Comparison of cancer incidence in domesticated versus wild animals, as the new insight into the cause and prevention of cancer in humans somayeh zaminpira- sorush niknamian
This document summarizes research comparing cancer rates in domesticated versus wild animals and discusses potential implications for human cancer prevention. It finds that domesticated animals like dogs and cats have much higher cancer rates than wild animals, likely due to differences in lifestyle and nutrition. Traditional diets and lifestyles may be important for preventing cancer in humans as well. Specific cancers that commonly occur in pets and their symptoms and risk factors are described. The role of the p53 tumor suppressor gene in various cancers is also discussed.
Updated version of molecular basis, with implied clinical aspect of the molecular basis.
(contents are taken from standard textbook and i dont own the copyright for the content details.)
This document provides an overview of cancer including types, causes, diagnosis, staging, treatment and prognosis. It discusses the major types of cancer that commonly affect men, women and children in the US. The pathophysiology section describes how genetic and epigenetic factors can cause normal cells to transform into cancer cells through mutations in oncogenes and tumor suppressor genes. Environmental exposures and lifestyle factors can also increase cancer risk by damaging DNA or altering gene expression through epigenetic changes. The progression of cancer involves a chain reaction of accumulating errors that allow cancer cells to evade controls on growth and spread.
Cancer is not one disease but many types with different characteristics. There are over 200 identified cancer types. Cancer is defined as uncontrolled cell growth and spread through the body. The global incidence of cancer is rising due to risk factors like lifestyle changes and aging populations. Common cancers worldwide include lung, breast, colorectal, prostate, and stomach cancers. Cancer development involves mutations that allow cells to evade controls on growth and survival.
On the cancer of wild animals somayeh zaminpira - sorush niknamianbanafsheh61
Cancer affects all animals containing eukaryotic cells. Less is known about the cancers that affect wild animals, since they move around and may not be easily observed for a long period of time. This review about cancers in wild animals may have useful data for the study of human cancers as well. Certain cancers in dinosaurs show that this metabolic disease is primitive and may have been around since the beginning of the multicellular organisms.
Cancer is characterized by uncontrolled cell growth and the spread of abnormal cells. It is caused by somatic mutations and disruptions to oncogenes and tumor suppressor genes. Many factors like environment, diet, smoking, and alcohol consumption can influence cancer risk. Researchers are studying the cancer genome to better understand carcinogenesis at the molecular level and identify new targeted therapies.
Introduction to cancer biology nerdy scientiststazib rahaman
This document discusses cancer initiation, promotion, and progression. It defines initiation as the creation of abnormal DNA from carcinogens. Promoters then stimulate replication of these neoplastic cells and tumor development. Enhancers increase the likelihood that nearby genes will be transcribed. Gene amplification and point mutations can further cancer progression. The document also summarizes a study finding COVID-19 infection is associated with severe outcomes in cancer patients, especially those undergoing immunosuppressive therapy, recommending screening and decreased immunosuppressive treatment during the pandemic.
Updated version of molecular basis, with implied clinical aspect of the molecular basis.
(contents are taken from standard textbook and i dont own the copyright for the content details.)
This document provides an overview of cancer including types, causes, diagnosis, staging, treatment and prognosis. It discusses the major types of cancer that commonly affect men, women and children in the US. The pathophysiology section describes how genetic and epigenetic factors can cause normal cells to transform into cancer cells through mutations in oncogenes and tumor suppressor genes. Environmental exposures and lifestyle factors can also increase cancer risk by damaging DNA or altering gene expression through epigenetic changes. The progression of cancer involves a chain reaction of accumulating errors that allow cancer cells to evade controls on growth and spread.
Cancer is not one disease but many types with different characteristics. There are over 200 identified cancer types. Cancer is defined as uncontrolled cell growth and spread through the body. The global incidence of cancer is rising due to risk factors like lifestyle changes and aging populations. Common cancers worldwide include lung, breast, colorectal, prostate, and stomach cancers. Cancer development involves mutations that allow cells to evade controls on growth and survival.
On the cancer of wild animals somayeh zaminpira - sorush niknamianbanafsheh61
Cancer affects all animals containing eukaryotic cells. Less is known about the cancers that affect wild animals, since they move around and may not be easily observed for a long period of time. This review about cancers in wild animals may have useful data for the study of human cancers as well. Certain cancers in dinosaurs show that this metabolic disease is primitive and may have been around since the beginning of the multicellular organisms.
Cancer is characterized by uncontrolled cell growth and the spread of abnormal cells. It is caused by somatic mutations and disruptions to oncogenes and tumor suppressor genes. Many factors like environment, diet, smoking, and alcohol consumption can influence cancer risk. Researchers are studying the cancer genome to better understand carcinogenesis at the molecular level and identify new targeted therapies.
Introduction to cancer biology nerdy scientiststazib rahaman
This document discusses cancer initiation, promotion, and progression. It defines initiation as the creation of abnormal DNA from carcinogens. Promoters then stimulate replication of these neoplastic cells and tumor development. Enhancers increase the likelihood that nearby genes will be transcribed. Gene amplification and point mutations can further cancer progression. The document also summarizes a study finding COVID-19 infection is associated with severe outcomes in cancer patients, especially those undergoing immunosuppressive therapy, recommending screening and decreased immunosuppressive treatment during the pandemic.
Natural history of human papillomavirus infections, cytologic and histologic ...Eliana Cordero
This document summarizes the natural history of human papillomavirus (HPV) infections and their relationship to abnormal cervical cytology and histology. It discusses that most HPV infections are transient and asymptomatic, but persistent infection with high-risk HPV types can sometimes lead to precancerous lesions and cervical cancer over many years. HPV type 16 is the most common high-risk type associated with cervical cancer. Screening programs have reduced cervical cancer rates in many countries, but it remains a health issue.
Squamous cell carcinoma is the most common head and neck malignancy, comprising over 90% of cases. Tobacco and alcohol are the most important causative agents, with risk increasing fourfold when used together. Tobacco contains over 40 known carcinogens like polycyclic hydrocarbons and nitrosamines. Cannabis smoking carries an even higher risk due to larger amounts of tar and aromatic hydrocarbons. While alcohol alone is not carcinogenic, it increases the risk from tobacco by facilitating tissue permeation of carcinogens. Viruses like HPV also contribute, with high-risk strains associated with malignant transformation. Prolonged sun exposure increases melanoma and lip cancer risk due to UV radiation. Occupational exposures like nickel, chromium,
Cancer is characterized by uncontrolled cellular growth and proliferation that can spread to other parts of the body. It is caused by both external factors like chemicals, radiation, viruses and internal factors such as genetic mutations. Cancer development is driven by changes in oncogenes and tumor suppressor genes. Tumor markers are substances produced by cancer cells or the body in response to cancer that can be detected in bodily fluids or tissues and used to diagnose certain cancer types. Some common tumor markers are CEA for colon cancer, AFP for liver cancer, and PSA for prostate cancer.
This document summarizes key concepts about cell biology and cancer. It states that cancer results from genetic changes related to cell division, growth control, genetic instability, and other cellular processes. These genetic changes disable normal controls that prevent uncontrolled cell growth and invasion. The abnormalities usually result from mutations in genes regulating cell division. Cancer development involves mutations in tumor suppressor genes and oncogenes. If cancer cells spread to other parts of the body, it can form new tumors in a process called metastasis.
Cancer is characterized by uncontrolled growth and spread of abnormal cells. If left untreated, cancer can result in death. The document discusses several types of cancer including lung cancer, the leading cause of cancer death, and colon cancer, the second most common cancer. It also covers cancer statistics, risk factors, screening, treatment milestones, and specific cancers like lung and colon cancer. Preventable lifestyle factors contribute to nearly 1/3 of cancer deaths in the US. Early detection through screening improves diagnosis and survival rates.
1) The study investigated differences in microRNA expression profiles between MYC translocation-positive and MYC translocation-negative Burkitt lymphoma cases to uncover potential molecular differences.
2) Unsupervised and supervised analyses revealed distinct microRNA expression patterns between the two groups, with four microRNAs found to be differentially expressed.
3) The different microRNA expression patterns were found to impact gene expression profiles, with DNMT1 and MYCN mRNA expression found to be upregulated in MYC translocation-negative cases. This suggests alternative mechanisms of MYC dysregulation and lymphomagenesis in the absence of translocation.
MAIN MOLECULAR MARKERS OF ORAL SQUAMOUS CELL CARCINOMA / dental implant cour...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document compares risk factors and molecular analysis of right-sided colon cancer and left-sided colon cancer. It discusses that:
- Right-sided colon cancer predominantly follows a MSI pathway while left-sided colon cancer follows a CIN pathway.
- There are differences in the embryonic development, function, and gene expression between the right and left colon that influence cancer risk.
- Certain risk factors like family history, inflammatory bowel disease, diet, and geographic location are associated with increased rates of either right-sided or left-sided colon cancers.
