Seminario
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This study aimed to identify nucleolar proteins that are differentially expressed in leukemia cell lines. The researchers isolated nucleoli from acute myeloid leukemia and acute lymphoblastic leukemia cell lines. Proteomic analysis identified 36 proteins that differed between AML and ALL lines and 29 proteins between pre-B ALL and pre-T ALL lines. Western blot and immunofluorescence analysis showed higher nucleolar expression of prohibitin and TDP-43 in some leukemia lines compared to others. The results demonstrate differences in nucleolar protein composition between leukemia subtypes that could be exploited for leukemia identification and classification.
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Seminario 2
This study aimed to identify nucleolar proteins that are differentially expressed in various leukemia cell lines. The researchers isolated nucleoli from acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), pre-B ALL and pre-T ALL cell lines. Two-dimensional difference gel electrophoresis (2D-DIGE) identified proteins with different expression levels between cell lines. Western blot and immunofluorescence analysis showed prohibitin (PHB) and TAR DNA-binding protein 43 (TDP-43) were more strongly expressed in some cell line nucleoli. The results demonstrate differences in nucleolar protein composition between leukemia subtypes that could be used to identify them.
Unlocking the Phytotherapeutic Synergism between Beta-lapachone and Soybean-...
Unlocking the Phytotherapeutic Synergism between Beta-lapachone and Soybean-...Saheed Oluwasina Oseni
The present in vitro study demonstrates that combination treatments with β-lap and genistein are more potent in killing both PC3 and LNCaP cancer cells than treatment with either genistein or β-lap alone, and therefore, could offer an effective chemotherapy against androgen dependent and independent prostate cancer. This result provides a rationale for in vivo studies and other therapeutic synergism.cancer biology
Autophagy is a catabolic process in which cells degrade unnecessary or dysfunctional components through lysosomes. It plays an important but complex role in cancer by modulating cell death, quality control, the immune response, and acting as a tumor suppressor. The PI3K/AKT/mTOR pathway is a key regulator of autophagy and is often deregulated in cancer, leading to abnormal autophagy. Recent studies suggest autophagy may be important in cancer development, progression, and response to treatment, though its specific effects depend on the context.
molecular pathogenesis of carcinogenesis
Molecular Pathogenesis and mechanisms of carcinogenesis involve several key hallmarks and changes in cell physiology that drive cancer development and progression. The hallmarks include self-sufficiency in growth signals, evasion of growth suppression, resistance to cell death, replication immortality, induction of angiogenesis, activation of invasion and metastasis, immune evasion, microRNA involvement, and epigenetic alterations. Cancer results from dysregulation of oncogenes and tumor suppressor genes that control the normal cell cycle and proliferation.
Apoptosis Hussein Sabit
Cancer arises from genetic damage to DNA, disrupted cell differentiation, and blocked apoptosis. The six hallmarks of cancer cells are self-sufficient growth signals, resistance to anti-growth signals, immortality, resistance to cell death, sustained angiogenesis, and invasion/metastasis. Proto-oncogenes stimulate cell growth but can cause cancer when mutated, while tumor suppressor genes like p53 regulate the cell cycle to prevent cancer by activating apoptosis. Apoptosis is a genetically programmed process of cell death that is important for development and tissue homeostasis, and imbalances in apoptosis can lead to diseases.
Hallmarks of cancer
Cancer cells acquire several hallmarks that allow malignant growth and spread. These include self-sufficiency in growth signals, evading growth suppression, resisting cell death, unlimited replication potential, inducing angiogenesis, invading locally and spreading to distant sites, reprogramming metabolism, and avoiding immune destruction. Specifically, cancer cells overexpress growth factors and receptors, mutate tumor suppressors and cell death pathways, activate telomerase to achieve immortality, secrete angiogenic factors, degrade the extracellular matrix, and suppress their own immunogenicity. These hallmark capabilities collectively enable cancer to develop and progress.
Seminario biologia molecular
This document summarizes a study exploring the effects of baicalein (BAI) on bladder cancer cells. The study found that BAI inhibits proliferation and promotes apoptosis in bladder cancer cells. It also inhibits bladder cancer cell migration by down-regulating microRNA (miR)-106 expression. Specifically, BAI affects bladder cancer cells by inhibiting the JNK and MEK/ERK pathways through reducing miR-106 levels. P21 was also identified as a target of miR-106. The study utilized techniques like transfection, PCR, western blot analysis, and cell migration assays to analyze these regulatory mechanisms and effects of BAI on bladder cancer cells.
Carcinogenesis
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.
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Seminario 2
This study aimed to identify nucleolar proteins that are differentially expressed in various leukemia cell lines. The researchers isolated nucleoli from acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), pre-B ALL and pre-T ALL cell lines. Two-dimensional difference gel electrophoresis (2D-DIGE) identified proteins with different expression levels between cell lines. Western blot and immunofluorescence analysis showed prohibitin (PHB) and TAR DNA-binding protein 43 (TDP-43) were more strongly expressed in some cell line nucleoli. The results demonstrate differences in nucleolar protein composition between leukemia subtypes that could be used to identify them.
Unlocking the Phytotherapeutic Synergism between Beta-lapachone and Soybean-...
