The document discusses the role of inflammation in cancer promotion. It describes an experiment using Mdr2-KO mice, which develop hepatocellular carcinoma in the context of chronic hepatitis. Nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) activation is involved in hepatocarcinogenesis in these mice and is predominantly located near inflamed portal tracts. Treatment with anti-inflammatory drugs or anti-TNFα decreases inflammation and NFkB activation in these mice. Generating double mutant mice with NFkB inactivated in hepatocytes showed that NFkB is critical for tumor promotion but dispensable for early stages of hepatocellular carcinoma development.
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.
The document discusses various types of tumor antigens recognized by T cells and immune mechanisms of tumor rejection. It covers tumor-associated antigens and tumor-specific antigens, and describes four main categories of tumor antigens: 1) abnormally expressed but unmutated cellular proteins, 2) products of mutated self genes, 3) oncogenes and mutated tumor suppressor genes, and 4) antigens of oncogenic viruses. It also discusses how tumors can evade immune responses through mechanisms like antigen loss, inhibiting immune molecules, regulatory T cells, and secreting immunosuppressive factors. Novel immunotherapies discussed include therapeutic cancer vaccines, monoclonal antibodies, immune checkpoint inhibitors, adoptive cell therapies, and oncolytic viruses.
The presentation outlines aspects of immunity against cancer, evasion strategies by cells, immunotherapy in cancer, cancer vaccines etc. Download and view the slideshow for better experience.
Prepared in Sept 2014
A detailed ppt about cancer immunotherapy.
includes:-
Immunosurveillance and Immunoediting
Dentritic cell vaccines
Antibody therapy
Combined therapy
immune blockades
Cytokine therapy
T cell therapy
Include latest research finding about therapy.
Tumors arise from mutations in genes regulating cell growth and division. Malignant tumors can invade other tissues and metastasize. The immune system normally eliminates cancerous cells, but tumors use escape mechanisms to avoid detection. Laboratory tests detect tumor antigens, characterize tumors, screen for cancers, monitor treatment response, and detect recurrence. Immunotherapy uses passive transfer of antibodies or active stimulation of the immune system to fight tumors.
This document discusses cancer stem cells (CSCs), which are rare cells in tumors that have the ability to self-renew and differentiate into the diverse cells that comprise the tumor. CSCs were first hypothesized in the 1870s and experiments in the 1950s-60s provided early evidence for their existence. The concept of CSCs was revived in the 2000s, with the definition that they can recapitulate tumor growth. CSCs are identified experimentally by markers and assays. They are thought to originate from somatic or adult stem/progenitor cells and have properties of self-renewal, differentiation, immortality. CSCs may cause metastases, therapy resistance and recurrence. Targeting CSCs may improve cancer treatment and CSCs may serve
The document discusses cancer immunosurveillance and immunoediting. It describes how the immune system plays an important role in controlling cancer development through 3 phases - elimination, equilibrium, and escape. In the elimination phase, innate and adaptive immunity work to eliminate cancer cells. Some cancer cells may survive this phase if they acquire properties to evade the immune system, entering the equilibrium phase. Eventually, in the escape phase, cancer cells are able to avoid immune destruction through various mechanisms and form clinically detectable tumors. Immunotherapy aims to enhance the immune response against cancer cells.
This document discusses immunosurveillance and immunotherapy for cancer treatment. It explains that the immune system normally surveils and destroys mutated cells to prevent tumor development, but tumors can evade this response through various mechanisms such as antigen shedding or fast proliferation. Immunotherapy aims to boost the immune system's ability to fight cancer, for example through monoclonal antibodies, non-specific stimulants, cancer vaccines, or T-cell therapies.
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.
The document discusses various types of tumor antigens recognized by T cells and immune mechanisms of tumor rejection. It covers tumor-associated antigens and tumor-specific antigens, and describes four main categories of tumor antigens: 1) abnormally expressed but unmutated cellular proteins, 2) products of mutated self genes, 3) oncogenes and mutated tumor suppressor genes, and 4) antigens of oncogenic viruses. It also discusses how tumors can evade immune responses through mechanisms like antigen loss, inhibiting immune molecules, regulatory T cells, and secreting immunosuppressive factors. Novel immunotherapies discussed include therapeutic cancer vaccines, monoclonal antibodies, immune checkpoint inhibitors, adoptive cell therapies, and oncolytic viruses.
The presentation outlines aspects of immunity against cancer, evasion strategies by cells, immunotherapy in cancer, cancer vaccines etc. Download and view the slideshow for better experience.
Prepared in Sept 2014
A detailed ppt about cancer immunotherapy.
includes:-
Immunosurveillance and Immunoediting
Dentritic cell vaccines
Antibody therapy
Combined therapy
immune blockades
Cytokine therapy
T cell therapy
Include latest research finding about therapy.