This document discusses the etiology of human cancer. It classifies the etiologic factors into 3 main groups: extrinsic, intrinsic, and unknown factors. Extrinsic factors include chemical, physical (radiation), and infectious agents (oncogenic viruses) and account for 85% of cancer etiology, particularly in adults. Intrinsic genetic factors are the main contributors to pediatric malignancies. Some key points made include that tobacco is responsible for 30% of cancers in the US, diet accounts for 35%, and viruses cause around 5% of cancers. Specific cancers are also linked to certain infectious agents, chemicals, radiation exposure, and genetic syndromes.
Cancer is an abnormal and uncontrolled division of cells, known as cancer cells that invade and destroy the surrounding tissues.
Generally cancer is defined as uncontrolled proliferation of cells without any differentiation. Cancer cells are different from normal cells in some aspects. They do not remain confined to one part of the body. They penetrate and infiltrate into the adjoining tissues and dislocate their functions. Some of the cancer cells get detached from the main site of origin and travel by blood and lymph to sites distant from the original tumour and form fresh colonies, called metastasis or secondary growth.
Cancer develops through a process called carcinogenesis where normal cells are transformed into cancer cells through genetic and epigenetic mutations. These mutations activate oncogenes and inactivate tumor suppressor genes, altering the biochemistry of the cell and causing uncontrolled cell growth. The mutations disrupt the typical cell division and growth factor signaling pathways, leading cells to proliferate autonomously without dependence on external growth signals. Common alterations include overproduction of growth factors, changes to growth factor receptors and intracellular signaling proteins, and autocrine signaling loops.
Cancer is abnormal and uncontrolled cell growth that can invade tissues and spread to other parts of the body. It is caused by changes in gene expression leading to imbalanced cell proliferation and death. The document defines several key cancer-related terms and describes how cancers are classified based on their origin, morphology, grade, and stage. It also lists several hallmarks of cancer cells, including unlimited growth, self-sufficiency, evasion of cell death, angiogenesis, and metastasis.
The document provides information about oncology nursing including objectives, cancer pathophysiology, risk factors, prevention, screening, detection methods, grading and staging of cancer, common cancer types, and nursing interventions. Key points include identifying risk factors from a patient's history, formulating nursing diagnoses, utilizing interventions to maintain health, providing spiritual care, and displaying caring behavior in the delivery of cancer nursing care.
Survivin is highly expressed in many cancers including oral cancer. It inhibits apoptosis and regulates cell cycle progression. The document discusses survivin expression in oral cancer tissues and pre-malignant lesions. Downregulation of survivin using siRNA inhibited oral cancer cell proliferation and induced apoptosis. Survivin inhibition also sensitized cancer cells to chemotherapy with paclitaxel and radiation therapy. Overexpression of survivin conferred resistance to these therapies. A lentivirus vector was developed to deliver survivin siRNA for cancer gene therapy.
Basic concept of Cancer and cancer cell.Madhur sharma
Cancer is a genetic disease caused by alterations in genes that can result from mutations during cell division, exposure to external agents, or randomly. There are four main types of cancer - carcinomas, sarcomas, lymphomas, and leukemias. Cancer is characterized by cellular changes that promote uncontrolled growth. Some key cancer genes include oncogenes that promote growth and tumor suppressor genes that normally inhibit growth. Examples are discussed like MYC, RAS, P53, and RB. New strategies to treat cancer focus on immunotherapy, inhibiting cancer-promoting proteins, and blocking angiogenesis within tumors.
The document lists over 100 "Supplementary Sidebars" numbered from 1.1 to 16.11. Each sidebar appears to cover a different topic related to cancer biology, with many sidebars focusing on specific experiments, findings, techniques, or hypotheses discussed in the field. The sidebars range widely in their subject matter and depth.
This document provides an overview of cancer biology. It defines cancer as the abnormal proliferation of cells and discusses the study of cancer (oncology). The document outlines the different types of tumors and cancers based on cell type and tissue of origin. It also explores the causes of cancer including radiation, chemicals and viruses. Key properties of cancer cells like lack of contact inhibition and defective differentiation are examined. The roles of oncogenes and tumor suppressor genes in cancer development are described. The document concludes with a review of cancer treatment methods such as surgery, chemotherapy, radiation therapy and prevention strategies.
Cancer is the second leading cause of death worldwide after cardiovascular disease. In India, an estimated 2.25 million people are living with cancer, with over 11 lakh new cases registered annually. Some key statistics for India include one woman dying of cervical cancer every 8 minutes and two women dying of breast cancer for every one diagnosed. Tumor markers are substances produced by cancerous tissues or the body in response to cancer that can help detect or monitor cancer. Some common tumor markers are CEA, AFP, CA125, and PSA. Tumor markers can be used for screening, diagnosis, staging, prognosis, and monitoring treatment effectiveness and recurrence. Characteristics of ideal tumor markers include cancer specificity, high sensitivity and specificity for detection
Cancer Report by SVCT Intern Neetu yadav(JBS)Svct Delhi
This social internship report summarizes Neetu Yadav's work with the Siddhartha Vashisht Charitable Trust to raise awareness about cancer. The report provides background information on cancer including common causes like tobacco, diet, infections, and environmental factors. It also describes signs and symptoms of cancer and different types of cancers. The report covers Neetu's internship activities from February 23rd to March 25th, 2011 with the goal of educating the public about cancer prevention and early detection.
Cancer arises from genetic changes in cells that cause uncontrolled growth and spread. The document discusses cancer pathogenesis, classification, stages, risk factors like carcinogens, and prevention strategies. It notes that in 2012 there were estimated 14 million new cancer cases worldwide resulting in 7.6 million deaths, with lung, breast, colorectal, and stomach cancer being most common. Prevention involves controlling risk factors like tobacco, promoting hygiene, vaccinations, and treating precancerous lesions.
This document discusses gene therapy as a promising treatment for breast cancer. It begins by providing background on breast cancer prevalence and current treatment options. It then describes how gene therapy could target mutated genes, cancer cell markers, block metastasis, and induce apoptosis. The document focuses on gene therapy approaches for breast cancer, including using antisense technology to inhibit pathogenic genes, RNA interference to downregulate genes like c-myc, and suicide genes to make cancer cells more sensitive to chemotherapy.
This document discusses neoplasia (new growths) and tumor classification. It defines neoplasia as abnormal tissue growth that exceeds normal limits. Tumors are classified based on their tissue of origin and whether they are benign or malignant. Benign tumors are named by adding "-oma" to the tissue type, such as fibroma. Malignant tumors arising from mesenchymal tissue are called sarcomas, while those from epithelial tissue are called carcinomas, such as adenocarcinoma. Classification can also be based on histological appearance, anatomical location, or cell of origin.
Natural history of human papillomavirus infections, cytologic and histologic ...Eliana Cordero
This document summarizes the natural history of human papillomavirus (HPV) infections and their relationship to abnormal cervical cytology and histology. It discusses that most HPV infections are transient and asymptomatic, but persistent infection with high-risk HPV types can sometimes lead to precancerous lesions and cervical cancer over many years. HPV type 16 is the most common high-risk type associated with cervical cancer. Screening programs have reduced cervical cancer rates in many countries, but it remains a health issue.
Squamous cell carcinoma is the most common head and neck malignancy, comprising over 90% of cases. Tobacco and alcohol are the most important causative agents, with risk increasing fourfold when used together. Tobacco contains over 40 known carcinogens like polycyclic hydrocarbons and nitrosamines. Cannabis smoking carries an even higher risk due to larger amounts of tar and aromatic hydrocarbons. While alcohol alone is not carcinogenic, it increases the risk from tobacco by facilitating tissue permeation of carcinogens. Viruses like HPV also contribute, with high-risk strains associated with malignant transformation. Prolonged sun exposure increases melanoma and lip cancer risk due to UV radiation. Occupational exposures like nickel, chromium,
Cancer is characterized by uncontrolled cellular growth and proliferation that can spread to other parts of the body. It is caused by both external factors like chemicals, radiation, viruses and internal factors such as genetic mutations. Cancer development is driven by changes in oncogenes and tumor suppressor genes. Tumor markers are substances produced by cancer cells or the body in response to cancer that can be detected in bodily fluids or tissues and used to diagnose certain cancer types. Some common tumor markers are CEA for colon cancer, AFP for liver cancer, and PSA for prostate cancer.
This document summarizes key concepts about cell biology and cancer. It states that cancer results from genetic changes related to cell division, growth control, genetic instability, and other cellular processes. These genetic changes disable normal controls that prevent uncontrolled cell growth and invasion. The abnormalities usually result from mutations in genes regulating cell division. Cancer development involves mutations in tumor suppressor genes and oncogenes. If cancer cells spread to other parts of the body, it can form new tumors in a process called metastasis.