Unlocking the Phytotherapeutic Synergism between Beta-lapachone and Soybean-...Saheed Oluwasina Oseni
The present in vitro study demonstrates that combination treatments with β-lap and genistein are more potent in killing both PC3 and LNCaP cancer cells than treatment with either genistein or β-lap alone, and therefore, could offer an effective chemotherapy against androgen dependent and independent prostate cancer. This result provides a rationale for in vivo studies and other therapeutic synergism.cancer biology
Autophagy is a catabolic process in which cells degrade unnecessary or dysfunctional components through lysosomes. It plays an important but complex role in cancer by modulating cell death, quality control, the immune response, and acting as a tumor suppressor. The PI3K/AKT/mTOR pathway is a key regulator of autophagy and is often deregulated in cancer, leading to abnormal autophagy. Recent studies suggest autophagy may be important in cancer development, progression, and response to treatment, though its specific effects depend on the context.
molecular pathogenesis of carcinogenesis
Molecular Pathogenesis and mechanisms of carcinogenesis involve several key hallmarks and changes in cell physiology that drive cancer development and progression. The hallmarks include self-sufficiency in growth signals, evasion of growth suppression, resistance to cell death, replication immortality, induction of angiogenesis, activation of invasion and metastasis, immune evasion, microRNA involvement, and epigenetic alterations. Cancer results from dysregulation of oncogenes and tumor suppressor genes that control the normal cell cycle and proliferation.
Apoptosis Hussein Sabit
Cancer arises from genetic damage to DNA, disrupted cell differentiation, and blocked apoptosis. The six hallmarks of cancer cells are self-sufficient growth signals, resistance to anti-growth signals, immortality, resistance to cell death, sustained angiogenesis, and invasion/metastasis. Proto-oncogenes stimulate cell growth but can cause cancer when mutated, while tumor suppressor genes like p53 regulate the cell cycle to prevent cancer by activating apoptosis. Apoptosis is a genetically programmed process of cell death that is important for development and tissue homeostasis, and imbalances in apoptosis can lead to diseases.
Hallmarks of cancer
Cancer cells acquire several hallmarks that allow malignant growth and spread. These include self-sufficiency in growth signals, evading growth suppression, resisting cell death, unlimited replication potential, inducing angiogenesis, invading locally and spreading to distant sites, reprogramming metabolism, and avoiding immune destruction. Specifically, cancer cells overexpress growth factors and receptors, mutate tumor suppressors and cell death pathways, activate telomerase to achieve immortality, secrete angiogenic factors, degrade the extracellular matrix, and suppress their own immunogenicity. These hallmark capabilities collectively enable cancer to develop and progress.
Seminario biologia molecular
This document summarizes a study exploring the effects of baicalein (BAI) on bladder cancer cells. The study found that BAI inhibits proliferation and promotes apoptosis in bladder cancer cells. It also inhibits bladder cancer cell migration by down-regulating microRNA (miR)-106 expression. Specifically, BAI affects bladder cancer cells by inhibiting the JNK and MEK/ERK pathways through reducing miR-106 levels. P21 was also identified as a target of miR-106. The study utilized techniques like transfection, PCR, western blot analysis, and cell migration assays to analyze these regulatory mechanisms and effects of BAI on bladder cancer cells.
Carcinogenesis
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.
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In this presentation I review the article Hallmarks of cancer: next generation, from Hanahan and Weinberg, and make a parallel with potential and current targets of radiopharmaceuticals for diagnosis and treatment.
Apoptosis
Apoptosis is a tightly regulated process of programmed cell death that removes unnecessary or damaged cells. It is mediated by caspases, cysteine-dependent aspartate-directed proteases, that cleave key cellular proteins and lead to cell death. Apoptosis occurs through the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and plays an important role in development, tissue homeostasis, and defense against infection and cancer. Defects in apoptosis can lead to neurodegenerative diseases, autoimmunity, and cancer.
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Hallmarks of cancer
The document discusses the hallmarks of cancer as proposed by Hanahan and Weinberg. It identifies the eight hallmarks as sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, deregulating cellular energetics, and avoiding immune destruction. It also discusses two enabling characteristics - genome instability and mutation, and tumor-promoting inflammation. Finally, it summarizes how several of these hallmarks, including sustaining proliferative signaling, activating invasion and metastasis, resisting cell death, and genome instability and mutation have been identified in breast cancer and contribute to its heterogeneity and treatment resistance.
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1. The document discusses fundamentals of host defense and innate immunity, focusing on physical and chemical defenses, the inflammatory response, and cellular defenses as part of the innate immune system.
2. Pattern recognition receptors (PRRs) play an important role in innate immunity by recognizing pathogen-associated molecular patterns (PAMPs) from microbes. Toll-like receptors (TLRs) are a major class of PRRs that signal the presence of various pathogens.
3. Innate immunity provides rapid response to infection prior to adaptive immunity and helps initiate adaptive immune responses through cytokines and antigen presentation. Therapeutic manipulation of TLRs may enhance or suppress immune responses.
N E O P L A S I A 2
The document discusses the molecular basis of neoplasia and carcinogenesis. It states that non-lethal genetic damage underlies carcinogenesis, which can be acquired or inherited. A tumor forms from the clonal expansion of a single damaged cell and further acquires mutations as it progresses. The four main classes of regulatory genes targeted are proto-oncogenes, tumor suppressor genes, apoptosis genes, and DNA repair genes. Carcinogenesis is a multistep process involving accumulating genetic lesions.
Hallmarks of Cancer
The document summarizes Hanahan and Weinberg's hallmarks of cancer. It describes the six original hallmarks proposed in 2000 of self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. In 2011, they added two emerging hallmarks of deregulating cellular energetics and avoiding immune detection, as well as two enabling characteristics of genome instability and tumor-promoting inflammation.
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Cancer is a deadly disease where cells in the body attack and destroy healthy tissue, leading to sickness and death. A tumour forms from cells that multiply uncontrollably due to DNA mutations caused by carcinogens like tobacco smoke and radiation. Common cancer treatments are surgery to remove tumours, chemotherapy using chemicals to kill cancer cells, and radiation therapy employing radiation to damage cancer cell DNA. Preventing cancer involves eating a healthy diet, limiting red meat and sugar, and maintaining an active lifestyle.