Tumors arise from mutations in genes regulating cell growth and division. Malignant tumors can invade other tissues and metastasize. The immune system normally eliminates cancerous cells, but tumors use escape mechanisms to avoid detection. Laboratory tests detect tumor antigens, characterize tumors, screen for cancers, monitor treatment response, and detect recurrence. Immunotherapy uses passive transfer of antibodies or active stimulation of the immune system to fight tumors.
This document discusses cancer stem cells (CSCs), which are rare cells in tumors that have the ability to self-renew and differentiate into the diverse cells that comprise the tumor. CSCs were first hypothesized in the 1870s and experiments in the 1950s-60s provided early evidence for their existence. The concept of CSCs was revived in the 2000s, with the definition that they can recapitulate tumor growth. CSCs are identified experimentally by markers and assays. They are thought to originate from somatic or adult stem/progenitor cells and have properties of self-renewal, differentiation, immortality. CSCs may cause metastases, therapy resistance and recurrence. Targeting CSCs may improve cancer treatment and CSCs may serve
The document discusses cancer immunosurveillance and immunoediting. It describes how the immune system plays an important role in controlling cancer development through 3 phases - elimination, equilibrium, and escape. In the elimination phase, innate and adaptive immunity work to eliminate cancer cells. Some cancer cells may survive this phase if they acquire properties to evade the immune system, entering the equilibrium phase. Eventually, in the escape phase, cancer cells are able to avoid immune destruction through various mechanisms and form clinically detectable tumors. Immunotherapy aims to enhance the immune response against cancer cells.
This document discusses immunosurveillance and immunotherapy for cancer treatment. It explains that the immune system normally surveils and destroys mutated cells to prevent tumor development, but tumors can evade this response through various mechanisms such as antigen shedding or fast proliferation. Immunotherapy aims to boost the immune system's ability to fight cancer, for example through monoclonal antibodies, non-specific stimulants, cancer vaccines, or T-cell therapies.
This document provides definitions and explanations of key cancer-related terms:
- Cancer is characterized by uncontrolled cell growth and spread. Benign tumors are not invasive while malignant tumors continue growing and spreading. Metastasis occurs when cancer cells spread from the original tumor to other parts of the body.
- Carcinomas arise from epithelial tissues, sarcomas from connective tissues, and leukemia from blood-forming tissues in the bone marrow. Carcinogens are agents that can cause cancer. Tumor antigens include those from mutated genes and overexpressed proteins. Immunotherapy harnesses the immune system to fight cancer using approaches like monoclonal antibody treatment, adoptive cell transfer, and cancer vaccines.
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.
This document discusses the history and science of organ transplantation. It begins with a brief history, highlighting Nobel Prize-winning discoveries such as the first successful organ transplant between twins in 1954. It then covers key topics like the major histocompatibility complex and mechanisms of graft rejection, such as acute cellular rejection mediated by T cells. The types of transplantation are defined, from autologous to xenogeneic grafts. Prevention of rejection involves tissue typing, immunosuppression, and vaccination. Complications like graft-versus-host disease are also summarized.
This presentation deals with the concept of Tumor immunity. It cover different types of Tumor and tumor antigens. How immunology plays role in tumor detection and diagnosis is also explained in this presentation. Concept of Tumor imunoprophylaxis and tumor immunotherapy is also explained.
This lecture discusses how the immune system responds to tumors and how tumors evade the immune system. It covers various types of tumor antigens recognized by the immune system, including products of mutated genes, overexpressed proteins, and oncofetal antigens. The immune system mounts cellular and humoral responses against tumors through cytotoxic T cells, NK cells, macrophages, and antibodies. However, tumors have developed mechanisms to evade the immune system, such as antigen loss, lack of costimulation, immunosuppression, and inducing T cell apoptosis. Understanding the immune response and evasion is crucial for developing immunotherapies against cancer.
This document provides an overview of tumor immunology, including definitions of cancer and carcinogenesis, tumor antigens, the immune response to cancer, and mechanisms by which tumors escape the immune system. It discusses how tumors stimulate an immune response through antigens but also ways they can evade immunity, such as through low immunogenicity, antigen modulation, and immune suppression. It describes experimental evidence for tumor antigens and the immune response against tumors.
This document discusses tumor immunology and immunotherapy. It provides evidence that the immune system can recognize and react against tumors. It describes tumor-associated antigens that can be recognized by the immune system. However, tumors also have mechanisms for escaping immune surveillance, such as not expressing immunogenic antigens or secreting immunosuppressive molecules. The document discusses various tumor-associated antigens and oncofetal antigens. It also outlines approaches for tumor immunotherapy, including using cytokines and immunopotentiating agents to enhance anti-tumor immunity.
