Cancer is caused by multiple factors and develops through a multi-step process. Key causes of cancer include tobacco use, certain viruses and bacteria, radiation, and hereditary factors. Cancers arise with different frequencies in different parts of the world, influenced by environmental and behavioral risks prevalent in each location. There is often a significant lag time, sometimes decades, between exposure to a carcinogen like tobacco smoke and the development of cancer. While most cancers are not inherited, some familial cancer syndromes exist that increase cancer risk due to a genetic predisposition.
This document discusses cancer invasion and metastasis. It begins by introducing the concepts of invasion and metastasis, where cancer spreads from the primary site to distant tissues. It then discusses the somatic evolution of cancer and the multiple genetic alterations required for malignancy. The document covers clinical and pathological correlations with metastasis risk, and the "seed and soil" hypothesis of why cancers metastasize to certain organs. It outlines the basic steps in the metastatic cascade, including invasion, intravasation, arrest and extravasation at distant sites. Finally, it discusses the implications of the traditional progression model, including the rarity of metastatic cells and prevention of metastasis through early detection and treatment.
The document outlines six hallmarks of cancer cells:
1. Self-sufficiency in growth signals through autocrine or paracrine signaling and expression of growth-promoting extracellular matrix receptors.
2. Insensitivity to antigrowth signals through mutations that block cell cycle inhibitors like Rb or induce differentiation.
3. Evading apoptosis by mutations in genes like p53 that derail cell suicide pathways and activate pro-survival signals.
4. Limitless replicative potential enabled by mechanisms like telomerase that maintain telomere length indefinitely.
5. Sustained angiogenesis driven by factors like VEGF that promote growth of blood vessels.
6. Tissue invasion and
Cancer and its types, all tumours are not cancer, cancer, diagnosis of cancer, how cancer differ, how cancer spread, how cancer start, how normal cells act
This document discusses molecular perspectives on cancer development. It describes how cancer cells differ from normal cells in their loss of growth regulation and increased proliferation. The key characteristics of cancer include clonality, autonomy, anaplasia, metastasis. Cancer development is driven by mutations in oncogenes, tumor suppressor genes, and mutator genes. Various carcinogens like chemicals, radiation, and viruses can cause these genetic mutations and ultimately lead to cancer. The major pathways of malignancy include uncontrolled proliferation, defects in cell cycle regulation, impaired DNA repair, immortalization, inhibited apoptosis, angiogenesis, and metastasis.
This document discusses various diagnostic tools used in oncology, including tumor markers, immunohistochemistry, immunocytology, cytogenetics, molecular diagnosis, and gene expression analysis. It provides details on tumor markers including their definition, classification, factors that affect serum levels, and indications for use. It also discusses immunohistochemistry in detail, covering tumor antigens, immunoreactivity, clinical applications for diagnosis, predicting therapy response and prognosis, and specific carcinoma markers like cytokeratins, CEA, and hormone receptors.
Malignant tumors are cancerous and can invade nearby tissues, spread to other parts of the body through the bloodstream, and form new tumors (metastasis). Benign tumors are not cancerous, do not invade tissues or spread, and can be surgically removed without threat to life. Cancer cells have characteristics like sustained growth signaling, evading growth suppression, resisting cell death, increased replication ability, inducing angiogenesis, and spreading to other areas (metastasis). These characteristics arise through genetic mutations that alter the functions of oncogenes and tumor suppressor genes.
Cancer Stem Cells (CSCs) have become a vital target for biologists and researchers.
The following presentation focuses on the treatment of cancer through targeting CSCs and its advantages.
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.
This document discusses cancer invasion and metastasis. It begins by introducing the concepts of invasion and metastasis, where cancer spreads from the primary site to distant tissues. It then discusses the somatic evolution of cancer and the multiple genetic alterations required for malignancy. The document covers clinical and pathological correlations with metastasis risk, and the "seed and soil" hypothesis of why cancers metastasize to certain organs. It outlines the basic steps in the metastatic cascade, including invasion, intravasation, arrest and extravasation at distant sites. Finally, it discusses the implications of the traditional progression model, including the rarity of metastatic cells and prevention of metastasis through early detection and treatment.
The document outlines six hallmarks of cancer cells:
1. Self-sufficiency in growth signals through autocrine or paracrine signaling and expression of growth-promoting extracellular matrix receptors.
2. Insensitivity to antigrowth signals through mutations that block cell cycle inhibitors like Rb or induce differentiation.
3. Evading apoptosis by mutations in genes like p53 that derail cell suicide pathways and activate pro-survival signals.
4. Limitless replicative potential enabled by mechanisms like telomerase that maintain telomere length indefinitely.
5. Sustained angiogenesis driven by factors like VEGF that promote growth of blood vessels.
6. Tissue invasion and
Cancer and its types, all tumours are not cancer, cancer, diagnosis of cancer, how cancer differ, how cancer spread, how cancer start, how normal cells act
This document discusses molecular perspectives on cancer development. It describes how cancer cells differ from normal cells in their loss of growth regulation and increased proliferation. The key characteristics of cancer include clonality, autonomy, anaplasia, metastasis. Cancer development is driven by mutations in oncogenes, tumor suppressor genes, and mutator genes. Various carcinogens like chemicals, radiation, and viruses can cause these genetic mutations and ultimately lead to cancer. The major pathways of malignancy include uncontrolled proliferation, defects in cell cycle regulation, impaired DNA repair, immortalization, inhibited apoptosis, angiogenesis, and metastasis.
This document discusses various diagnostic tools used in oncology, including tumor markers, immunohistochemistry, immunocytology, cytogenetics, molecular diagnosis, and gene expression analysis. It provides details on tumor markers including their definition, classification, factors that affect serum levels, and indications for use. It also discusses immunohistochemistry in detail, covering tumor antigens, immunoreactivity, clinical applications for diagnosis, predicting therapy response and prognosis, and specific carcinoma markers like cytokeratins, CEA, and hormone receptors.