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The document describes the nCounter Analysis System, a technology for multiplexed digital detection of target molecules without compromising data quality or quantity. Key points:
- It allows multiplexing of up to 800 targets in a single tube with a simple workflow and automated processing requiring only 15 minutes of hands-on time.
- Data output includes target identifiers, count numbers, and internal controls, enabling high quantitative reproducibility across assays.
- The system directly assays tissue, cell, and blood lysates as well as FFPE samples with no need for amplification, reverse transcription, or sample partitioning.
Hallmarks of cancer
Cancer cells exhibit six hallmarks that allow tumor growth and metastasis. They are: self-sufficiency in growth signals, insensitivity to anti-growth signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Cancer cells achieve these hallmarks through genetic and epigenetic alterations that disrupt normal cell signaling pathways.
Clinical characteristics of a group of patients with multiple myeloma who had...
This document summarizes key information about multiple myeloma (MM), including its characteristics, diagnosis, and treatments. MM is a type of cancer caused by uncontrolled plasma cell proliferation, resulting in monoclonal immunoglobulin production. It is characterized by low blood counts, bone problems, infections, kidney failure, and monoclonal gammopathy. Diagnosis involves medical history, physical exam, laboratory tests (including blood counts, protein electrophoresis), bone marrow biopsy, and imaging. Treatments discussed include chemotherapy regimens containing bortezomib, thalidomide, dexamethasone, and stem cell transplantation. The objective of the study was to analyze clinical characteristics of MM patients with two different lambda light chains.
SEMINARIO BIOMOL - Isabella Buitrago
This document summarizes a study that examined the relationship between arsenic trioxide, intravesical bacillus Calmette-Guerin (BCG), and bladder cancer. The study found that arsenic trioxide and BCG work together to counter cancer by disabling the IER3/Nrf2 pathway and promoting IL-6 and IL-8 expression. Various methods were used including RT-qPCR, western blot, immunohistochemistry, and ELISA. The results showed that arsenic trioxide and BCG were able to promote apoptosis of bladder tumor cells and decrease tumor volume and weight. The conclusions state that more research is needed to develop innovative cancer treatments using toxic agents and inactivated bacteria.
The Genetic Basis of Cancer
Introduction to Cancer
Stem cells and cancer cells
major pathways that lead to formation of tumors.
Tumor Supressors
Colon cancer to prove Knudson hypothesis.
The modern treatments available to treat cancer.
Apoptosis and the response to chemotherapy
1) Apoptosis is a programmed cell death mechanism that is important for normal development and tissue homeostasis, but is often inhibited in cancer cells to allow uncontrolled growth.
2) There are three main apoptotic pathways - extrinsic, intrinsic, and granzyme-mediated - that involve initiator and executioner caspases.
3) Cancer therapies like chemotherapy and radiation can induce apoptosis in tumor cells, but tumors evolve mechanisms to evade apoptosis like downregulating death receptors or overexpressing anti-apoptotic proteins.
4) New targeted therapies are being developed to manipulate the apoptotic pathway in cancer cells by inhibiting anti-apoptotic proteins or activating death receptors to selectively kill tumor cells.
Part 2 Nhl
Follicular lymphoma is the most common form of indolent NHL in the United States. It arises from germinal center B cells and is strongly associated with a translocation involving BCL2, which leads to overexpression of the BCL2 protein and promotes cell survival. Diffuse large B-cell lymphoma is the most common form of aggressive NHL, often presenting as a rapidly enlarging mass. Burkitt lymphoma is very aggressive and occurs in three clinical variants associated with distinct epidemiological factors and EBV infection status. Multiple myeloma is characterized by proliferation of plasma cells in the bone marrow leading to lytic bone lesions and organ dysfunction.
9.3 Prelude To Cancer
Mutations in genes that regulate the cell cycle, such as proto-oncogenes and tumor suppressor genes, can lead to cancer if they cause cells to continuously divide. Multiple mutations are often required for cancer to develop, including mutations that allow uncontrolled growth and inhibit anchorage dependence. Cancer progresses as mutations accumulate, first forming benign tumors that could develop into malignant tumors if additional mutations occur, allowing invasion of other tissues and organs.
Carcinogenesis
Carcinogenesis refers to the process by which a normal cell is transformed into a malignant cell and repeatedly divides to become a cancer
Chemicals which initiate this process is called chemical carcinogens
Chemicals which increase the effectiveness of carcinogens is called co-carcinogens
REGULATORY BACKGROUND
ROLE OF PROTO-ONCOGENES AND TUMOR SUPPRESSOR GENES
ACTIVATION OF PROTO ONCOGENES
OXIDATIVE STRESS IN CARCINOGENESIS
OECD guidelines
451- Carcinogenecity studies
453- Combined chronic toxicity/carcinogenecity
ICH guidelines
S1A- Guideline on the need for carcinogenicity studies of
pharmaceuticals
S1B- Testing for carcinogenicity of pharmaceuticals
S1C- Dose selection for carcinogenicity studies of pharmaceuticals
Metabolism and cancer 2013
The document discusses the relationship between cancer and cellular metabolism. It provides a brief history of how Otto Warburg first observed that cancer cells metabolize glucose differently than normal cells through aerobic glycolysis. More recently, there has been a renaissance in studying how oncogenes and tumor suppressor genes can alter cellular metabolism in cancer. The document then overviews key metabolic pathways and regulators that are altered in cancer, such as mutations in the TCA cycle enzymes IDH1 and IDH2. It describes techniques that can be used to study metabolism and cancer, such as analyzing mutations, gene expression, epigenetic changes, and cellular pathways. Throughout, it provides examples of studies investigating specific metabolic changes in cancer, such as how miRNAs
Tumor And Microenvironment
1) Tumors exist within a complex microenvironment consisting of various cell types that influence tumor growth, progression, and metastasis.