Immunotherapy utilizes the body's immune system to fight cancer by improving its ability to detect and kill cancer cells. Chimeric antigen receptors (CARs) are engineered receptors that are used to graft the specificity of a monoclonal antibody onto a T cell. CARs are under investigation as a cancer therapy using adoptive cell transfer. To produce CAR T cells, T cells are engineered using a virus-based gene delivery system containing packaging elements and a vector to transfer genetic material that encodes the CAR receptor structure. CAR T cell therapy shows promise but also risks toxicity that requires careful management. Ongoing research focuses on improving CAR specificity and controlling their activity in the body.
1) The document discusses cancer and the immune system, covering topics like tumor antigens, immune responses to tumors, and tumor escape mechanisms.
2) It provides an overview of tumor immunology, including how tumors evade the immune system through mechanisms like down-regulating class I MHC expression and antigen modulation.
3) The document also summarizes different immunotherapy approaches, such as treatments using cytokines, monoclonal antibodies, and vaccination strategies using isolated tumor peptides or transfected tumor cells.
Hallmarks of Cancer - Classical vs Metabolic approachSreepadmanabh M
The document summarizes the "Hallmarks of Cancer" proposed by Douglas Hanahan and Robert Weinberg in 2000. It identified six common traits or hallmarks that allow normal cells to transform into cancer cells: (1) self-sufficiency in growth signals, (2) insensitivity to anti-growth signals, (3) evading apoptosis, (4) limitless replicative potential, (5) sustained angiogenesis, and (6) tissue invasion and metastasis. In 2011, Hanahan proposed four additional hallmarks: deregulated metabolism, immune evasion, severe chromosomal abnormalities, and chronic inflammation inducing cancer. The document discusses evidence that a metabolic approach may provide further insights into understanding cancer.
immunology chapter 9 : activation of T lymphocytesprincesa_mera
1. T lymphocyte activation involves recognition of antigen peptides presented by MHC molecules on antigen presenting cells. This provides an initial activation signal that is enhanced by costimulatory molecules like B7 and CD28.
2. Upon activation, naive T cells proliferate extensively through clonal expansion, increasing the number of antigen-specific T cells by 100,000-fold. They also differentiate into effector T cell subsets.
3. The main effector T cell subsets are TH1 and TH2 cells, distinguished by their cytokine production. TH1 cells produce IFNγ and activate macrophages, while TH2 cells produce IL-4 and stimulate antibody class switching and eosinophil responses.
MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and affect multiple cellular processes. Dysregulation of miRNAs is common in cancer and can impact cancer hallmarks like sustained proliferation, evading growth suppression, resisting cell death, and activating invasion and metastasis. Certain miRNAs are considered oncogenes when their expression is increased in tumors, while others act as tumor suppressors when their expression is decreased. Altered miRNA expression and biogenesis machinery defects contribute to cancer development and progression. miRNAs also show potential as cancer biomarkers and therapeutic targets.
Cell within a tumor that possess the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor”.
“CSC can thus only be defined experimentally by their ability to recapitulate the generation of a continuously growing tumor”.
Metastatic cascade and Epithelial Mesenchymal TransitionShruti Dogra
This document provides an overview of cancer metastasis and the epithelial-mesenchymal transition (EMT) process. It discusses the metastatic cascade, which involves tumor cell invasion, intravasation into blood vessels, transport through circulation, extravasation and homing to distant sites, and formation of secondary tumors. EMT is described as a key step in metastasis that allows epithelial cells to detach from primary tumors and migrate. The molecular and cellular changes involved in EMT include loss of epithelial markers like E-cadherin and gain of mesenchymal markers. Transcription factors such as Snail, Slug, Twist, and ZEB play important roles in inducing EMT. Understanding metastasis and EMT can help develop strategies to prevent cancer spread
Tumor, Tumor immunology, cancer, hallmarks of cancer, carcinoma, lymphoma, metastasis, malignant, benign, angiogenesis, oncogenes and cancer induction, kuby detailed study quick revision, proto-oncogenes, tumor antigens, antibody, experiments for tumor antigens, methods for characterization of TSTA, Immunoediting, Current research n new approaches, monoclonal antibody
Therapeutic prospects in Cancer Immunotherapy.
Interleukins for Renal Cell Carcinoma.
BCG for Bladder Cancer.
Vaccination Strategies: Oncolytic virus for melanoma, Dendritic Cell therapy for CA Prostate.
Immune Checkpoint inhibitors. PD1 and PD L1 inhibitors.
Adoptive Cell Therpay. CAR T Cell Therapy
Clinical efficacy. Costs.
The immune system plays an important role in tumor immunity by recognizing and destroying tumor cells. However, tumors have developed several mechanisms to evade the immune system. Tumors express a variety of tumor antigens that can elicit an immune response, but they often downregulate antigen expression or lose antigenicity over time. Additionally, tumors employ immunosuppressive strategies like increasing immunosuppressive cytokines or reducing co-stimulatory molecules to avoid immune detection and destruction. While immune surveillance exists, tumors have found ways to circumvent it through immune escape mechanisms.