Cancer is characterized by uncontrolled growth and spread of abnormal cells. If left untreated, cancer can result in death. The document discusses several types of cancer including lung cancer, the leading cause of cancer death, and colon cancer, the second most common cancer. It also covers cancer statistics, risk factors, screening, treatment milestones, and specific cancers like lung and colon cancer. Preventable lifestyle factors contribute to nearly 1/3 of cancer deaths in the US. Early detection through screening improves diagnosis and survival rates.
1) The study investigated differences in microRNA expression profiles between MYC translocation-positive and MYC translocation-negative Burkitt lymphoma cases to uncover potential molecular differences.
2) Unsupervised and supervised analyses revealed distinct microRNA expression patterns between the two groups, with four microRNAs found to be differentially expressed.
3) The different microRNA expression patterns were found to impact gene expression profiles, with DNMT1 and MYCN mRNA expression found to be upregulated in MYC translocation-negative cases. This suggests alternative mechanisms of MYC dysregulation and lymphomagenesis in the absence of translocation.
MAIN MOLECULAR MARKERS OF ORAL SQUAMOUS CELL CARCINOMA / dental implant cour...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
This document compares risk factors and molecular analysis of right-sided colon cancer and left-sided colon cancer. It discusses that:
- Right-sided colon cancer predominantly follows a MSI pathway while left-sided colon cancer follows a CIN pathway.
- There are differences in the embryonic development, function, and gene expression between the right and left colon that influence cancer risk.
- Certain risk factors like family history, inflammatory bowel disease, diet, and geographic location are associated with increased rates of either right-sided or left-sided colon cancers.
This document discusses the etiology of human cancer. It classifies the etiologic factors into 3 main groups: extrinsic, intrinsic, and unknown factors. Extrinsic factors include chemical, physical (radiation), and infectious agents (oncogenic viruses) and account for 85% of cancer etiology, particularly in adults. Intrinsic genetic factors are the main contributors to pediatric malignancies. Some key points made include that tobacco is responsible for 30% of cancers in the US, diet accounts for 35%, and viruses cause around 5% of cancers. Specific cancers are also linked to certain infectious agents, chemicals, radiation exposure, and genetic syndromes.
Cancer is an abnormal and uncontrolled division of cells, known as cancer cells that invade and destroy the surrounding tissues.
Generally cancer is defined as uncontrolled proliferation of cells without any differentiation. Cancer cells are different from normal cells in some aspects. They do not remain confined to one part of the body. They penetrate and infiltrate into the adjoining tissues and dislocate their functions. Some of the cancer cells get detached from the main site of origin and travel by blood and lymph to sites distant from the original tumour and form fresh colonies, called metastasis or secondary growth.
Cancer develops through a process called carcinogenesis where normal cells are transformed into cancer cells through genetic and epigenetic mutations. These mutations activate oncogenes and inactivate tumor suppressor genes, altering the biochemistry of the cell and causing uncontrolled cell growth. The mutations disrupt the typical cell division and growth factor signaling pathways, leading cells to proliferate autonomously without dependence on external growth signals. Common alterations include overproduction of growth factors, changes to growth factor receptors and intracellular signaling proteins, and autocrine signaling loops.
Cancer is abnormal and uncontrolled cell growth that can invade tissues and spread to other parts of the body. It is caused by changes in gene expression leading to imbalanced cell proliferation and death. The document defines several key cancer-related terms and describes how cancers are classified based on their origin, morphology, grade, and stage. It also lists several hallmarks of cancer cells, including unlimited growth, self-sufficiency, evasion of cell death, angiogenesis, and metastasis.
The document provides information about oncology nursing including objectives, cancer pathophysiology, risk factors, prevention, screening, detection methods, grading and staging of cancer, common cancer types, and nursing interventions. Key points include identifying risk factors from a patient's history, formulating nursing diagnoses, utilizing interventions to maintain health, providing spiritual care, and displaying caring behavior in the delivery of cancer nursing care.
Survivin is highly expressed in many cancers including oral cancer. It inhibits apoptosis and regulates cell cycle progression. The document discusses survivin expression in oral cancer tissues and pre-malignant lesions. Downregulation of survivin using siRNA inhibited oral cancer cell proliferation and induced apoptosis. Survivin inhibition also sensitized cancer cells to chemotherapy with paclitaxel and radiation therapy. Overexpression of survivin conferred resistance to these therapies. A lentivirus vector was developed to deliver survivin siRNA for cancer gene therapy.
Basic concept of Cancer and cancer cell.Madhur sharma
Cancer is a genetic disease caused by alterations in genes that can result from mutations during cell division, exposure to external agents, or randomly. There are four main types of cancer - carcinomas, sarcomas, lymphomas, and leukemias. Cancer is characterized by cellular changes that promote uncontrolled growth. Some key cancer genes include oncogenes that promote growth and tumor suppressor genes that normally inhibit growth. Examples are discussed like MYC, RAS, P53, and RB. New strategies to treat cancer focus on immunotherapy, inhibiting cancer-promoting proteins, and blocking angiogenesis within tumors.
The document lists over 100 "Supplementary Sidebars" numbered from 1.1 to 16.11. Each sidebar appears to cover a different topic related to cancer biology, with many sidebars focusing on specific experiments, findings, techniques, or hypotheses discussed in the field. The sidebars range widely in their subject matter and depth.
This document provides an overview of cancer biology. It defines cancer as the abnormal proliferation of cells and discusses the study of cancer (oncology). The document outlines the different types of tumors and cancers based on cell type and tissue of origin. It also explores the causes of cancer including radiation, chemicals and viruses. Key properties of cancer cells like lack of contact inhibition and defective differentiation are examined. The roles of oncogenes and tumor suppressor genes in cancer development are described. The document concludes with a review of cancer treatment methods such as surgery, chemotherapy, radiation therapy and prevention strategies.
Similar to Comparison of cancer incidence in domesticated versus wild animals, as the new insight into the cause and prevention of cancer in humans somayeh zaminpira- sorush niknamian
Cancer is the second leading cause of death worldwide after cardiovascular disease. In India, an estimated 2.25 million people are living with cancer, with over 11 lakh new cases registered annually. Some key statistics for India include one woman dying of cervical cancer every 8 minutes and two women dying of breast cancer for every one diagnosed. Tumor markers are substances produced by cancerous tissues or the body in response to cancer that can help detect or monitor cancer. Some common tumor markers are CEA, AFP, CA125, and PSA. Tumor markers can be used for screening, diagnosis, staging, prognosis, and monitoring treatment effectiveness and recurrence. Characteristics of ideal tumor markers include cancer specificity, high sensitivity and specificity for detection
Cancer Report by SVCT Intern Neetu yadav(JBS)Svct Delhi
This social internship report summarizes Neetu Yadav's work with the Siddhartha Vashisht Charitable Trust to raise awareness about cancer. The report provides background information on cancer including common causes like tobacco, diet, infections, and environmental factors. It also describes signs and symptoms of cancer and different types of cancers. The report covers Neetu's internship activities from February 23rd to March 25th, 2011 with the goal of educating the public about cancer prevention and early detection.
Cancer arises from genetic changes in cells that cause uncontrolled growth and spread. The document discusses cancer pathogenesis, classification, stages, risk factors like carcinogens, and prevention strategies. It notes that in 2012 there were estimated 14 million new cancer cases worldwide resulting in 7.6 million deaths, with lung, breast, colorectal, and stomach cancer being most common. Prevention involves controlling risk factors like tobacco, promoting hygiene, vaccinations, and treating precancerous lesions.
This document discusses gene therapy as a promising treatment for breast cancer. It begins by providing background on breast cancer prevalence and current treatment options. It then describes how gene therapy could target mutated genes, cancer cell markers, block metastasis, and induce apoptosis. The document focuses on gene therapy approaches for breast cancer, including using antisense technology to inhibit pathogenic genes, RNA interference to downregulate genes like c-myc, and suicide genes to make cancer cells more sensitive to chemotherapy.
This document discusses neoplasia (new growths) and tumor classification. It defines neoplasia as abnormal tissue growth that exceeds normal limits. Tumors are classified based on their tissue of origin and whether they are benign or malignant. Benign tumors are named by adding "-oma" to the tissue type, such as fibroma. Malignant tumors arising from mesenchymal tissue are called sarcomas, while those from epithelial tissue are called carcinomas, such as adenocarcinoma. Classification can also be based on histological appearance, anatomical location, or cell of origin.
Cancer is caused by uncontrolled cell growth and can affect people of all ages. While genetics play a small role, environmental factors are responsible for the vast majority of cancers. Some known causes of cancer include tobacco use, certain infections, radiation, poor diet/obesity, and environmental pollutants. There is no single cause of cancer for most individuals, as cancer is usually the result of multiple factors. Certain inherited genetic mutations do significantly increase cancer risk for some people. Prolonged exposure to carcinogens like asbestos can also cause specific types of cancer. Overall, cancer remains a major public health problem worldwide.