2) Chronic inflammation can promote tumor development by increasing genetic mutations while also stimulating angiogenesis and tumor cell proliferation.
3) The tumor microenvironment interacts bidirectionally with cancer cells to encourage processes like angiogenesis, immune suppression, invasion, and metastasis through factors such as TGF-β, VEGF, and cytokines.
4) Therapies targeting the tumor microenvironment can impact its composition and make cancer cells more invasive, highlighting the need for combination treatments.
Development of cancer
Cancer is characterized by uncontrolled cell growth and spread. Key points:
- Oncogenes are mutated proto-oncogenes that regulate cell growth. Carcinogens and hereditary factors can cause mutations.
- Cancer cells lack contact inhibition and crowd out healthy cells. They reproduce rapidly, forming tumors.
- Tumors can be benign or malignant, with malignant tumors spreading to other sites (metastasizing).
- Early detection through screening and self-exams improves cancer treatment outcomes. Risk-reducing behaviors include not smoking, limiting alcohol, eating fruits/veggies, wearing sunscreen, and exercising regularly.
Cell Mechanisms Presentation.pdf
This document provides an overview of a presentation on cell mechanisms that covers four main topics:
1) The mechanisms that confine cells and tissues to specific anatomical sites through intercellular adhesion and memory.
2) Four types of cellular adaptations.
3) A comparison of necrosis and apoptosis, the two main types of cell death. Necrosis is unregulated cell death that causes inflammation, while apoptosis is a regulated process of cell suicide.
4) At least 20 slides are required to be created in PowerPoint or Impress covering these topics using at least four scholarly sources.
2018 BDSRA Cotman MGH Center for Genomic Medicine
This document summarizes the research of the MGH Center for Genomic Medicine Ba>en Disease Research Program. They are invesFgaFng the molecular basis of neuronal ceroid lipofuscinosis (NCL) through geneFc research with the goal of developing drugs. Their objecFves include understanding how geneFc mutaFons lead to NCL at the cellular level and which processes cause disease symptoms. They use geneFc model organisms and human cell cultures to test hypotheses and idenFfy drug targets. Their research aims to improve detecFon of geneFc causes, further the understanding of NCL proteins, and advance translaFon of findings to help human paF
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Hallmarks of cancer and radiopharmaceuticals
In this presentation I review the article Hallmarks of cancer: next generation, from Hanahan and Weinberg, and make a parallel with potential and current targets of radiopharmaceuticals for diagnosis and treatment.
Apoptosis
Apoptosis is a tightly regulated process of programmed cell death that removes unnecessary or damaged cells. It is mediated by caspases, cysteine-dependent aspartate-directed proteases, that cleave key cellular proteins and lead to cell death. Apoptosis occurs through the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and plays an important role in development, tissue homeostasis, and defense against infection and cancer. Defects in apoptosis can lead to neurodegenerative diseases, autoimmunity, and cancer.
Biology of cancer lecture 5 cell cycle Karobi Moitra
The document discusses the cell cycle, which is a programmed series of events that allows a cell to duplicate its contents and divide into two daughter cells. It describes the stages of the cell cycle including gap phases, DNA synthesis, and mitosis. Checkpoint controls ensure each step is completed before advancing to the next. Cancer cells often lose these checkpoint controls, allowing uncontrolled cell division. The roles of cyclins, CDKs, and inhibitors like pRb in regulating the cell cycle are also summarized. Understanding the cell cycle can aid developing anticancer drugs that target specific regulatory proteins.
Hallmarks of cancer
The document discusses the hallmarks of cancer as proposed by Hanahan and Weinberg. It identifies the eight hallmarks as sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, deregulating cellular energetics, and avoiding immune destruction. It also discusses two enabling characteristics - genome instability and mutation, and tumor-promoting inflammation. Finally, it summarizes how several of these hallmarks, including sustaining proliferative signaling, activating invasion and metastasis, resisting cell death, and genome instability and mutation have been identified in breast cancer and contribute to its heterogeneity and treatment resistance.
10884 2
1. The document discusses fundamentals of host defense and innate immunity, focusing on physical and chemical defenses, the inflammatory response, and cellular defenses as part of the innate immune system.
2. Pattern recognition receptors (PRRs) play an important role in innate immunity by recognizing pathogen-associated molecular patterns (PAMPs) from microbes. Toll-like receptors (TLRs) are a major class of PRRs that signal the presence of various pathogens.
3. Innate immunity provides rapid response to infection prior to adaptive immunity and helps initiate adaptive immune responses through cytokines and antigen presentation. Therapeutic manipulation of TLRs may enhance or suppress immune responses.
N E O P L A S I A 2
The document discusses the molecular basis of neoplasia and carcinogenesis. It states that non-lethal genetic damage underlies carcinogenesis, which can be acquired or inherited. A tumor forms from the clonal expansion of a single damaged cell and further acquires mutations as it progresses. The four main classes of regulatory genes targeted are proto-oncogenes, tumor suppressor genes, apoptosis genes, and DNA repair genes. Carcinogenesis is a multistep process involving accumulating genetic lesions.
Hallmarks of Cancer
The document summarizes Hanahan and Weinberg's hallmarks of cancer. It describes the six original hallmarks proposed in 2000 of self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. In 2011, they added two emerging hallmarks of deregulating cellular energetics and avoiding immune detection, as well as two enabling characteristics of genome instability and tumor-promoting inflammation.