Malignant tumors are cancerous and can invade nearby tissues, spread to other parts of the body through the bloodstream, and form new tumors (metastasis). Benign tumors are not cancerous, do not invade tissues or spread, and can be surgically removed without threat to life. Cancer cells have characteristics like sustained growth signaling, evading growth suppression, resisting cell death, increased replication ability, inducing angiogenesis, and spreading to other areas (metastasis). These characteristics arise through genetic mutations that alter the functions of oncogenes and tumor suppressor genes.
Cancer Stem Cells (CSCs) have become a vital target for biologists and researchers.
The following presentation focuses on the treatment of cancer through targeting CSCs and its advantages.
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.
This document provides an overview of cancer biology, covering topics such as the definition of cancer, types of cancers like carcinomas and sarcomas, common cancers by incidence rate, key characteristics of specific cancers like lung cancer and colon cancer, cancer genetics including oncogenes and tumor suppressor genes, hallmarks of cancer, and the process of metastasis. It includes descriptions, risk factors, images and literature references.
This document discusses chemoprevention for cancer. It defines chemoprevention as using chemicals to interfere with cell division processes so cancer cells commit suicide. Chemoprevention is divided into primary, secondary, and tertiary prevention based on risk levels. The ideal chemopreventive agent is inexpensive, safe, and effective with minimal side effects for long-term use. The document then discusses how chemoprevention works on tumor cells and by histone modifications. It describes epigenetic therapy and drugs used for this therapy. Finally, it discusses how phytochemicals from plants like green tea, curcumin, caffeine, and gingerol can also help prevent cancer.
Epithelial and mesenchymal transition in invasion and metastasisAshwini Gowda
This document discusses neoplasia and the process of metastasis. It defines neoplasia as new, uncontrolled growth and describes the hallmarks of cancer cells, including autonomous growth, loss of differentiation, invasion and metastasis. It explains the multi-step process of metastasis, beginning with local invasion of tumor cells into surrounding tissue facilitated by degradation of the extracellular matrix and migration of cells. The document then discusses the vascular dissemination of tumor cells and colonization at distant sites, outlining several theories for how metastatic potential arises in tumors. Key genes and pathways involved in epithelial-mesenchymal transition and the generation of cancer stem cells are also reviewed.
Genetic testing and counseling can help determine cancer risk based on family history and genetic mutations. Most cancers are sporadic but 5-10% are hereditary due to inherited gene mutations. Genetic counselors use family histories and genetic tests to assess cancer risks, recommend screening, and provide counseling to relatives. While some cancers have clear high-risk genes, most have contributions from multiple common and rare variants, so interpretation requires expertise.
The document discusses the eight hallmarks of cancer identified by Hanahan and Weinberg: 1) sustaining proliferative signaling, 2) evading growth suppressors, 3) resisting cell death, 4) enabling replicative immortality, 5) inducing angiogenesis, 6) activating invasion and metastasis, 7) evading immune destruction, and 8) deregulating cellular metabolism. It provides details on the molecular mechanisms cancer cells use to acquire these hallmark capabilities, such as generating their own growth signals, inactivating tumor suppressors, increasing anti-apoptotic factors, maintaining telomeres, secreting angiogenic factors, enhancing proteases, and adapting metabolism.
This document provides an overview of the molecular foundations of cancer. It discusses how cancer arises from genetic and epigenetic aberrations that accumulate in cells and lead to altered gene expression and the acquisition of hallmark capabilities that allow tumors to form and progress. Key points covered include the types of genomic changes like mutations and chromosome defects that occur; the roles of oncogenes and tumor suppressor genes; how cancer risk can be inherited; and the uses of genomics in cancer diagnosis and targeted treatment.
This document discusses cancer types, properties, symptoms, prevention, screening, and treatment. It defines cancer as abnormal cell growth with the potential to invade other parts of the body. The six hallmarks of cancer are described as uncontrolled cell growth, growth despite growth-inhibiting signals, evading cell death, unlimited cell division potential, inducing blood vessel growth, and spreading to other tissues. Common cancer symptoms depend on the location and can include lumps, bleeding, weight loss, and fever. Prevention methods include vaccines, medication like aspirin and tamoxifen, and diet low in processed meat. Screening considers test accuracy, potential harms, treatment options, and cost. Cancer treatment includes chemotherapy, radiation, palliative care
Gene therapy involves inserting genetic material into cells to give them a new or restore a missing function. It can be used to treat cancer by modifying cancer cells at the molecular level, such as replacing a defective tumor suppressor gene like p53 to stop uncontrolled cell growth or induce cell death. Several approaches for gene therapy for cancer have shown promise in preclinical studies, including restoring tumor suppressor gene function, blocking oncogenes, and introducing "suicide genes" to selectively kill cancer cells. However, challenges remain to effectively target all cancer cells, including metastases.
1. Several molecular pathways are involved in breast cancer pathogenesis, including steroid hormone receptors, HER2/neu, cell cycle proteins, and growth factors.
2. Risk factors for breast cancer include increasing age, female gender, family history, genetic mutations, personal history of breast cancer or other breast diseases, reproductive factors, and hormone use.
3. High risk patients are identified using tools like the Gail model and managed through increased screening including breast self-exams, clinical exams, mammograms, and MRI. Preventive options include tamoxifen, raloxifen, and prophylactic surgeries.
This document summarizes recent research on cancer stem cells. It discusses that some cancers are driven by rare cancer stem cells that have properties similar to normal stem cells, such as self-renewal. These cancer stem cells can be identified in several cancers including colorectal cancer, breast cancer, and leukemias. Several signaling pathways important for regulating normal stem cells, such as Wnt and Notch, also appear to play roles in cancer stem cells. Targeting and eliminating cancer stem cells may be necessary for more effective cancer treatments.
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.
There are many types of cancer treatment that depend on the type and stage of cancer, including surgery, radiation therapy, chemotherapy, immunotherapy, targeted therapy, hormone therapy, stem cell transplants, and precision medicine. Surgery attempts to remove the entire tumor mass and sometimes lymph nodes, while radiation therapy uses radiation to damage cancer cell DNA. Chemotherapy uses cytotoxic drugs to kill rapidly dividing cells, and can be used with other treatments. Targeted therapy and immunotherapy target specific molecular differences in cancer cells. Hormone therapy slows the growth of cancers that use hormones, and stem cell transplants restore blood-forming stem cells after other treatments destroy them. Precision medicine selects individualized treatments based on the genetics of a patient's cancer.