This document discusses neoplasia and cancer. It defines key terms like neoplasm, tumor, benign and malignant tumors. It explains that neoplasia is abnormal cell growth, and tumors can be benign (non-cancerous) or malignant (cancerous). Malignant tumors are able to invade other tissues and metastasize (spread) to other parts of the body. The document also discusses cancer risk factors, carcinogenesis (the process of cancer development), common carcinogens (cancer-causing agents) like chemicals, radiation and viruses, and the process of metastasis (cancer spreading).
Oncology and surgical practice are becoming more integrated, as surgeons are often responsible for initially diagnosing and managing solid tumors. A thorough understanding of cancer epidemiology, etiology, staging, and natural history is required to determine the optimal surgical therapy for each patient. Tumor cells acquire several characteristics before becoming fully malignant, including establishing independence from normal growth controls, achieving immortality and angiogenesis, and developing the abilities to invade other tissues and disseminate throughout the body. Both genetic and environmental factors contribute to cancer development in complex ways. A combination of inherited predispositions and exposures to carcinogenic chemicals, viruses, radiation, and other external factors drive the transformation of normal cells into malignant tumors.
This document summarizes research on the effect of bacteria on healthy and cancerous cells. It finds that while most bacteria do not cause disease, some types of bacteria can increase the risk of cancer, such as Helicobacter pylori which increases the risk of stomach cancer. The document also discusses how some bacterial infections can transform into malignant tumors through genetic mutations. It provides background on cancer development and the role of genetic and epigenetic factors in normal cells transforming into cancerous cells.
This document discusses the genetic and epigenetic changes that cause cancer. It explains that cancer arises due to alterations that disrupt normal cell proliferation, senescence, and death. Key changes include mutations in oncogenes that increase cell growth and tumor suppressor genes that normally inhibit growth. Cancer development involves multiple genetic hits over time that transform cells and allow unchecked growth. Epigenetic alterations like DNA methylation and histone modifications also contribute to carcinogenesis. The complex interplay between a person's genetic factors and environmental exposures ultimately leads to the development of cancer.
This document discusses oncogenic viruses and their role in cancer development. It begins with an introduction to viruses and cancer. Key points include that viruses can integrate into host cell DNA and express viral oncoproteins that alter cell growth pathways, leading to cellular transformation over multiple steps. Major oncogenic viruses discussed are human papillomavirus (HPV), hepatitis B and C viruses, Epstein-Barr virus, Kaposi's sarcoma-associated herpesvirus, and human T-cell leukemia virus. The mechanisms of oncogenesis include introducing new oncogenes, altering expression of cellular genes, and affecting DNA repair and genetic stability.
Cancer is caused by uncontrolled cell growth and can spread throughout the body. The three main properties of cancer cells are that they grow aggressively, can invade nearby tissues, and may spread (metastasize) to distant areas. Nearly all cancers are caused by genetic abnormalities within cells that affect genes regulating cell growth and death. Some genetic changes are inherited, but many are acquired from environmental exposures like tobacco smoke, radiation, chemicals or infectious agents. Cancer development involves multiple genetic mutations that cause cells to proliferate uncontrollably and evade the immune system.
Professor Jurasunas explains what is cancer and how it develops. He explains the nature of this disease, and why cells mutate, elaborating on P53 and apoptosis. He explains why Cancer is a silent killer, while addressing the cellular cycle.
Cancer is caused by mutations in genes that control cell growth called oncogenes and tumor suppressor genes. Oncogenes are mutated forms of normal genes that cause cells to grow uncontrollably, while tumor suppressor genes normally slow cell growth but are inactivated in cancer. Many cancers are caused by a combination of inherited gene mutations and acquired mutations from environmental exposures. Identifying mutations in specific oncogenes and tumor suppressor genes can help determine cancer risk and guide treatment decisions. The drug Herceptin targets the HER2/neu oncogene expressed in some breast cancers.
Human health has many aspects, we need to feed the diet which provides better nutrition and gives good health, an absence of disease and good behaviour. There are many health-related problems and conditions are responsible for the weak health and sometimes death causing illness, in which cancer is one most common health risk in human healthcare. Cancer is the state in which cell division is uncontrolled which damage the cells and in the last stage, if incurable caused death. There are many reasons why cell got infected due to cancerous infections, in which food habits and quality of foodstuffs are also increased the risk of cancer, like mycotoxins contamination in the food. MSG additives, taste enhancer, food colouring etc. done by the chemical processing which produces toxins inside the during the oxidation process of food. Cancer is causes of death rate higher than other health risks all over the world. The number of cancer cases is likely to rise up to 24 million by 2035. Several studies were performed in the last years in order to explore and analyze associations between diet and risk of cancer. The risk of cancer is depending on the degree of exposure to contaminated food, availability of nutrients in the body, dietary pattern and lifestyle as well as food behaviour. Research from a number of sources provides information that some vegetables, fruits, and whole grains, dietary fibre, certain micronutrients, few fatty acids and physical activity protect against cancers. Whereas poor dietary intake, imbalanced nutrition, less physical activity trances fatty acids, food processing and cooking method may increase risks.
Keywords: Cancer, death, nutrition, fruits and vegetable
This document provides information on childhood tumors, with a focus on Burkitt lymphoma. Some key points:
- Burkitt lymphoma is the most common childhood cancer in tropical Africa, associated with Epstein-Barr virus and malaria. It is characterized by very rapid proliferation and a "starry sky" appearance on histology.
- The disease is staged based on tumor location and spread. Treatment involves chemotherapy like cyclophosphamide and vincristine, with central nervous system prophylaxis. Prognosis is generally good if caught early, though relapse is common.
- Other childhood cancers discussed include acute leukemias, brain tumors, Hodgkin's lymphoma, and the role of genes like TP53 and
The document discusses paediatric oncology and acute leukemia. It notes that acute leukemia is the most common childhood malignancy, representing 35% of cases, with acute lymphoblastic leukemia (ALL) making up 27% specifically. ALL is most common in children aged 2-6 years old and presents with pallor, bruising, hepatosplenomegaly and lymphadenopathy. Proper treatment can cure approximately 70% of children with ALL. Treatment involves induction of remission, consolidation therapy, and 2-3 years of maintenance therapy to eliminate remaining leukemia cells.
Similar to Comparison of cancer incidence in domesticated versus wild animals, as the new insight into the cause and prevention of cancer in humans somayeh zaminpira- sorush niknamian (20)
The Impact of Serotonin on the Cause and Treatment of Cancerbanafsheh61
This review article goes through many researches based on the effectiveness of the neurotransmitter serotonin on cancer cells and also the impact of SSRIs (selective serotonin reuptake inhibitors) drugs on the cause of certain types of cancers. Serotonin has been shown to be a mutagenic factor for a wide range of normal and tumor cells. Serotonin exhibits a growth stimulatory effect in aggressive cancers and carcinoids usually through 5- HT1 and 5-HT2 receptors. In contrast, low doses of serotonin can inhibit tumor growth via the decrease of blood supply to the tumor, suggesting that the role of serotonin on tumor growth is concentration-dependent. Serum serotonin level was found to be suitable for prognosis evaluation of urothelial carcinoma in the urinary bladder, adenocarcinoma of the prostate and renal cell carcinoma.The mechanism that connect serotonin with tumor evolution seem to be related to the serotonin impact on tumor associated macrophages.
Introducing the Evolutionary Cell Memory (ECM) Hypothesis banafsheh61
This research study has gone through more than 34 sample tumors in Violet Cancer Institute (VCI) to find the cancer
cells’ resemblances to the primitive eukaryote cells in 3.5 billion years ago before the entrance of the mitochondria
into the eukaryote cells as endosymbionts. Nearly all the samples showed that the mitochondria inside the cells were
not working properly. Their cristae were damaged or the mitochondria did not work or better said “shut down”
inside the cancer cells. This study introduces a new hypothesis called the Evolutionary Cell Memory (ECM) based on
the Lamarckian Evolutionary Hypothesis and the Evolutionary Metabolic Hypothesis of Cancer introduced by the
Somayeh Zaminpira and Sorush Niknamian in 2017.
Introducing the Prodotis M1-Macrophage Hypothesis of Cancer Metastasis (PMMH)banafsheh61
ancer tumor would metastasize. To find the best answer, we have reviewed the cases from 1889 to 2017 in humans, animals and plants tumors. Metastasis involves a complex series of steps in which cancer cells leave the original tumor site and migrate to other parts of the body. The macrophage type M1, seems the main cause of metastasis in humans and animal cancers. In plants, we have not found any case of metastasis and the reason is that they lack the macrophages. Nearly all metastasis hypothesis cannot bring out the next target tissue by even 80%, however; the most correct hypothesis is James Ewing’s theory which challenged the seed and soil theory and proposed that metastasis occurs purely by anatomic and mechanical routes. By putting together all the findings and data from the mentioned dates, we have put forth a new hypothesis which
The main cause and prevention of multiple sclerosis and its relation to cancerbanafsheh61
This document summarizes a research paper on the Evolutionary Metabolic Hypothesis of Multiple Sclerosis (EMHMS). It was authored by Somayeh Zaminpira and Sorush Niknamian from the University of Cambridge. The paper proposes that multiple factors may cause MS, including viral infections, oxidative stress, lack of sunlight exposure, and increased inflammation. It finds that environmental temperature and proximity to the equator are important factors, with higher rates of MS and cancer seen in populations farther from the equator like Australia. The paper argues that mitochondrial dysfunction leading to increased reactive oxygen species is a likely primary cause of MS and cancer.