04 cancer
Cancer is a deadly disease where cells in the body attack and destroy healthy tissue, leading to sickness and death. A tumour forms from cells that multiply uncontrollably due to DNA mutations caused by carcinogens like tobacco smoke and radiation. Common cancer treatments are surgery to remove tumours, chemotherapy using chemicals to kill cancer cells, and radiation therapy employing radiation to damage cancer cell DNA. Preventing cancer involves eating a healthy diet, limiting red meat and sugar, and maintaining an active lifestyle.
cancer
The document describes the nCounter Analysis System, a technology for multiplexed digital detection of target molecules without compromising data quality or quantity. Key points:
- It allows multiplexing of up to 800 targets in a single tube with a simple workflow and automated processing requiring only 15 minutes of hands-on time.
- Data output includes target identifiers, count numbers, and internal controls, enabling high quantitative reproducibility across assays.
- The system directly assays tissue, cell, and blood lysates as well as FFPE samples with no need for amplification, reverse transcription, or sample partitioning.
Hallmarks of cancer
Cancer cells exhibit six hallmarks that allow tumor growth and metastasis. They are: self-sufficiency in growth signals, insensitivity to anti-growth signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Cancer cells achieve these hallmarks through genetic and epigenetic alterations that disrupt normal cell signaling pathways.
Clinical characteristics of a group of patients with multiple myeloma who had...
This document summarizes key information about multiple myeloma (MM), including its characteristics, diagnosis, and treatments. MM is a type of cancer caused by uncontrolled plasma cell proliferation, resulting in monoclonal immunoglobulin production. It is characterized by low blood counts, bone problems, infections, kidney failure, and monoclonal gammopathy. Diagnosis involves medical history, physical exam, laboratory tests (including blood counts, protein electrophoresis), bone marrow biopsy, and imaging. Treatments discussed include chemotherapy regimens containing bortezomib, thalidomide, dexamethasone, and stem cell transplantation. The objective of the study was to analyze clinical characteristics of MM patients with two different lambda light chains.
SEMINARIO BIOMOL - Isabella Buitrago
This document summarizes a study that examined the relationship between arsenic trioxide, intravesical bacillus Calmette-Guerin (BCG), and bladder cancer. The study found that arsenic trioxide and BCG work together to counter cancer by disabling the IER3/Nrf2 pathway and promoting IL-6 and IL-8 expression. Various methods were used including RT-qPCR, western blot, immunohistochemistry, and ELISA. The results showed that arsenic trioxide and BCG were able to promote apoptosis of bladder tumor cells and decrease tumor volume and weight. The conclusions state that more research is needed to develop innovative cancer treatments using toxic agents and inactivated bacteria.
The Genetic Basis of Cancer
Introduction to Cancer
Stem cells and cancer cells
major pathways that lead to formation of tumors.
Tumor Supressors
Colon cancer to prove Knudson hypothesis.
The modern treatments available to treat cancer.
Apoptosis and the response to chemotherapy
1) Apoptosis is a programmed cell death mechanism that is important for normal development and tissue homeostasis, but is often inhibited in cancer cells to allow uncontrolled growth.
2) There are three main apoptotic pathways - extrinsic, intrinsic, and granzyme-mediated - that involve initiator and executioner caspases.
3) Cancer therapies like chemotherapy and radiation can induce apoptosis in tumor cells, but tumors evolve mechanisms to evade apoptosis like downregulating death receptors or overexpressing anti-apoptotic proteins.
4) New targeted therapies are being developed to manipulate the apoptotic pathway in cancer cells by inhibiting anti-apoptotic proteins or activating death receptors to selectively kill tumor cells.
Part 2 Nhl
Follicular lymphoma is the most common form of indolent NHL in the United States. It arises from germinal center B cells and is strongly associated with a translocation involving BCL2, which leads to overexpression of the BCL2 protein and promotes cell survival. Diffuse large B-cell lymphoma is the most common form of aggressive NHL, often presenting as a rapidly enlarging mass. Burkitt lymphoma is very aggressive and occurs in three clinical variants associated with distinct epidemiological factors and EBV infection status. Multiple myeloma is characterized by proliferation of plasma cells in the bone marrow leading to lytic bone lesions and organ dysfunction.
9.3 Prelude To Cancer
Mutations in genes that regulate the cell cycle, such as proto-oncogenes and tumor suppressor genes, can lead to cancer if they cause cells to continuously divide. Multiple mutations are often required for cancer to develop, including mutations that allow uncontrolled growth and inhibit anchorage dependence. Cancer progresses as mutations accumulate, first forming benign tumors that could develop into malignant tumors if additional mutations occur, allowing invasion of other tissues and organs.
Carcinogenesis
Carcinogenesis refers to the process by which a normal cell is transformed into a malignant cell and repeatedly divides to become a cancer
Chemicals which initiate this process is called chemical carcinogens
Chemicals which increase the effectiveness of carcinogens is called co-carcinogens
REGULATORY BACKGROUND
ROLE OF PROTO-ONCOGENES AND TUMOR SUPPRESSOR GENES
ACTIVATION OF PROTO ONCOGENES
OXIDATIVE STRESS IN CARCINOGENESIS
OECD guidelines
451- Carcinogenecity studies
453- Combined chronic toxicity/carcinogenecity
ICH guidelines
S1A- Guideline on the need for carcinogenicity studies of
pharmaceuticals
S1B- Testing for carcinogenicity of pharmaceuticals
S1C- Dose selection for carcinogenicity studies of pharmaceuticals
Metabolism and cancer 2013
The document discusses the relationship between cancer and cellular metabolism. It provides a brief history of how Otto Warburg first observed that cancer cells metabolize glucose differently than normal cells through aerobic glycolysis. More recently, there has been a renaissance in studying how oncogenes and tumor suppressor genes can alter cellular metabolism in cancer. The document then overviews key metabolic pathways and regulators that are altered in cancer, such as mutations in the TCA cycle enzymes IDH1 and IDH2. It describes techniques that can be used to study metabolism and cancer, such as analyzing mutations, gene expression, epigenetic changes, and cellular pathways. Throughout, it provides examples of studies investigating specific metabolic changes in cancer, such as how miRNAs
Tumor And Microenvironment
1) Tumors exist within a complex microenvironment consisting of various cell types that influence tumor growth, progression, and metastasis.