This document discusses cancer cachexia, beginning with an introduction that notes weight loss in cancer patients is associated with poor quality of life and increased morbidity. It then defines cachexia as a complex metabolic syndrome characterized by loss of muscle and fat mass. The pathophysiology section explains cachexia is multifactorial, involving anorexia, abnormal metabolism, and cytokine changes. Management involves treating the underlying cancer, nutritional intervention such as supplements by various routes, and pharmacological treatments including progestational agents, corticosteroids, and cytokine inhibitors, with some promising animal research on combinations. The document concludes by recommending various steps to address cachexia in clinical practice.
There are several methods used to diagnose cancer, including radiological, cytological, histological, and molecular methods. Radiological exams like CT scans and MRIs can detect cancers non-invasively, while biopsies provide tissue samples for pathological examination under a microscope. Newer diagnostic tools analyze tumor markers in blood and cells as well as genetic changes at the molecular level to characterize cancers and detect them earlier. Making an accurate cancer diagnosis often requires integrating multiple diagnostic techniques and a second opinion from an oncologist or pathologist.
This document discusses cancer and genetic influences. It defines cancer as uncontrolled cell proliferation that occurs due to an imbalance in cellular proliferation and death. Cancer is caused by mutations in genes controlling processes like proliferation, the cell cycle, and programmed cell death. The document summarizes the major types of cancer and characteristics of cancer cells. It describes how cancer can be influenced by genetics, with some forms having a higher incidence in families. Cancer is considered a genetic disease caused by mutations in genes regulating cell growth and death. Key genes involved include oncogenes, tumor suppressors, and genes responsible for DNA repair. Specific oncogenes discussed are RAS, RET, MET, and MYC. RAS family proto-oncogenes are described in
Breast cancer is caused by heterogeneous tumor cells whose behavior depends on biological features. Molecular subtyping through gene expression profiling can classify tumor types, recognize hereditary implications, identify appropriate therapies, determine prognosis, and avoid unnecessary treatment. The major subtypes are luminal A/B, HER2-enriched, and basal-like, which differ in gene expression, sensitivity to therapies, and clinical outcomes. Understanding the molecular biology of breast cancer is crucial for precision medicine approaches to management.
Cancer is caused by genetic mutations in somatic cells. Whole genome sequencing can identify all genetic alterations in cancer including single nucleotide mutations, small insertions/deletions, copy number changes, and chromosomal rearrangements. Earlier methods focused on sequencing protein kinase genes known to be involved in cancer signaling pathways. Current methods like whole exome sequencing focus on coding exons to identify damaging mutations at lower cost compared to whole genome sequencing. Non-coding mutations in regulatory regions and microRNAs are also important in cancer development.
This presentation provides an overview of cancer including statistics, causes, types, symptoms, diagnosis, treatment, and top cancer hospitals in India. Cancer is characterized by uncontrolled cell growth that can form tumors. Over 1.3 million new cancer cases are diagnosed in the US each year, resulting in over 500,000 deaths. Risk factors include genetic factors, tobacco use, viruses, radiation, and obesity. The main types of cancer are carcinomas, sarcomas, lymphomas, and leukemias. Diagnosis involves imaging tests and biopsies. Treatment options include surgery, radiation, chemotherapy, immunotherapy, and targeted therapy.
Introduction to Targeted Therapies in OncologyMohamed Abdulla
Describes the molecular background which represents the core for developing targeted therapies against specific biological events in malignant cellular clones.
Cancer is not a single disease but rather a group of related diseases characterized by uncontrolled cell growth and division. There are many types of cancer that are classified based on the tissue affected, growth patterns, and ability to metastasize. Cancer begins when genetic changes cause normal cells to multiply uncontrollably and form tumors. If left untreated, cancer cells can invade nearby tissues and spread via the bloodstream and lymphatic system to other parts of the body.
This document discusses benign and malignant tumors. It defines neoplasia as new abnormal growth and divides tumors into benign and malignant. Benign tumors are slow-growing, localized masses that are not life-threatening, while malignant tumors rapidly proliferate, invade surrounding tissues, and metastasize to distant sites, potentially causing death. Malignant tumors are also known as cancers. The document describes characteristics of benign versus malignant tumors such as growth rate, circumscription, differentiation, and metastasis. It also lists factors that can predispose individuals to developing neoplasms.
This document provides an overview of cancer biology, covering topics such as the definition of cancer, types of cancers like carcinomas and sarcomas, common cancers by incidence rate, key characteristics of specific cancers like lung cancer and colon cancer, cancer genetics including oncogenes and tumor suppressor genes, hallmarks of cancer, and the process of metastasis. It includes descriptions, risk factors, images and literature references.
This document discusses chemoprevention for cancer. It defines chemoprevention as using chemicals to interfere with cell division processes so cancer cells commit suicide. Chemoprevention is divided into primary, secondary, and tertiary prevention based on risk levels. The ideal chemopreventive agent is inexpensive, safe, and effective with minimal side effects for long-term use. The document then discusses how chemoprevention works on tumor cells and by histone modifications. It describes epigenetic therapy and drugs used for this therapy. Finally, it discusses how phytochemicals from plants like green tea, curcumin, caffeine, and gingerol can also help prevent cancer.
Epithelial and mesenchymal transition in invasion and metastasisAshwini Gowda
This document discusses neoplasia and the process of metastasis. It defines neoplasia as new, uncontrolled growth and describes the hallmarks of cancer cells, including autonomous growth, loss of differentiation, invasion and metastasis. It explains the multi-step process of metastasis, beginning with local invasion of tumor cells into surrounding tissue facilitated by degradation of the extracellular matrix and migration of cells. The document then discusses the vascular dissemination of tumor cells and colonization at distant sites, outlining several theories for how metastatic potential arises in tumors. Key genes and pathways involved in epithelial-mesenchymal transition and the generation of cancer stem cells are also reviewed.
Genetic testing and counseling can help determine cancer risk based on family history and genetic mutations. Most cancers are sporadic but 5-10% are hereditary due to inherited gene mutations. Genetic counselors use family histories and genetic tests to assess cancer risks, recommend screening, and provide counseling to relatives. While some cancers have clear high-risk genes, most have contributions from multiple common and rare variants, so interpretation requires expertise.