How butterfly effect or deterministic chaos theory in theorical physics expla...banafsheh61
The document discusses how chaos theory and the butterfly effect can explain the main cause of cancer. It proposes that small increases in reactive oxygen species above normal limits can cause chaos in normal cells by damaging mitochondria. This mitochondrial damage disrupts communication between the nucleus and mitochondria, causing the nucleus to signal fermentation rather than apoptosis, similar to early single-celled organisms. Over time, this evolutionary reversion enables cancer progression by allowing cells to produce energy without intact mitochondria.
Introduction to the evolutionary metabolic medicine based on mitochondrial dy...banafsheh61
This document provides information about a company called Evolutionary Metabolic Medicine based in Tehran, Iran that studies mitochondrial dysfunction. It introduces mitochondrial evolution and function, describing how mitochondria originated from bacteria and regulate cell metabolism. Nearly all human diseases are related to mitochondrial dysfunction caused by reactive oxygen species production during respiration. The summary introduces a new branch of medicine focused on treating diseases by addressing mitochondrial metabolic changes.
INTRODUCTION TO THE EVOLUTIONARY METABOLIC MEDICINE BASED ON MITOCHONDRIAL DY...banafsheh61
This document introduces evolutionary metabolic medicine, which focuses on mitochondrial dysfunction and metabolic changes in cells. It discusses how mitochondria produce energy and reactive oxygen species, and how damage to mitochondria can lead to diseases. Nearly all human diseases are related to mitochondrial dysfunction and inheritance. While reactive oxygen species are normal byproducts, excessive amounts can cause oxidative damage over time, accumulating in tissues and decreasing fitness. This damage contributes to aging and diseases like Alzheimer's. The conclusion proposes that mitochondrial dysfunction is a primary cause of many major diseases, and that an evolutionary perspective on cellular metabolism and dysfunction is needed to develop new treatments.
HOW BUTTERFLY EFFECT OR DETERMINISTIC CHAOS THEORY IN THEORETICAL RHYSICS EXP...banafsheh61
This document discusses how chaos theory and the butterfly effect from physics can explain the main cause of cancer. It introduces chaos theory and the butterfly effect, which states that small changes can lead to large differences later on. It then discusses how increasing reactive oxygen species above normal limits inside cells can damage mitochondria and cause chaos, changing cells from apoptosis to fermentation. This evolutionary change may be the main driver of cancer as it allows cells to avoid death and produce energy without mitochondria. The document provides background on mitochondria, reactive oxygen species, oxidative damage, and the connection between the nucleus and mitochondria.
THE MAIN CAUSE AND PREVENTION OF MULTIPLE SCLEROSIS AND ITS RELATION TO CANCERbanafsheh61
This document discusses the potential causes of multiple sclerosis (MS) and its relationship to cancer. It introduces the Evolutionary Metabolic Hypothesis of MS, which proposes that MS is caused by an increase in reactive oxygen species and reactive nitrogen species inside cells. This oxidative stress damages mitochondria and leads to inflammation and demyelination in the brain and spinal cord. The document reviews several studies that link mitochondrial dysfunction and oxidative damage to MS. It also discusses how cancer cells revert to an ancient fermentation process instead of using mitochondria, in order to avoid apoptosis. Therefore, both MS and cancer may be caused by mitochondrial damage and the resulting oxidative stress.
the main treatment of cancer, somayeh zaminpira and sorush niknamianbanafsheh61
This research article summarizes the key differences between how cancer cells and normal cells produce energy. It finds that the main difference is that cancer cells rely primarily on fermentation to produce energy rather than the more efficient aerobic respiration that normal cells use. Fermentation produces much less ATP than aerobic respiration. The article reviews over 200 studies on the topic and finds consistent evidence that cancer cells have damaged and abnormal mitochondria that prevent them from efficiently performing aerobic respiration. This forces cancer cells to use the less efficient fermentation process to produce energy and survive.
EVOLUTIONARY METABOLIC HYPOTHESIS OF CANCERbanafsheh61
This document summarizes the Evolutionary Metabolic Hypothesis of Cancer (EMHC) proposed by the authors. The EMHC builds upon the Warburg Hypothesis, which posits that cancer cells generate energy through fermentation of glucose rather than oxidative phosphorylation in mitochondria. The authors conducted a study treating 54 cancer patients with a ketogenic diet and ozone therapy, finding significant reductions in tumor size across several cancer types. They propose a mathematical model describing cancer growth based on energy conservation principles, similarly to models of organism development. The EMHC views cancer as both an evolutionary and metabolic disease influenced by mutations affecting energy production pathways.
HOW BOHR EFFECT ADMIT THE OZONE THERAPY PLUS SPECIFIC KETO DIETIN TREATMENT O...banafsheh61
This document discusses how the Bohr effect and a specific ketogenic diet plus ozone therapy can help treat cancer. The Bohr effect explains that hemoglobin releases more oxygen when the blood's pH is lower. Cancer tumors produce lactic acid, lowering pH in tissues. Ozone therapy and a ketogenic diet both raise blood pH, allowing more oxygen to be absorbed from the lungs and transported to acidic tumor tissues. This extra oxygen supply may help force cancer cells into apoptosis and treat the cancer.
Agricultural revolution in the line of human evolution is the onset of nutrit...banafsheh61
This document discusses human evolution and shifts in human diet and nutrition over time. It outlines the following key points:
1) Early primates starting 65 million years ago ate mostly insects and later shifted to a mostly plant-based diet.
2) The first hominids like Australopithecus around 3.7 million years ago were herbivorous but evidence suggests they ate some meat.
3) Genus Homo emerged around 2.3 million years ago and species like Homo habilis were gatherer-hunters that scavenged and potentially hunted meat, though plants remained the staple.
4) Later humans like Homo erectus from 1.7-230,
The impact of the serotonin on the cause and treatment of cancerbanafsheh61
Serotonin plays a role in cancer development and progression through several mechanisms:
1. Serotonin can stimulate the growth of some cancer cells through serotonin receptors.
2. Low doses of serotonin can inhibit tumor growth by decreasing blood supply.
3. Serotonin impacts tumor-associated macrophages and their production of proteins that influence angiogenesis.
4. Serotonin levels have been found to correlate with prognosis for some cancer types like bladder and prostate cancer.
Agricultural revolution in the line of human evolution is the onset of nutrit...banafsheh61
This document discusses human evolution and shifts in human diet and nutrition over time. It outlines the following key points:
1) Early primates starting 65 million years ago ate mostly insects and later shifted to a mostly plant-based diet.
2) The first hominids like Australopithecus around 3.7 million years ago were herbivorous but evidence suggests they ate some meat.
3) Genus Homo emerged around 2.3 million years ago and ate a diet of plants and increasing amounts of scavenged and hunted meat, though plants remained the primary food source.
4) Homo erectus between 1.7-230,000 years ago consumed more meat and
On the cancer of wild animals somayeh zaminpira - sorush niknamianbanafsheh61
This document summarizes research on cancers found in wild animals. It discusses reports of cancer in dinosaur fossils, showing cancer has affected multi-cellular organisms for millions of years. It also describes an unusual transmissible cancer affecting Tasmanian devils, where cancer cells are transmitted between animals. Finally, it mentions several other reports of cancer in sharks, fish, and naked mole rats, demonstrating cancer can impact a wide range of wild species.
Consumption of saturated animal fats in the diet of humans may decrease the r...banafsheh61
This document summarizes research on the relationship between saturated fat consumption and heart disease risk. It discusses several studies that found no correlation or an inverse correlation between saturated fat intake and heart disease rates. It also profiles the diets of various tribes and populations that consume high amounts of saturated fat from animals but have low rates of heart disease. The document concludes that based on studies of healthy populations and biological needs, consuming saturated fats from animals may not increase and could potentially decrease risk of heart disease.
Vegetable oils consumption as one of the leading cause of cancer and heart di...banafsheh61
This review takes a deep look at increases in the incidence of cancer and heart disease after the introduction of industrial vegetable oils in the world. Most vegetable oils are highly processed and refined products, which completely lack the essential nutrients. Omega-6 Linoleic acid from vegetable oils increases oxidative stress in the body of humans, contributing to endothelial dysfunction and heart disease. The consumption of these harmful oils which are high in mega-6 polyunsaturated fats results in changing the structure of cell membrane which contribute to increasing inflammation and the incidence of cancer.