2) Chronic inflammation can promote tumor development by increasing genetic mutations while also stimulating angiogenesis and tumor cell proliferation.
3) The tumor microenvironment interacts bidirectionally with cancer cells to encourage processes like angiogenesis, immune suppression, invasion, and metastasis through factors such as TGF-β, VEGF, and cytokines.
4) Therapies targeting the tumor microenvironment can impact its composition and make cancer cells more invasive, highlighting the need for combination treatments.
Development of cancer
Cancer is characterized by uncontrolled cell growth and spread. Key points:
- Oncogenes are mutated proto-oncogenes that regulate cell growth. Carcinogens and hereditary factors can cause mutations.
- Cancer cells lack contact inhibition and crowd out healthy cells. They reproduce rapidly, forming tumors.
- Tumors can be benign or malignant, with malignant tumors spreading to other sites (metastasizing).
- Early detection through screening and self-exams improves cancer treatment outcomes. Risk-reducing behaviors include not smoking, limiting alcohol, eating fruits/veggies, wearing sunscreen, and exercising regularly.
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Cell Mechanisms Presentation.pdf
This document provides an overview of a presentation on cell mechanisms that covers four main topics:
1) The mechanisms that confine cells and tissues to specific anatomical sites through intercellular adhesion and memory.
2) Four types of cellular adaptations.
3) A comparison of necrosis and apoptosis, the two main types of cell death. Necrosis is unregulated cell death that causes inflammation, while apoptosis is a regulated process of cell suicide.
4) At least 20 slides are required to be created in PowerPoint or Impress covering these topics using at least four scholarly sources.
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Chromosomal abnormalities often involve gaining or losing chromosomes together across cancer types and can develop different cancers like kidney, bone, and liver cancers. Studies of consistent chromosomal aberrations in specific cancer types have identified some cancer-causing genes. Understanding chromosomal patterns may be key to preventing cancer development and progression.
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2017 BDSRA Cotman, Chandrachud, Hillje, Ilo, Sci, Nowell and Klein CLN2, CLN3...Batten Disease Support and Research Association
This document summarizes research being conducted at MGH on neuronal ceroid lipofuscinoses (NCL), also known as Batten disease. The research aims to understand how genetic mutations lead to NCL at the molecular level in order to develop therapies. The researchers use genetic model organisms and human cell cultures to study NCL protein function and disease processes. They also work to identify unknown genetic causes of NCL and modifiers through sequencing. The findings from these models are helping identify new drug targets currently under study for drug development.Applications of molecular genetics
Molecular genetics is the study of DNA structure, replication, and influence on organisms. Techniques of molecular genetics include gene therapy, amplification, polymerase chain reaction (PCR), cell culture, DNA cloning in bacteria, gel electrophoresis, and isolation of DNA. Gene therapy is an experimental technique that uses genes to treat or prevent disease. PCR amplifies a segment of DNA, allowing scientists to study small samples. Cell culture provides model systems to study cell physiology. DNA cloning makes copies of DNA fragments in bacteria. Gel electrophoresis separates DNA fragments by size. Isolation of DNA extracts free DNA molecules for further analysis. These techniques have applications in medicine, research, forensics, and molecular biology.
Anti-Neoplastic agents (Anti-Cancer)
This document discusses cancer and chemotherapy. It defines cancer as uncontrolled growth and spread of abnormal cells that can lead to death if left untreated. Malignant tumors can invade tissues and spread, while benign tumors do not. Chemotherapy refers to drugs used to kill cells, including anticancer agents. The effects of chemotherapy depend on the cancer's stage and location. Cancer development is influenced by genetic and environmental factors. The document then discusses the cell cycle, tumor suppressor genes, apoptosis pathways, limitations of chemotherapy, adverse effects, and classifications of chemotherapy drugs including alkylating agents.
2016 BDSRA Cotman, Chandrachud, Hillje, Ilo, Nowell, Oh CLN2, CLN3, CLN6, Adu...
2016 BDSRA Cotman, Chandrachud, Hillje, Ilo, Nowell, Oh CLN2, CLN3, CLN6, Adu...Batten Disease Support and Research Association
This document summarizes research investigating the molecular basis of neuronal ceroid lipofuscinosis (NCL), a group of genetic disorders. The research aims to improve diagnosis and develop treatments by:
1) Using genetic model organisms and human cell cultures to study how mutations in NCL genes disrupt cellular processes and lead to symptoms;
2) Identifying new drug targets and screening drug libraries to find potential treatments; and
3) Collaborating with other groups to advance understanding of NCL diseases at the molecular level in order to develop better targeted therapies.Seminario molecular!!!!!
This study aimed to determine the relationship between differential DNA methylation and mRNA expression in uterine leiomyoma. The researchers obtained tissue samples from hysterectomy patients and isolated DNA and RNA. They performed genome-wide DNA methylation sequencing and RT-PCR. Their results demonstrated that hypermethylation of CpG islands in gene promoter regions was associated with transcriptional repression of tumor suppressor genes in uterine leiomyoma. Understanding the epigenetic mechanisms involved in leiomyoma pathogenesis could help develop diagnostic biomarkers and therapeutic targets for the disease.