The document discusses the eight hallmarks of cancer identified by Hanahan and Weinberg: 1) sustaining proliferative signaling, 2) evading growth suppressors, 3) resisting cell death, 4) enabling replicative immortality, 5) inducing angiogenesis, 6) activating invasion and metastasis, 7) evading immune destruction, and 8) deregulating cellular metabolism. It provides details on the molecular mechanisms cancer cells use to acquire these hallmark capabilities, such as generating their own growth signals, inactivating tumor suppressors, increasing anti-apoptotic factors, maintaining telomeres, secreting angiogenic factors, enhancing proteases, and adapting metabolism.
This document provides an overview of the molecular foundations of cancer. It discusses how cancer arises from genetic and epigenetic aberrations that accumulate in cells and lead to altered gene expression and the acquisition of hallmark capabilities that allow tumors to form and progress. Key points covered include the types of genomic changes like mutations and chromosome defects that occur; the roles of oncogenes and tumor suppressor genes; how cancer risk can be inherited; and the uses of genomics in cancer diagnosis and targeted treatment.
This document discusses cancer types, properties, symptoms, prevention, screening, and treatment. It defines cancer as abnormal cell growth with the potential to invade other parts of the body. The six hallmarks of cancer are described as uncontrolled cell growth, growth despite growth-inhibiting signals, evading cell death, unlimited cell division potential, inducing blood vessel growth, and spreading to other tissues. Common cancer symptoms depend on the location and can include lumps, bleeding, weight loss, and fever. Prevention methods include vaccines, medication like aspirin and tamoxifen, and diet low in processed meat. Screening considers test accuracy, potential harms, treatment options, and cost. Cancer treatment includes chemotherapy, radiation, palliative care
Gene therapy involves inserting genetic material into cells to give them a new or restore a missing function. It can be used to treat cancer by modifying cancer cells at the molecular level, such as replacing a defective tumor suppressor gene like p53 to stop uncontrolled cell growth or induce cell death. Several approaches for gene therapy for cancer have shown promise in preclinical studies, including restoring tumor suppressor gene function, blocking oncogenes, and introducing "suicide genes" to selectively kill cancer cells. However, challenges remain to effectively target all cancer cells, including metastases.
1. Several molecular pathways are involved in breast cancer pathogenesis, including steroid hormone receptors, HER2/neu, cell cycle proteins, and growth factors.
2. Risk factors for breast cancer include increasing age, female gender, family history, genetic mutations, personal history of breast cancer or other breast diseases, reproductive factors, and hormone use.
3. High risk patients are identified using tools like the Gail model and managed through increased screening including breast self-exams, clinical exams, mammograms, and MRI. Preventive options include tamoxifen, raloxifen, and prophylactic surgeries.
This document summarizes recent research on cancer stem cells. It discusses that some cancers are driven by rare cancer stem cells that have properties similar to normal stem cells, such as self-renewal. These cancer stem cells can be identified in several cancers including colorectal cancer, breast cancer, and leukemias. Several signaling pathways important for regulating normal stem cells, such as Wnt and Notch, also appear to play roles in cancer stem cells. Targeting and eliminating cancer stem cells may be necessary for more effective cancer treatments.
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.
There are many types of cancer treatment that depend on the type and stage of cancer, including surgery, radiation therapy, chemotherapy, immunotherapy, targeted therapy, hormone therapy, stem cell transplants, and precision medicine. Surgery attempts to remove the entire tumor mass and sometimes lymph nodes, while radiation therapy uses radiation to damage cancer cell DNA. Chemotherapy uses cytotoxic drugs to kill rapidly dividing cells, and can be used with other treatments. Targeted therapy and immunotherapy target specific molecular differences in cancer cells. Hormone therapy slows the growth of cancers that use hormones, and stem cell transplants restore blood-forming stem cells after other treatments destroy them. Precision medicine selects individualized treatments based on the genetics of a patient's cancer.
This document discusses cancer cachexia, beginning with an introduction that notes weight loss in cancer patients is associated with poor quality of life and increased morbidity. It then defines cachexia as a complex metabolic syndrome characterized by loss of muscle and fat mass. The pathophysiology section explains cachexia is multifactorial, involving anorexia, abnormal metabolism, and cytokine changes. Management involves treating the underlying cancer, nutritional intervention such as supplements by various routes, and pharmacological treatments including progestational agents, corticosteroids, and cytokine inhibitors, with some promising animal research on combinations. The document concludes by recommending various steps to address cachexia in clinical practice.
There are several methods used to diagnose cancer, including radiological, cytological, histological, and molecular methods. Radiological exams like CT scans and MRIs can detect cancers non-invasively, while biopsies provide tissue samples for pathological examination under a microscope. Newer diagnostic tools analyze tumor markers in blood and cells as well as genetic changes at the molecular level to characterize cancers and detect them earlier. Making an accurate cancer diagnosis often requires integrating multiple diagnostic techniques and a second opinion from an oncologist or pathologist.
This document discusses cancer and genetic influences. It defines cancer as uncontrolled cell proliferation that occurs due to an imbalance in cellular proliferation and death. Cancer is caused by mutations in genes controlling processes like proliferation, the cell cycle, and programmed cell death. The document summarizes the major types of cancer and characteristics of cancer cells. It describes how cancer can be influenced by genetics, with some forms having a higher incidence in families. Cancer is considered a genetic disease caused by mutations in genes regulating cell growth and death. Key genes involved include oncogenes, tumor suppressors, and genes responsible for DNA repair. Specific oncogenes discussed are RAS, RET, MET, and MYC. RAS family proto-oncogenes are described in
Breast cancer is caused by heterogeneous tumor cells whose behavior depends on biological features. Molecular subtyping through gene expression profiling can classify tumor types, recognize hereditary implications, identify appropriate therapies, determine prognosis, and avoid unnecessary treatment. The major subtypes are luminal A/B, HER2-enriched, and basal-like, which differ in gene expression, sensitivity to therapies, and clinical outcomes. Understanding the molecular biology of breast cancer is crucial for precision medicine approaches to management.