The prime cause and treatment of cancer somayeh zaminpira - sorush niknamianbanafsheh61
This meta-analysis research has gone through more than 200 studies from 1934 to 2016 to find the differences and similarities in cancer cells, mostly the cause. The most important difference between normal cells and cancer cells is how they respire. Normal cells use the sophisticated process of respiration to efficiently turn any kind of nutrient that is fat, carbohydrate or protein into high amounts of energy in the form of ATP. This process requires oxygen and breaks food down completely into harmless carbon dioxide and water. Cancer cells use a primitive process of fermentation to inefficiently turn either glucose from carbohydrates or the amino acid glutamine from protein into small quantities of energy in the form of ATP. This process does not require oxygen, and only partially breaks down food molecules into lactic acid and ammonia, which are toxic waste products. The most important result is that fatty acids or better told fats cannot be fermented by cells. This research mentions the role of ROS and inflammation in causing mitochondrial damage and answers the most important questions behind cancer cause and mentions some beneficial methods in preventing and treatment of cancer.
Reactive oxygen species along with reactive nitrogen species (rosrns) as the ...banafsheh61
Multiple Sclerosis is a condition of demyelination of the nerve cells in the brain and spinal cord. It is possible that multiple factors are involved in causing multiple sclerosis, including DNA defects in nuclear and mitochondrial genomes, viral infection, hypoxia, oxidative stress, lack of sunlight, and increased macrophages and lymphocytes in the brain. This meta-analysis has gone through many researches and reviews to find the similarities and differences in the cause of this disease. The role of mitochondrial metabolism, environmental temperature and distance from the equator has been discussed in this research, and the amounts of Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) has been found to be the most possible cause of multiple sclerosis in men and women
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
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Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Comparison of cancer incidence in domesticated versus wild animals, as the new insight into the cause and prevention of cancer in humans somayeh zaminpira- sorush niknamian
1. Journal of Multidisciplinary Engineering Science and Technology (JMEST)
ISSN: 2458-9403
Vol. 4 Issue 7, July - 2017
www.jmest.org
JMESTN42352028 7579
Comparison of Cancer Incidence in
Domesticated Versus Wild Animals, as the New
Insight into the Cause and Prevention of
Cancer in Humans
*
Somayeh Zaminpira Ms.c.
Ms.c. in Clinical Psychology, Olom Tahghighat University
1
Young Researchers and Elite club, Tehran, Iran
Banafsheh_pira@yahoo.com
Sorush Niknamian Bs.c.
2
Young Researchers and Elite Club, Tehran. Iran
Sorushniknamian61@gmail.com
Abstract—This review research article has gone
through the cancer incidence in domesticated and
wild animals. Cancer causes approximately 50
percent of deaths in pets over the age of 10. Some
common types of cancers in pets include are skin,
breast, head and neck, lymphoma, leukemia,
testicular, abdominal, and bone. Cancers
commonly found in pets that are also commonly
found in humans are lymphoma, melanoma, and
osteosarcoma. The two most common household
pets, dogs tend to get cancer at a higher rate than
cats. The cancer may be treatable depending on
cancer type and the treatment options for dogs
and cats are similar to those for humans. The
cancer incidence in wild animals is much less
than domesticated animals which are due to their
lifestyle and nutrition type. The reason behind the
cancer incidence in wild animals is the
environmental parasites, viruses, bacteria and
fungi. It seems the traditional lifestyle and
nutrition is very important in the prevention of the
cancer in humans as well.
Keywords—Domesticated animals, wild
animals, cancer, traditional nutrition
I. INTRODUCTION
Peto's paradox
Peto's Paradox is the observation, that at the
species level, the incidence of cancer does not appear
to correlate with the number of cells in an organism.
[58] For instance, the incidence of cancer in humans
is much higher than the incidence of cancer in whales.
[59] This is despite the fact that a whale has many
more cells than a human. If the probability of
carcinogenesis were constant across cells, one would
expect whales to have a higher incidence of cancer
than humans. The same is true of elephants. In
October 2015, two independent studies showed that
elephants have 20 copies of a tumor suppressor gene
TP53 in their genome, where humans and other
mammals have only one, thus providing a possible
solution to the paradox. [60]
P53 gene and the role in cancer
If the TP53 gene is damaged, tumor suppression is
severely compromised. People who inherit only one
functional copy of the TP53 gene will most likely
develop tumors in early adulthood, a disorder known
as Li-Fraumeni syndrome. The TP53 gene can also
be modified by mutagens like chemicals, radiation, or
viruses, increasing the likelihood for uncontrolled cell
division. More than 50 percent of human tumors
contain a mutation or deletion of the TP53 gene. [61]
Loss of p53 creates genomic instability that most often
results in an aneuploidy phenotype. [62] Increasing
the amount of p53 may seem a solution for treatment
of tumors or prevention of their spreading. This,
however, is not a usable method of treatment, since it
can cause premature aging. [63] Restoring
endogenous normal p53 function holds some promise.
Research has shown that this restoration can lead to
regression of certain cancer cells without damaging
other cells in the process. The ways by which tumor
regression occurs depends mainly on the tumor type.
For example, restoration of endogenous p53 function
in lymphomas may induce apoptosis, while cell growth
may be reduced to normal levels. Thus,
pharmacological reactivation of p53 presents itself as
a viable cancer treatment option. [64][65] The first
commercial gene therapy, Gendicine, was approved
in China in 2003 for the treatment of head and neck
squamous cell carcinoma. It delivers a functional copy
of the p53 gene using an engineered adenovirus. [66]
Certain pathogens can also affect the p53 protein that
the TP53 gene expresses. One such example, human
papillomavirus (HPV), encodes a protein, E6, which
binds to the p53 protein and inactivates it. This
mechanism, in synergy with the inactivation of the cell
cycle regulator pRb by the HPV protein E7, allows for
repeated cell division manifested clinically as warts.
Certain HPV types, in particular types 16 and 18, can
also lead to progression from a benign wart to low or
high-grade cervical dysplasia, which are reversible
forms of precancerous lesions. Persistent infection of
the cervix over the years can cause irreversible
changes leading to carcinoma in situ and eventually
2. Journal of Multidisciplinary Engineering Science and Technology (JMEST)
ISSN: 2458-9403
Vol. 4 Issue 7, July - 2017
www.jmest.org
JMESTN42352028 7580
invasive cervical cancer. This results from the effects
of HPV genes, particularly those encoding E6 and E7,
which are the two viral oncoproteins that are
preferentially retained and expressed in cervical
cancers by integration of the viral DNA into the host
genome. [67] The p53 protein is continually produced
and degraded in cells of healthy people, resulting in
damped oscillation. The degradation of the p53
protein is associated with binding of MDM2. In a
negative feedback loop, MDM2 itself is induced by the
p53 protein. Mutant p53 proteins often fail to induce
MDM2, causing p53 to accumulate at very high levels.
Moreover, the mutant p53 protein itself can inhibit
normal p53 protein levels. In some cases, single
missense mutations in p53 have been shown to
disrupt p53 stability and function. [68] Suppression of
p53 in human breast cancer cells is shown to lead to
increased CXCR5 chemokine receptor gene
expression and activated cell migration in response to
chemokine CXCL13. [69] One study found that p53
and Myc proteins were the key to the survival of
Chronic Myeloid Leukaemia (CML) cells. Targeting
p53 and Myc proteins with drugs gave positive results
on mice with CML. [70][71]
Materials and Methods
Cancer causes almost 50% of deaths in pets over
the age of 10. Some common types of cancers in pets
include: skin, breast, head and neck, lymphoma,
leukemia, testicular, abdominal, and bone. Cancers
commonly found in pets that are also commonly found
in humans are lymphoma, melanoma, and
osteosarcoma. [2] Of the two most common
household pets, dogs tend to get cancer at a higher
rate than cats. The cancer may be treatable
depending on cancer type and the treatment options
for dogs and cats are similar to those for humans.
Surgery, radiation therapy, chemotherapy, and
immunotherapy are all considered and will usually
result in less side effects in animals than in humans.
[3]
Cancer in Cats
Cats can get a variety of cancers. The most
common are lymphoma, squamous cell carcinoma,
mammary cancer, mast cell tumors, oral tumors,
fibrosarcoma, osteosarcoma, respiratory carcinoma,
intestinal adenocarcinoma, and pancreatic-liver
adenocarcinoma. The disease has become so
prevalent that it is now the most common cause of
death in cats. [4] Certain breeds are more prone to
certain cancers than others. Signs and symptoms are
different depending on the type and stage of the
cancer. Tumors that are visible or detectable by touch
are most easily identified. The American Veterinary
Medical Association recommends twice-a-year
wellness exams for all cats. [5] Because the causes of
cancer in cats are similar to those in humans, risk can
be reduced by lowering the animal's exposure to
harmful carcinogens, including tobacco smoke. [6]
Feline Leukemia
In humans, some viruses can lead to cancer.