Molecular techniques for pathology research - MDX .pdf
This document discusses molecular techniques used in pathology research such as PCR, microarrays, next generation sequencing, immunohistochemistry, ELISA, and Western blotting. It provides details on each technique including the basic principles, applications in research, and examples of uses in studies of gene expression, cancer, bone disease, and growth retardation. The learning outcomes are to understand these techniques and their uses in basic and clinical research.
DNA REPLICATION NEWS
The document discusses DNA replication and recent research findings. It begins with an introduction to DNA replication and how it allows cells to duplicate their genome during cell division. It then summarizes two recent studies: one finding that the replication stress response protein SMARCAL1 plays a key role in maintaining telomere stability, and the other showing that the protein APOBEC can induce mutations by taking advantage of single-stranded DNA during replication of the lagging strand. The studies provide new insights into cancer cell replication pathways and genes that could be targeted for new cancer therapies.
DNA Methylation and Epigenetic Events Underlying Renal Cell Carcinomas
Renal cell carcinoma (RCC) refers to a group of tumors that develop from the epithelium of the kidney tubes, including clear cell
RCC, papillary RCC, and chromophobe RCC. Most clear cell renal
carcinomas have a large histologic subtype, genetic or epigenetic
genetic von Hippel-Lindau (VHL). A comprehensive analysis of
the genetic modification genome suggested that chromosome 3p
loss and chromosome gains 5q and 7 may be a significant copy
defect in the development of clear kidney cell cancer. A more potent renal cell carcinoma may develop if chromosome 1p, 4, 9,
13q, or 14q is also lost. Renal carcinogenesis is not associated with
chronic inflammation or histological changes. However, regional hypermethylation of DNA in CpG C-type islands has already
accumulated in cancer-free kidney tissue, implying that the presence of malignant kidney lesions may also be detected by modified
DNA methylation. Modification of DNA methylation in cancerous
kidney tissue may advance kidney tissue to epigenetic mutations
and genes, leading to more serious cancers and even determining
a patient’s outcome
Topic of the month.... Primary CNS lymphoma
Non-Hodgkin's lymphoma can invade the brain and central nervous system, leading to primary central nervous system lymphoma (PCNSL). PCNSL resembles diffuse large B-cell lymphoma but the molecular mechanisms that cause PCNSL are uncertain. Survival has improved with methotrexate-based chemotherapy instead of radiation, but most patients eventually relapse. Advances in imaging and molecular markers have improved diagnosis but better tools are still needed to monitor treatment response and identify therapeutic targets.
Juan carlos review paper final
Proteomics and metabolomics studies are investigating biomarkers for early detection of amyotrophic lateral sclerosis (ALS). Proteomics identified three biomarkers, including decreased transthyretin and increased cystatin C levels. Metabolomics identified 17 potential biomarkers by analyzing cerebrospinal fluid and found perturbations in glucose metabolism. While these areas of research have advanced biomarker identification, validation of results is still needed. Continued studies may allow biomarkers to be used in routine patient checkups to enable early diagnosis and treatment of ALS.
Order a20171110 83
Acute lymphocytic leukemia (ALL) is a cancer of the lymphoid cells in the bone marrow. Early symptoms include fever, fatigue, and enlarged lymph nodes. Diagnostic tests include blood tests, bone marrow biopsies, imaging scans, and spinal fluid tests to determine the extent of the cancer's spread. Treatment involves induction therapy to eliminate leukemia cells, consolidation therapy to destroy remaining cells, and maintenance therapy to prevent regrowth of the cancer.
Apoptosis
Apoptosis is a programmed cell death process that occurs in multicellular organisms. During apoptosis, cells undergo changes such as blebbing, shrinkage, and nuclear fragmentation. Between 50-70 billion cells die per day in the human body through apoptosis. Defects in apoptotic processes can lead to diseases such as cancer by allowing non-functional cells to continue proliferating. Apoptosis involves signaling pathways, regulation of mitochondria, caspase activation, and removal of dead cells.
Abstract Triennale
This document summarizes a thesis that uses induced pluripotent stem cells (iPSCs) as an in vitro model of Parkinson's disease. The thesis reprogrammed fibroblasts from patients with a genetic form of Parkinson's caused by SNCA gene duplication and from healthy donors into iPSCs. It then differentiated these iPSCs into dopaminergic neurons to evaluate differences in phenotype between healthy and affected cells. In particular, the thesis aims to investigate autophagy in these neurons under stress conditions, as autophagy has been linked to the clearance of alpha-synuclein, which seems impaired in Parkinson's disease.
A Detailed study on Lupus Nephritis
This document summarizes a study on lupus nephritis. It begins by explaining that lupus nephritis is a disease caused by systemic lupus erythematosus (SLE) that results in kidney inflammation. It then discusses the pathogenesis of lupus nephritis, including genetic factors, immune system activation by nuclear particles, and lymphocyte expansion. Symptoms, diagnosis, and treatment options are also outlined, including corticosteroids, immunosuppressive drugs, managing blood pressure, and dialysis or kidney transplantation in severe cases. The conclusion states that lupus nephritis remains a major SLE complication but improved understanding of its causes and management have led to more effective therapies.
Microvascular complication (m)(t)
This document discusses retinopathy of prematurity (ROP), including its types, causes, pathology, treatment, and prevention. ROP is a disease affecting the retina of premature infants, caused by abnormal blood vessel growth. It begins with incomplete retinal vascularization and can progress to elevated ridges and extra-retinal fibrovascular proliferation. Treatment involves laser therapy or cryotherapy to ablate the abnormal blood vessels. Vitamin supplementation and controlling oxygen exposure can help prevent ROP.