Cancer is caused by genetic mutations in somatic cells. Whole genome sequencing can identify all genetic alterations in cancer including single nucleotide mutations, small insertions/deletions, copy number changes, and chromosomal rearrangements. Earlier methods focused on sequencing protein kinase genes known to be involved in cancer signaling pathways. Current methods like whole exome sequencing focus on coding exons to identify damaging mutations at lower cost compared to whole genome sequencing. Non-coding mutations in regulatory regions and microRNAs are also important in cancer development.
This presentation provides an overview of cancer including statistics, causes, types, symptoms, diagnosis, treatment, and top cancer hospitals in India. Cancer is characterized by uncontrolled cell growth that can form tumors. Over 1.3 million new cancer cases are diagnosed in the US each year, resulting in over 500,000 deaths. Risk factors include genetic factors, tobacco use, viruses, radiation, and obesity. The main types of cancer are carcinomas, sarcomas, lymphomas, and leukemias. Diagnosis involves imaging tests and biopsies. Treatment options include surgery, radiation, chemotherapy, immunotherapy, and targeted therapy.
Introduction to Targeted Therapies in OncologyMohamed Abdulla
Describes the molecular background which represents the core for developing targeted therapies against specific biological events in malignant cellular clones.
Cancer is not a single disease but rather a group of related diseases characterized by uncontrolled cell growth and division. There are many types of cancer that are classified based on the tissue affected, growth patterns, and ability to metastasize. Cancer begins when genetic changes cause normal cells to multiply uncontrollably and form tumors. If left untreated, cancer cells can invade nearby tissues and spread via the bloodstream and lymphatic system to other parts of the body.
This document discusses benign and malignant tumors. It defines neoplasia as new abnormal growth and divides tumors into benign and malignant. Benign tumors are slow-growing, localized masses that are not life-threatening, while malignant tumors rapidly proliferate, invade surrounding tissues, and metastasize to distant sites, potentially causing death. Malignant tumors are also known as cancers. The document describes characteristics of benign versus malignant tumors such as growth rate, circumscription, differentiation, and metastasis. It also lists factors that can predispose individuals to developing neoplasms.
This document discusses the characteristics of neoplasms. It states that all tumors have two basic components - the parenchyma made of neoplastic cells, and the stroma which provides support. The parenchyma determines the nature and behavior of the tumor. Benign and malignant tumors can be distinguished by their differentiation, rate of growth, local invasion, and ability to metastasize. Malignant tumors are less differentiated, grow faster, invade surrounding tissue, and spread to distant sites through lymphatic or hematogenous routes.
Neoplasia refers to abnormal growth of cells. Benign tumors remain localized, do not invade other tissues or metastasize. They are well-differentiated and grow slowly. Malignant tumors are poorly differentiated, invade surrounding tissues and spread to distant sites. They grow rapidly and can be fatal if not treated. The key differences between benign and malignant tumors are their ability to invade other tissues and metastasize to other parts of the body.
Chemical carcinogenesis involves multiple stages: initiation, promotion, and progression. Initiation involves DNA damage from mutagenic chemicals and fixes a heritable mutation. Promotion involves clonal expansion of initiated cells. Progression leads to malignant tumors through additional mutations. Initiation is irreversible while promotion and progression are reversible. Carcinogens are classified as genotoxic if they directly damage DNA or non-genotoxic if they modify gene expression without direct DNA damage. The multi-stage model of carcinogenesis with initiation, promotion and progression explains the process at a molecular level.
This document defines key terms related to chemical carcinogenesis and provides an overview of the topic. It begins by defining terms like tumor, neoplasia, benign vs malignant tumors. It describes classical concepts of carcinogenesis as well as modern molecular understanding. It also discusses various assays and methods used to study carcinogenesis and assess toxicological risk. The overall goal is to explain the mechanisms and measurement of how chemicals can cause cancer at a molecular level.
Neoplasia refers to abnormal cell growth. Benign tumors grow slowly, are self-limited and non-invasive, while malignant tumors grow rapidly, invade surrounding tissues, and can metastasize to distant sites. The mechanism of neoplasia involves loss of differentiation, increased growth rate, local invasion, and metastasis in malignant tumors compared to benign tumors. Nomenclature of tumors is based on the cell of origin and suffix, such as carcinoma for epithelial tumors and sarcoma for mesenchymal tumors.
Understanding cancer -_what_is_cancer_editedvjcummins
This document provides a high-level overview of cancer, including what it is, its causes, and types. It discusses that cancer is a group of diseases involving uncontrolled cell growth. Genes and their mutations play a key role in cancer development, with oncogenes accelerating cell growth and tumor suppressor genes normally restraining growth. The precise balance between these genes can be disrupted by various external and internal factors, leading to cancer.
This document defines neoplasia as abnormal new growth resulting from uncontrolled cellular proliferation. It distinguishes neoplasia from hyperplasia based on lack of normal control and persistence after stimulus removal. Neoplasms contain proliferating parenchymal cells and supporting stromal tissue. Benign tumors are well-differentiated, encapsulated, and do not metastasize, while malignant tumors are poorly differentiated, infiltrative, and can metastasize. The document also discusses tumor nomenclature, characteristics, causes, pathways of spread including lymphatic and hematogenous routes, common metastatic sites, staging, and grading of cancers.
This document discusses neoplasia (tumors) and provides details on their characteristics, types, growth patterns, spread, effects on the host, and grading and staging. Malignant tumors are described as having anaplastic cells with irregular shapes and sizes, abnormal nuclei, frequent mitosis, and loss of organization. They grow rapidly, invade locally and metastasize to distant sites. In contrast, benign tumors remain confined without invasion or metastasis. Grading reflects tumor differentiation while staging assesses tumor size, lymph node involvement, and presence of metastases using the TNM system.
This document defines key terms related to tumors and cancer progression. It discusses the types of tumors as benign or malignant. Malignant tumors can invade nearby tissues and metastasize to other parts of the body. Key terms defined include anaplasia, where cells lose their defining characteristics; pleomorphism, variability in cell size and shape; loss of polarity, a hallmark of cancer; dysplasia, abnormal but not cancerous cells; and carcinoma-in-situ, abnormal cells that have not spread from their origin. The summary emphasizes that cancer is uncontrolled cell growth that can occur in any tissue, and tumors can be either cancerous or noncancerous.