Papilloma virus or HPV, which is the causative agent
of most cases of cervical cancer. Viral infection can
also lead to cancer in animals. Feline leukemia (FeLV)
is an RNA virus that infects less than 2% of healthy,
domestic cats. [8] Infection is more prevalent in high-
risk populations that mean cats with outdoor access or
frequent social interactions. [7] The virus can spread
from one cat to another via saliva, nasal secretions,
feces, and milk. [9][10] It is transmitted during various
forms of contact, from friendly grooming to biting. The
virus can also be passed to a developing kitten during
pregnancy. The age and time of infection affect the
progression and clinical outcome of the virus. Kittens
are more likely to be infected and more likely to
develop more severe complications. [11] In most
cases, FeLV initially infects lymphocytes in the
oropharynx, which travel to the bone marrow, where
virally infected cells are produced very rapidly. [12] In
most environments, the Feline leukemia virus cannot
survive for long outside of the host. It can be killed
with soap and disinfectants. At this time, studies show
no evidence that FeLV can be transmitted from
infected cats to humans. [13] Infected animals may
develop anemia or lymphoma. The FeLV-C subtype
binds to and impedes the function of a heme transport
protein on the surface of developing red blood cells.
The result is a decrease in red blood cell numbers.
[14][15] Signs of anemia in cats include paleness of
the skin, tongue, gums, and mucous membranes
surrounding the eye. FeLV- induced lymphomas are
some of the most frequent tumors seen in cats.
Symptoms depend on the location of the tumor, and
may include weight loss, rough hair coat, loss of
appetite, vomiting, diarrhea, respiratory distress,
swelling of the lymph nodes and more. FeLV is also
linked to diseases of the kidneys, joints, lymph nodes,
small intestine, liver and nervous system. Depression
of the immune system makes infected cats more
susceptible to infections. Therefore, they may be
infected by organisms that healthy cats usually fend
off. It is possible for FeLV positive cats to remain
healthy. However, the prognosis is poor for cats with
persistent active infection. [12]
There are several different laboratory tests to
detect FeLV. These include
1) an antigen enzyme-linked immunosorbent assay
(ELISA)
2) an indirect immunofluorescent antibodyassay
(IFA).
Both tests use blood samples to detect the
presence of a protein that indicates FeLV infection.
This protein is called p27, and is part of the structure
of the virus. [12] Inconclusive results may require
additional testing with other methods, such as a
specific type of polymerase chain reaction (PCR),
which can detect FeLV-DNA in infected animals.
Infection with FeLV can be prevented by vaccination.
The vaccine is classified as non-core, which means it
3. Journal of Multidisciplinary Engineering Science and Technology (JMEST)
ISSN: 2458-9403
Vol. 4 Issue 7, July - 2017
www.jmest.org
JMESTN42352028 7581
can be considered optional. However both the
American Association of Feline Practitioners (AAFP)
and the European Advisory Board on Cat Disease
(ABCD) recommend that all cats with uncertain FeLV
status and/or are at risk of exposure be vaccinated.
Kittens are often vaccinated at 8-9 weeks of age and
again at 12 weeks of age. Research shows that the
vaccine will confer immunity for up to 1 year. Many
vets recommend a booster vaccination 1 year after
initial vaccination and annually thereafter. Because
cats become less susceptible with age, some vets
consider vaccination every 2-3 years sufficient for
older animals. [12]
Feline Squamous Cell Carcinoma
Squamous Cell Carcinoma (SCC) is a cancer that
occurs in cats and dogs. The tumors can appear
many places but are seen most commonly on and
around the eyes, ears, nose, mouth, and areas with
little hair. The primary cause of SCC is sunlight over-
exposure, which is especially harmful to fair-haired
cats. Age and exposure to cigarette smoke also
increase the risk for SCC. [16] At first, SCC tumors
look much like other common skin irritations, making
them difficult to identify. Scabs, hair loss, irritated skin,
loss of teeth with limited healing, and raised red
bumps on the skin are all possible sign of SCC. [16]
Crusty sores can appear and develop into deep ulcers
that bleed when irritated. In later stages, the cancer
may spread to the lymph nodes and lungs. Staging of
the cancer may involve chest X-rays and testing
lymph fluid. [17] In advanced cases, SCC tumors can
cause tissue death and destroy bone structure,
leading to pain, discomfort, and possibly death.
Feline Mammary Cancer
Feline mammary cancer (FMC) is the third most
common cancer in female cats. It is very uncommon
in males, but some cases have been reported. [22]
The mammary gland tumors that result from FMC can
be benign or malignant. However, 80-96% of
mammary tumors are malignant, meaning that they
can invade nearby tissues, and are capable of
metastasis. [22] Unfortunately malignant mammary
tumors tend to be much more harmful. [23] Cats have
four mammary glands on each side of their body, any
of which can be affected by FMC. They are referred to
as axillary, thoracic, abdominal, and inguinal glands.
These glands are the sites of primary tumor growth.
As with breast cancer in women, FMC is highly
metastatic. As a result, this type of cancer can spread
to the lungs, the lining of the lungs and pleura, liver,
regional lymph nodes, and other parts of the body.
Genes that have been targeted in human breast
cancer research have also been studied in feline
mammary cancer. HER-2/neu is the gene that
encodes the human epidermal growth factor receptor
protein. This protein resides on cell surfaces, where it
can interact with growth signals. If gene
amplificationcreates extra copies of the HER-2 gene,
then its corresponding protein will also be
overexpressed. This is thought to lead to increased
cell proliferation. HER-2 overexpression has been
detected in up to 30% of human breast cancer cases.
[22] Similarly, it occurs in 30% of feline mammary
cancer cases. [4] While all feline breeds may be
affected by FMC, some are at a higher risk than
others. [4] Studies have shown the Siamese breed to
have twice the risk of developing this type of cancer.
[22][24] Risk increases with age up to 14 years, with
an average age of tumor development between 10
and 11 years. [23] According to one study, intact
females are 7 times more likely to develop mammary
tumors than cats that are spayed at a young age. [25]
FMC is most often detected when pet owners or
veterinarians feel a mass during examination of the
mammary region. However, masses can also indicate
other conditions, such as severely inflamed lesions,
cysts, follicular tumors, and others. [4] Histology can
be used to confirm the diagnosis and classify the
lesion. Tumors are graded as well differentiated,
moderately differentiated, or poorly differentiated,
based on the appearance of the tissue-cells under a
microscope. Tumor size is the most important
prognostic factor in FMC cases, affecting the
progression of the disease and the survival time. [4]
Generally, larger tumors have a worse prognosis.
Lymph node involvement and degree of metastasis
also determine the severity of FMC cases.
Cancer in Dogs
Dogs have 35 times as much skin cancer as do
humans, 4 times as many breast tumors, 8 times as
much bone cancer, and twice as high an incidence of
leukemia. [28] Other common types of cancer found in
dogs include cancer of the mouth, lymphoma,
testicular, and abdominal tumors. [2] Osteosarcoma,
is most common in large dog breeds, such as Great
Danes, mastiffs, Labrador Retrievers, and Rottweilers.
[3]
Canine Transmissible Venereal Tumor
Cancer in humans is practically never transmitted
from one person to another. Only very rare
documented exceptions exist, usually involving
surgical mishaps. Canine Transmissible Venereal
Tumor (CTVT) is a very unusual form of cancer
affecting canines. CTVT is transmitted by mating,
licking, or other direct contact. [29] The tumor affects
the genitalia. In some cases the urethra becomes
blocked making it difficult for the affected animal to
urinate. [30] If the cancer is located at the mouth and
nose, nosebleeds, facial swelling, and nostril
discharge are common symptoms.
Many human cancers are caused by viruses,
including the human papilloma virus (HPV), a major
cause of cervical cancer. Infection with viruses can
lead to changes in normal cells within the infected
person and lead to the development of cancer.