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Seminario
- 1. Nucleolar proteins with altered expression in leukemic cell lines. Kaisa J. Teittinena, Pauliina Kärkkäinena, Johanna Salonenb, Gunilla Rönnholmc, Hanna Korkeamäkia, Mauno Vihinenb, Nisse Kalkkinenc, Olli Lohia
- 2. leukemia. Leukemia is cancer of the blood cells. It starts in the bone marrow (the soft tissue inside most bones. Bone marrow is where blood cells are made). Normally the bone marrow makes: White blood cells (which help body fight Infection), Red blood cells (which carry oxygen to all parts of body) and Platelets (which help blood clot). With leukemia, the bone marrow starts to make a lot of abnormal white blood cells, called leukemia cells. They don't do the work of normal white blood cells, they grow faster than normal cells, and they don't stop growing when they should. Over time, leukemia cells can crowd out the normal blood cells. This can lead to serious problems such as anemia, bleeding, and infections. Leukemia cells can also spread to the lymph nodes or other organs and cause swelling or pain. INTRODUCTION.
- 3. leukemia is grouped by how fast it gets worse and what kind of white blood cell it Affects: -Acute leukemia gets worse very fast and cause symptoms in few time. -Chronic leukemia gets worse slowly and may not cause symptoms for years. -Lymphocytic (or lymphoblastic) leukemia affects white blood cells called lymphocytes. -Myelogenousleukemia affects white blood cells called myelocytes. types .
- 4. Acute lymphoblastic leukemia, or ALL. Acute myelogenous leukemia, or AML. Chronic lymphocytic leukemia, or CLL. Chronic myelogenous leukemia, or CML. types .
- 5. There are more likely to get leukemia when people: Was exposed to large amounts of radiation. Was exposed to certain chemicals at work, such as benzene. Had some types of chemotherapy to treat another cancer. Have Down syndrome or some other genetic problems. Smoke. Risk factors.
- 6. Prohibitin. Mitochondrial prohibitin complexes control cell proliferation, cristae morphogenesis and the functional integrity of mitochondria. TDP-43. has been shown to be involved in regulation of pre-mRNA splicing and repression of transcription. Nuclear proteins.
- 7. Nucleophosmin. It is essential for normal embryonic development and, specifically, for the control of centrosome duplication and genomic stability. Nuclear proteins.
- 8. Some Proteins can be find with an altered expression in the nucleoli of leukemic cells (changes in nucleolar proteomes). Prohibitin (PHB) and TAR-DNA-binding protein-43 (TDP-43) were strongly expressed in the nucleoli. Our results demonstrate that leukemic cells have differences in their nucleolar protein composition, and suggest that it may be possible to exploit these differences in identification of leukemia subtypes. Nucleolar protein-leukemia
- 9. This study aimed to identify nucleolar proteins that are differen- tially expressed in various cell lines derived from acute leukemias. Objective.
- 11. FUNDAMENTO: aislar células (ya sean células procariotas, eucariotas o vegetales), cultivarse en condiciones controladas y obtener poblaciones celulares homogéneas para estudiar los procesos que ocurren en las células. ¿Para que?: Se realizo el cultivo para poder estudiar en el laboratorio estas células plasmáticas. CULTIVO.
- 12. FUNDAMENTO: una manera eficiente para aislar y obtener nucléolos purificados sin las demás partes del núcleo. ¿para que?: para poder medir la concentración de proteínas totales en los nucléolos. AISLAMIENTO NUCLEOLOS.
- 13. FUNDAMENTO: Separa las proteínas según su punto isoeléctrico y peso molecular. ¿para que?: Análisis de los extractos nucleolares y sus características. 2 DIGE.
- 14. FUNDAMENTO: identificar proteínas. ¿para que?: identificar las proteínas nucleolares. IDENTIFICACION DE PROTEINAS.
- 15. FUNDAMENTO: detectar proteínas específicas en una muestra determinada. ¿Para que?: Detectar las proteínas: PHB y TDP-43. WESTERN BLOT.
- 16. FUNDAMENTO: se emplean anticuerpos para tinción de las proteínas. ¿para que?: producir la tinción de las proteínas: PHB y TDP-43. INMUNOFLUORECENCIA.
- 17. RESULTADOS Leucemogénesis nucleolar Fundamento: Aproximación proteómica para buscar proteínas cuya expresión varía entre diferentes tipos de células leucémicas.
- 20. RESULTADOS Para facilitar el lugar recogiendo los geles 2-DE fueron post-teñidas con plata. Por último, las manchas de las proteínas seleccionadas fueron digeridas "en gel" y luego sometidas anano LC-de masas en tándem análisis de espectrometría
- 21. RESULTADOS MASCOTA MS / MS programa de Búsqueda de Ion.
- 22. RESULTADOS Expresión nucleolar de PHB Western blot análisis en los extractos nucleolares de laslíneas de células leucémicas. Igualdad de cargas de las muestras. Expresión nucleolar de TDP-43 y su región terminal N (TDP-43-N) Western blot análisis. Igualdad de cargas de las muestras.
- 23. RESULTADOS Análisis densiométrico de las intensidades de las bandas en el panel A normalizado a los niveles de CCRF-CEM. 2.9 y 1.8 a 2.7
- 24. RESULTADOS Tinción de inmunofluorescencia de PHB en los preparativos nucleolares de CCRF-CEMy FH-CALL-3 células. Tinción de inmunofluorescencia de TDP-43 en los preparativos nucleolar de CCRF-CEM y las células MHH-CALL3. DAPI, 4,6-diamidino-2-phenylindole.
- 25. DISCUSSION
- 27. MAPA CONCEPTUAL
- 28. MAPA CONCEPTUAL
- 29. Mapa conceptual.
- 30. Gracias…