This document provides an overview of neoplasia (new growth or tumor). It defines a neoplasm as an abnormal mass of tissue with growth that exceeds and is uncoordinated with normal tissues. Neoplasms can be benign (non-cancerous) or malignant (cancerous). Malignant tumors are characterized by a lack of differentiation, local invasion, and metastasis (spread) to distant sites. The grading and staging of cancers provides information on the aggressiveness and extent of disease, which helps guide treatment decisions.
Neoplasms are characterized as either benign or malignant tumors. Benign tumors remain localized and do not invade surrounding tissue, while malignant tumors grow uncontrollably, invade surrounding areas, and metastasize to distant sites. Cancer development occurs through genetic mutations that alter cell growth and behavior over time. Malignant tumors are further classified by their site of origin, structure, and degree of differentiation through grading and staging systems.
This document provides an overview of cancer and its genetic basis. It defines cancer as a genetic disorder where normal cell growth control is lost. Cancer arises due to mutations in genes regulating cell proliferation, development, and other functions. These mutated genes, called oncogenes, promote uncontrolled cell growth. The document discusses various cancer risk factors and causes, including genetic predisposition, carcinogens, viruses, and lifestyle factors. It also describes the roles of oncogenes and tumor suppressor genes in cancer development.
Neoplasia refers to new or abnormal growth of tissue. Benign tumors remain localized and do not invade other tissues or spread to other parts of the body, while malignant tumors are invasive and metastatic. Malignant tumors are collectively referred to as cancer. The classification and diagnosis of tumors involves examining their histological features such as differentiation, growth rate, size, invasion and metastasis. Laboratory diagnosis of cancer involves histological examination of biopsies, cytological examination of cell samples, molecular analysis and identification of tumor markers. Staging of cancer determines the extent of disease spread and guides treatment decisions.
This document provides an overview of neoplasia (new growths) and cancer. It defines neoplasia as abnormal cell growth triggered by mutations affecting a single cell and its progeny. Neoplasms have two components - neoplastic cells that form the tumor and reactive stroma including connective tissue. Tumors are classified as benign or malignant based on their biological behavior and morphology. Malignant tumors invade, destroy structures, and metastasize, while benign tumors remain localized. Grading of cancers is based on differentiation, and staging incorporates tumor size, lymph node involvement, and metastasis. Laboratory diagnosis of cancer involves histologic, cytologic, molecular, and tumor marker methods.
Cancer is a group of diseases involving abnormal cell growth and potential to spread. It develops due to loss of normal growth control mechanisms. Cancers are classified by their primary site, tissue type, grade, and stage. The main tissue types are carcinomas (epithelial), sarcomas (connective tissues), myelomas (bone marrow), leukemias (blood), and lymphomas (lymph system). Cancers can also be classified based on their level of abnormality (grade) or extent of spread (stage). Understanding cancer classification helps determine diagnosis and treatment.
This document defines neoplasia and provides details on the classification and nomenclature of tumors. It begins by defining a neoplasm as an abnormal mass of tissue that grows in an uncoordinated manner. Benign tumors are non-invasive and localized, while malignant tumors are invasive and spreading. Tumors are classified based on the tissue of origin, such as carcinomas arising from epithelial tissue and sarcomas from connective tissue. The document further describes features of benign versus malignant tumors and provides examples of tumor classifications and histological slides.
This document provides an overview of neoplasia (abnormal growths) and cancer. It defines neoplasms and tumors, and distinguishes between benign and malignant types. Common cancer statistics in Bangladesh are presented. The key similarities and differences between hyperplasia and neoplasia, as well as benign versus malignant tumors are discussed. Various types of neoplasms are classified and examples are provided based on tissue of origin. Important cancer-related terminology like carcinoma, sarcoma, metastasis and anaplasia are explained. The document concludes with a comparison of carcinoma and sarcoma.
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Biology of cancer 134 L1 karobi moitra
1. WHAT IS CANCER AND HOW DOES IT AFFECT
THE HUMAN CONDITION ?
Karobi Moitra (Ph.D)
NCI Frederick , NIH
Cancer Inflammation Program
Human Genetics Section
Frederick MD.
2. Is cancer a single disease
or
a group of diseases ?
3. Cancer is a group of related diseases which are
characterized by uncontrolled cellular growth
and division
5. Origin of the word “Cancer”
The origin of the word cancer is credited to the Greek physician Hippocrates
(460–370 B.C.), considered the "Father of Medicine." Hippocrates used the
terms carcinos and carcinoma to describe non-ulcer forming and ulcer-forming
tumors. In Greek, these words refer to a crab, most likely applied to the
disease because the finger-like spreading projections from a cancer called to
mind the shape of a crab.
The Roman physician, Celsus (28-50 B.C.), later translated the Greek term
into cancer, the Latin word for crab.
Galen (130-200 A.D.), another Roman physician, used the word oncos (Greek
for swelling) to describe tumors. Galen's term is now used as a part of the
name for cancer specialists -- oncologists.
6. Cancer is associated with abnormal cellular
proliferation
Cells divide when they should not divide and they
lack the normal control systems to shut off unwanted
cell division
7. Loss of Normal Growth Control
Normal
cell division
Cell Suicide or Apoptosis
Cell damage—
no repair
Cancer
cell division
First Second Third Fourth or
mutation mutation mutation later mutation R
Uncontrolled growth
8. In most cases to form a contiguous cell mass
called a tumor
R
9. Example of Normal Growth
Dead cells
shed from
outer surface
Epidermis
Cell migration
Dividing cells
in basal layer
Dermis
Each time one of these basal cells divides, it produces two cells. One remains in the basal layer and
retains the capacity to divide. The other migrates out of the basal layer and loses the capacity to
divide. The number of dividing cells in the basal layer, therefore, stays the same. R
10. The Beginning of Cancerous Growth
During the development of skin cancer, the normal balance between cell division and cell loss is disrupted.