However, CTVT is different. In this case, the cancer
cells themselves are transmitted from animal to
animal. Once in the new animal, the tumor can grow
and eventually be spread to additional animals. [31]
CTVT is not transmissible via killed tumor cells or by
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cell contents. [29] Viruses are usually present in a
cell's liquid contents. If the liquid contents do not
transfer CTVT, it is evidence that viruses are not
responsible for the cancer. Also, all tumor cells
examined so far have a molecular fingerprint in their
DNA that is absent in normal cells. Specially, the
cancer cells contain a DNA sequence called Line-1
inserted near the oncogene c-myc. [32] Researchers
have compared tumor DNA and normal DNA within
different breeds of dogs. The results showed the
expected differences between the normal cell DNA,
but all tumor DNA samples were very similar despite
being from very different dogs. These results indicate
that the tumor cells themselves transfer CTVT
between animals. [31] In most cases, the immune
system recognizes and eliminates cells of other types
that are introduced into an animal or humans. This
does not happen with CTVT. Upon the initial infection,
CTVT begins a state of rapid and intense growth that
lasts anywhere from three to nine months and
possibly longer in old or weakened dogs and This is
usually followed by a variable regression phase. [29]
Canine Osteosarcoma
Osteosarcoma (OSA) is a cancer that develops
within bones. It is often invasive and metastatic. [35]
OSA is relatively rare in small domesticated animals,
accounting for only 5-6% of canine malignancies. But,
it is by far the most common primary bone tumor in
dogs, accounting for 80% of cases. [36] This type of
cancer occurs most commonly in the appendicular
skeleton, including the radius and ulna, femur, tibia,
scapila, humerus, and phalanges. The forelimbs are
more likely to be affected than the hind limbs. OSA
also occurs in the axial skeleton, including the spinal
bones, skull, mandible, and the vertebrae at the base
of the sacrum. In rare cases, it can affect extraskeletal
tissues, such as muscle. [37] Because of its ability to
metastasize, OSA can spread to other parts of the
body and invades the lungs in approximately 17% of
cases. [37] Osteosarcoma is more common in adult
dogs. Large animals, weighing from 20 to 40 kg, are
at a higher risk than smaller animals. [37] Large tumor
size is associated with poor prognosis. [38] The
location of the tumor can also affect the outcome of
the disease. Axial skeletal OSA and appendicular
OSA tend to have similar prognoses. [39] Tumors in
the humerus bone tend to have a poor prognosis
while tumors in the jaw tend to have better outcomes.
[38][39]
Canine Hemangiosarcoma
Hemangiosarcoma (HSA) is a cancer that
originates in cells that form blood vessels. HSA is
responsible for approximately 7% of canine cancer
cases. It is more common in dogs than any other
species of animal examined. [44] HSA occurs most
commonly in the spleen, skin, and the right atrium of
the heart. [45] Primary tumors have also been
reported in the lung, aorta, kidney, oral cavity, muscle,
bone, urinary bladder, prostate gland, vagina,
peritoneum, intestine, tongue, and conjunctiva. [46]
HSA is highly metastatic. When HSA is confined to
the skin, it is less apt to spread. Over 80% of all other
cases have already metastasized at the time of
diagnosis. [46] HSA cells may release proteins that
stimulate the growth of new blood vessels. This
process is known as angiogenesis, and is critical for
tumor formation. The presence of numerous blood
vessels helps supply growing tumors with nutrients
and oxygen and may serve as a highway for the
cancer cells to metastasize to distant parts of the
body.
Older animals are at higher risk for developing
hemangiosarcoma. Affected dogs are usually
diagnosed between 9 and 12 years of age. [47] HSA
tends to affect large breed animals more often than
smaller ones. Breeds that are more prone to this type
of cancer include German Shepherds, Golden
Retrievers, Labrador Retrievers, Pointers, Boxers,
English Settlers, Great Danes, Poodles, and Siberian
Huskies. Breeds with short hair, light hair, light skin, or
Whippets are more prone to hemangiosarcoma of the
skin. [46][48][49] Symptoms of HSA vary depending
on the location and stage of the cancer, but may
include weakness, weight loss, tachycardia,
tachypnea, abdominal swelling, lethargy, and
paleness of mucous membranes. Episodes of acute
weakness and collapse may indicate that a tumor has
ruptured, causing uncontrolled blood loss. If internal
bleeding occurs and the blood is reabsorbed from the
body cavity back into blood vessels, the animal may
gradually recover. In more severe cases, tumor
rupture can cause sudden death. [46] Veterinarians
often detect HSA during physical examinations. They
also use blood tests, urine analysis, chest x-rays,
abdominal ultrasound, echocardiogram, biopsy, and
more. One type of blood test, the complete blood
count (CBC), can detect anemia, misshapen or
fragmented red blood cells, and other signs of HSA.
Some tests can even indicate the organs being
affected by the disease. A blood smear that shows
normoblasts may indicate cancer of the spleen. [46]
Canine Mast Cell Tumors
Mast cell tumors, which also called mastocytomas,
are the most common skin cancer in dogs. [51]
Mastocytomas, develop most often in dogs seven and
a half to nine years of age, but can occasionally be
found in dogs as young as four to six months.
Different breeds also have different rates of mast cell
tumors. Boxers and Boston terriers have the highest
rates. [52] Mast cell tumors originate from mast cells,
immune system cells found in many tissues of the
body. [53] Because mast cells can be found almost
anywhere, mastocytomas have the potential to appear
in all different regions of the body. They are most
commonly located on the skin on hind legs, thorax, or
genital regions. [54] Mast cells contain a variety of
biologically active substances, including histamine,
heparin, serotonin, and prostaglandins. These
chemicals are released from the cells during an
allergic reaction. [55] These are the substances that
cause the symptoms associated with allergies.
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Redness, itching, swelling, blood pressure drops,
tearing, nausea and wheezing. Normally these
chemicals are highly regulated, but when mast cells
become cancerous, they no longer appropriately
control the release of the chemicals. The unregulated
release of chemicals by a mastocytoma can cause a
variety of symptoms. The symptoms any particular
dog shows is variable, but can include vomiting,
ulcers, bloody excrement, abdominal pain, and blood-
clotting difficulties; gastro-intestinal problems are the
most common signs. [56] Mastocytomas appear as
raised lumps that are often irritated or red in
appearance. Mast cell tumors have no characteristic
form or color and are impossible to identify without
laboratory testing. [51] Often when a mastocytoma is
touched the skin becomes red, itchy, and swollen.
[52][57] This response is also called Darier's Sign. It
occurs because when the mast cells in the tumor are
compressed they release the chemical histamine, and
this causes irritation of the skin. Although normal mast
cells are typically fairly stationary, advanced mast cell
tumors may metastasize to other places in the body.
Veterinarians stage mast cell tumors using a six tiered
system that is stages 0 to 5, based on the extent that
the cancer has spread in the body. Staging takes into
account the number and size of tumors, lymph node
involvement, and recurrence rate. [51] A higher stage
indicates greater body involvement with Stage 5
representing distant metastasis including bone
marrow or blood involvement. [52] Another
classification system, the histological grade which
values from 1 to 3, is based on the physical
appearance of the cells in the tumor. More abnormal
mast cells-tissues are associated with a higher
histological grade and have a higher possibility of
being malignant. [52]
Cancer in Wild Animals
There are some types of cancers have been
diagnosed in wild animals. Less is known about the
cancers that affect wild animals, since they move
around and may not be easily observed for a long
period of time. Tasmanian Devils, Nowadays are
plagued by an infectious cancer known as Tasmanian
devil facial tumor disease (DFTD). Since the
emergence of the disease in 1996, the population has
declined by more than 60 percent. [72] George
Washington University Medical Center researchers
reported over thirty tumors found in elasmobranchs, a
group of animals that includes sharks, rays, and
skates. [73] In August of 2012, an article was
published that described the discovery of melanoma
affecting a population of wild fish. [74]
Cancer incidence in naked mole rats, due to the
high amounts of hyaluronic acid, is rare. [75]
Although all analyzed human cancer genes are
present in chimpanzee, cancer incidence in non-
human primates is very rare. Additional factors
contributing to the observed differences could include
changes in diet, lifestyle or exposure to mutagenic
agents, [76][77][78] physiological differences in
immune system or in life expectancy and aging rates.
[79]
The most interesting wild animal which can resist
cancer incidence is elephant. A team led by Dr.
Joshua Schiffman at the University of Utah set out to
examine cancer rates in different species. They began
by studying 14 years of autopsy data collected by the
San Diego Zoo. They analyzed 36 species that
spanned up to 6 orders of magnitude in size and life
span ranging from the 51-gram striped grass mouse,
which lives a maximum of 4.5 years, to the elephant,
which can live up to 65 years. They also analyzed 644
documented deaths from a global database of captive
African and Asian elephants. The researchers found
no significant relationships between cancer risk and
body size, life span, or basic metabolic rate among
the species. For elephants, they estimated that the
overall lifetime chance of dying from cancer was less
than 5%. The lifetime cancer mortality rate for humans
is about 20%. Elephants may have evolved to resist
cancer by triggering apoptosis through p53 to
efficiently remove mutant cells. [80][81][82]
Conclusion
Cancer incidence in the wolf is lower than that in
the domestic dog. Cancer is low in the chimpanzee
than in the human despite the two species having very
similar cancer genes. The issue is not genetics, but it
is the environment or gene-environmental
interactions. Most chimpanzees eat their natural diet
while in the wild or in captivity. It is likely that the
incidence of cancer would be higher in chimpanzees
that would eat a Western human diet. Germ line
mutations might increase the incidence of some
cancers, but only in a certain provocative
environment. Cancer can occur in wild animals that
are infected with certain viruses. Viruses can damage
mitochondrial function thus producing cancer in the
infected cells. The somatic mutations would arise as a
downstream effect of the defective respiration. It is not
clear if viral infections would be more common in
domestic animals than in wild animals. Pollutants in
the environment, including in the diet, would damage
cellular respiration. Respiratory damage is largely
responsible for cancer in both humans and
domesticated animals that do not eat their natural
foods.
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