The basal cells now divide faster than is needed to replenish the cells being shed from the surface of the
skin. Each time one of these basal cells divides, the two newly formed cells will often retain the capacity to R
divide, thereby leading to an increase in the total number of dividing cells.
12. Tumors (Neoplasms)
Underlying tissue
R
This gradual increase in the number of dividing cells creates a growing mass of tissue called a “tumor” or “neoplasm.”
14. Types of cancer / precancerous subtypes:
According to growth type:
Neoplasia - growth of cells to form a new structure eg: a tumor
Hyperplasia - excessive no. of cells.
Dysplasia - loss of normal arrangement of tissue (precancerous)
Carcinoma-in-situ - uncontrolled growth of cells that remains
at the same place (non-invasive).
Invasive carcinoma - can invade surrounding tissue and also
undergo metastasis. R
15. Hyperplasia
Excessive growth
Normal Hyperplasia
R
16. Dysplasia
Excessive growth Loss of cellular structure
& tissue arrangement
Normal Hyperplasia Mild dysplasia
R
17. Normal to Invasive
Excessive growth Loss of cellular structure Excessive growth Invades
& tissue arrangement in place
Normal Hyperplasia Mild Carcinoma in
dysplasia situ (severe
dysplasia) Cancer
(invasive)
R
18. Types of cancer / precancerous subtypes:
According to growth type:
Neoplasia - growth of cells to form a new structure eg: a tumor
Hyperplasia - excessive no. of cells.
Dysplasia - loss of normal arrangement of tissue (precancerous)
Carcinoma-in-situ - uncontrolled growth of cells that remains
at the same place (non-invasive).
Invasive carcinoma - can invade surrounding tissue and also
undergo metastasis. R
19. According to tissue type affected :
Carcinoma - tumors made up of principally epithelial cells
(cells that line inner and outer surfaces).
eg: cervical and skin cancers.
Sarcoma - made up principally of connective tissue cells
(cartilage, bone etc.)
eg: osteosarcoma.
Leukemia - Neoplastic growth of leucocytes (WBC) .
Lymphoma - excessive production of lymphocytes by lymph
nodes and spleen.
eg: Hodgkins disease. R
20. Different Kinds of Cancer
Leukemias:
Some common
carcinomas: Bloodstream
Lung Lymphomas:
Lymph nodes
Breast (women)
Colon
Some common
Bladder sarcomas:
Prostate (men) Fat
Bone
Muscle R
21. According to tissue type affected :
Carcinoma - tumors made up of principally epithelial cells
(cells that line inner and outer surfaces).
eg: cervical and skin cancers.
Sarcoma - made up principally of connective tissue cells
(cartilage, bone etc.)
eg: osteosarcoma.
Leukemia - Neoplastic growth of leucocytes (WBC) .
Lymphoma - excessive production of lymphocytes by lymph
nodes and spleen.
eg: Hodgkins disease. R
22. According to metastasis (invading capacity)
Benign tumor - these tumors have restricted growth and tend
to remain localized.
eg: wart.
Malignant tumor - these tumors do not remain localized but
invade other tissue and give rise to
secondary tumors in other parts of the
body (metastasis).
R
23. Malignant versus Benign Tumors
Benign (not cancer) Malignant (cancer)
tumor cells grow cells invade
only locally and cannot neighboring tissues,
spread by invasion or enter blood vessels,
metastasis and metastasize to
different sites
Time
R
24. Invasion and Metastasis
1
Cancer cells invade
surrounding tissues
and blood vessels
2
Cancer cells are
transported by the
circulatory system
to distant sites
3
Cancer cells
reinvade and grow
at new location
R
25. Different kinds According to growth type:
of cancer Neoplasia - growth of cells to form a new structure eg: a tumor
Hyperplasia - excessive no. of cells.
Dysplasia - loss of normal arrangement of tissue (precancerous)
Carcinoma-in-situ - uncontrolled growth of cells that remains
at the same place (non-invasive).
Invasive carcinoma - can invade surrounding tissue and also
undergo metastasis.
According to tissue type affected : According to metastasis (invading capacity)
Carcinoma - tumors made up of principally epithelial cells Benign tumor - these tumors have restricted growth and tend
(cells that line inner and outer surfaces). to remain localized.
eg: cervical and skin cancers. eg: wart.
Sarcoma - made up principally of connective tissue cells
(cartilage, bone etc.)
eg: osteosarcoma. Malignant tumor - these tumors do not remain localized but
invade other tissue and give rise to
secondary tumors in other parts of the
Leukemia - Neoplastic growth of leucocytes (WBC) .
body (metastasis).
Lymphoma - excessive production of lymphocytes by lymph
nodes and spleen.
eg: Hodgkins disease.
R
26. Why Cancer Is Potentially Dangerous
Brain
Melanoma
cells travel
through
bloodstream
Liver
Melanoma
(initial tumor)
R
28. Naming Cancers
Cancer Prefixes Point to Location
Prefix Meaning
adeno- gland
chondro- cartilage
erythro- red blood cell
hemangio- blood vessels
hepato- liver
lipo- fat
lympho- lymphocyte
melano- pigment cell
myelo- bone marrow
myo- muscle
osteo- bone R
31. Characteristic adaptive features of cancer cells :
1. Loss of contact inhibition
Normal cells stop growing when their plasma membranes
come into contact with one another - normal cells stop
moving when they contact each other this is called
contact inhibition, cancer cells lose the property of
contact inhibition. Transformed cells do not stop dividing
after forming a monolayer division continues until several
layers of cells are formed.
R
32. 2. Unrestrained control of growth
Cancer cells lack the normal control systems to shut
off unwanted growth.
3. Metastasis
Metastasis is the spread of cancer cells from a primary
site of origin to other tissues where they grow as
secondary tumors.
R
33. Some biochemical properties of cancer cells :
1. Increased glycolysis (Warburg effect)
Otto Warburg observed that virtually every type of cancer
cells that form solid tumors excrete much larger quantities of
lactic acid than its normal counterpart. This is known as the
‘Warburg effect’.
Unlike normal cells, which break down sugar using oxidative
pathways (or the Krebs cycle), tumor cells used non-
oxidative pathways (glycolysis) to generate energy from
sugar.
R
34. 2. Alterations in cytoskeletal proteins
Less organized/ disorganized arrangement of
cytoskeletal proteins - such as myosin , tubulin etc.
R
35. 3. Loss of anchorage dependence
Cancer cells in culture can grow suspended in
media while most normal cells need to attach to a
substratum to grow (anchored).
R
36. 4. Cancer cells are seemingly immortal
Cancer cells in culture can continue to grow indefinitely.
R
37. The Somatic Mutation Theory
Of Cancer
Theodore Boveri 1914
He stated that the fundamental
cause of cancer was in chromatin
imbalance in the cells from which
cancer arises.
Evidence : Many cancers have
chromosomal abnormalities
R
44. What Causes Cancer?
Some viruses or bacteria
Some chemicals Radiation
Heredity
Diet
Hormones
R
45. Population-Based Studies
Regions of Highest Incidence
U.K.:
Lung
cancer
JAPAN:
Stomach CANADA:
cancer Leukemia
U.S.:
CHINA: Colon
Liver cancer
cancer BRAZIL:
AUSTRALIA: Cervical
Skin cancer
cancer
A striking finding to emerge from population studies is that cancers arise with different frequencies
in different areas of the world. For example, stomach cancer is especially frequent in Japan, colon
cancer is prominent in the United States, and skin cancer is common in Australia. What is the R
reason for the high rates of specific kinds of cancer in certain countries?
46. Heredity? Behaviors? Other Factors?
Colon Cancer Stomach Cancer
(Number of new cases (Number of new cases
per 100,000 people) per 100,000 people)
100 100
70
50
5 7
0 Japan Japanese U.S. 0 Japan Japanese U.S.
families families
in U.S. in U.S.
In theory, differences in heredity or environmental risk factors might be responsible for the different cancer
rates observed in different countries. Studies on people who have moved from one country to another
suggest that exposure to risk factors for cancer varies by geographic location. For example, in Japan, the
rate of colon cancer is lower, and the rate of stomach cancer is higher, than in the United States. But this
difference has been found to gradually disappear in Japanese families that have moved to the United States.
This suggests that the risk of developing the two kinds of cancer is not determined primarily by heredity. The R
change in risk for cancer for Japanese families could involve cultural, behavioral, or environmental factors
predominant in one location and not in the other.
47. Tobacco Use and Cancer
Some Cancer-Causing Chemicals in Tobacco Smoke
R
48. Low-Strength Radiation
High
Dallas
Skin
Cancer
Incidence Pittsburgh
Detroit
Low
Least Most
Annual Sunshine
(UV radiation)
Some atoms give off radiation, which is energy that travels through space. Prolonged or repeated
exposure to certain types of radiation can cause cancer. Cancer caused by the sun’s ultraviolet
radiation is most common in people who spend long hours in strong sunlight. Ultraviolet radiation
from sunlight is a low-strength type of radiation. Effective ways to protect against ultraviolet radiation
and to prevent skin cancer are to avoid going into strong, direct sunlight and to wear protective
clothing. Sunscreen lotions reduce the risk of some forms of skin cancers. R
49. High-Strength Radiation
High
Leukemia
Incidence
Low
Least Most
X-ray Dose
(atomic radiation)
Increased rates of cancer also have been detected in people exposed to high-strength forms of radiation such as
X-rays or radiation emitted from unstable atoms called radioisotopes. Because these two types of radiation are
stronger than ultraviolet radiation, they can penetrate through clothing and skin into the body. Therefore, high-
strength radiation can cause cancers of internal body tissues. Examples include cancer caused by nuclear fallout
R
from atomic explosions and cancers caused by excessive exposure to radioactive chemicals.
50. Lag Time
20-Year Lag Time Between
Smoking and Lung Cancer
Cigarette
consumption
(men)
4000
Lung
150
Cigarettes 3000 cancer
Smoked (men) Lung Cancer
per Person 100 Deaths (per
per Year 100,000 people)
2000
50
1000
1900 1920 1940 1960 1980
Year
Chemicals and radiation that are capable of triggering the development of cancer are called “carcinogens.” Carcinogens act through a
multistep process that initiates a series of genetic alterations (“mutations”) and stimulates cells to proliferate. A prolonged period of time is
usually required for these multiple steps. There can be a delay of several decades between exposure to a carcinogen and the onset of R
cancer. For example, young people exposed to carcinogens from smoking cigarettes generally do not develop cancer for 20 to 30 years.
This period between exposure and onset of disease is the lag time.
51. Viruses
Virus inserts
and changes
genes for
cell growth
Cancer-linked virus
R
52. Examples of Human Cancer Viruses
Some Viruses Associated with Human Cancers
R
53. Bacteria and Stomach Cancer
Patient’s H. pylori
tissue
sample
The bacterium Helicobacter pylori, which can cause stomach ulcers, has been associated with the
development of cancer, so people infected with H. pylori are at increased risk for stomach cancer.
Research is under way to define the genetic interactions between this infectious agent and its host
tissues that may explain why cancer develops. R
54. Heredity and Cancer
All Breast Cancer Patients
Inherited factor(s)
Other factor(s)
Cancer is not considered an inherited illness because most cases of cancer, perhaps 80 to 90 percent, occur in people
with no family history of the disease. However, a person’s chances of developing cancer can be influenced by the
inheritance of certain kinds of genetic alterations. These alterations tend to increase an individual’s susceptibility to
developing cancer in the future. For example, about 5 percent of breast cancers are thought to be due to inheritance of
particular form(s) of a “breast cancer susceptibility gene.”
R
55. Heredity Can Affect Many Types of Cancer
Inherited Conditions That Increase Risk for Cancer
Inherited mutations can influence a person’s risk of developing many types of cancer in
addition to breast cancer. For example, certain inherited mutations have been described
that increase a person’s risk of developing colon, kidney, bone, skin or other specific forms
of cancer. But these hereditary conditions are thought to be involved in only 10 percent or
fewer of all cancer cases.
R
56. Cancer is a group of related diseases which are
characterized by uncontrolled cellular growth
and division
Cells divide when they should not divide and they
lack the normal control systems to shut off unwanted
cell division
R