The document discusses immuno-oncology and the relationship between cancer and the immune system. It provides an overview of topics that will be covered in an upcoming webinar, including advances in immuno-oncology for different cancer types and combination immunotherapy approaches. The document then reviews key topics in more depth, including how immuno-oncology focuses on improving the body's immune response against cancer and recent immunotherapy approvals. It also discusses how cancer can evade the immune system and strategies for cancer immunotherapy, such as manipulating co-stimulatory signals, enhancing antigen presenting cells, and using cytokines, monoclonal antibodies, and cancer vaccines.
This document summarizes a case study on using exosomes for cancer therapy. Key points include:
1) Exosomes were loaded with the anticancer drug paclitaxel (PTX) using incubation, electroporation, or sonication methods. Sonication provided the greatest drug loading capacity and stability.
2) Loaded exosomes (exoPTX) accumulated more in drug-resistant cancer cells than free drug. ExoPTX also overcame P-glycoprotein mediated drug resistance.
3) In mouse studies, exoPTX treatment significantly inhibited lung metastasis growth compared to free drug or control treatments.
4) The results suggest that exosome carriers can deliver
The document discusses advances in genomic sequencing technology and its potential to revolutionize cancer treatment. James Hadfield of Cancer Research UK describes how sequencing costs have plummeted from $3 billion for the first human genome to $1,000 per genome today. Next-generation sequencing is enabling analysis of cancer genomes and monitoring of tumor evolution during treatment. Hadfield argues that personalized cancer genomic medicine, using sequencing to tailor treatments to individual patients' tumor mutations, should be implemented as quickly as possible, as it represents the most significant change in cancer care since chemotherapy.
The document discusses criteria for evaluating genomic tests, including whether the test is clinically meaningful, how it was validated, reliability, practicality, and cost-effectiveness. It emphasizes that tests must provide value beyond traditional measures and require multiple studies as evidence. Genomic tests are developed through a process similar to drug development, starting with initial studies to develop relevant profiles which are then validated in additional studies with prospective design. Sources of variability must be rigorously controlled and clinical context is important.
This document provides definitions and explanations of key cancer-related terms:
- Cancer is characterized by uncontrolled cell growth and spread. Benign tumors are not invasive while malignant tumors continue growing and spreading. Metastasis occurs when cancer cells spread from the original tumor to other parts of the body.
- Carcinomas arise from epithelial tissues, sarcomas from connective tissues, and leukemia from blood-forming tissues in the bone marrow. Carcinogens are agents that can cause cancer. Tumor antigens include those from mutated genes and overexpressed proteins. Immunotherapy harnesses the immune system to fight cancer using approaches like monoclonal antibody treatment, adoptive cell transfer, and cancer vaccines.
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.
This document discusses the history and science of organ transplantation. It begins with a brief history, highlighting Nobel Prize-winning discoveries such as the first successful organ transplant between twins in 1954. It then covers key topics like the major histocompatibility complex and mechanisms of graft rejection, such as acute cellular rejection mediated by T cells. The types of transplantation are defined, from autologous to xenogeneic grafts. Prevention of rejection involves tissue typing, immunosuppression, and vaccination. Complications like graft-versus-host disease are also summarized.
This presentation deals with the concept of Tumor immunity. It cover different types of Tumor and tumor antigens. How immunology plays role in tumor detection and diagnosis is also explained in this presentation. Concept of Tumor imunoprophylaxis and tumor immunotherapy is also explained.
This lecture discusses how the immune system responds to tumors and how tumors evade the immune system. It covers various types of tumor antigens recognized by the immune system, including products of mutated genes, overexpressed proteins, and oncofetal antigens. The immune system mounts cellular and humoral responses against tumors through cytotoxic T cells, NK cells, macrophages, and antibodies. However, tumors have developed mechanisms to evade the immune system, such as antigen loss, lack of costimulation, immunosuppression, and inducing T cell apoptosis. Understanding the immune response and evasion is crucial for developing immunotherapies against cancer.
This document provides an overview of tumor immunology, including definitions of cancer and carcinogenesis, tumor antigens, the immune response to cancer, and mechanisms by which tumors escape the immune system. It discusses how tumors stimulate an immune response through antigens but also ways they can evade immunity, such as through low immunogenicity, antigen modulation, and immune suppression. It describes experimental evidence for tumor antigens and the immune response against tumors.
This document discusses tumor immunology and immunotherapy. It provides evidence that the immune system can recognize and react against tumors. It describes tumor-associated antigens that can be recognized by the immune system. However, tumors also have mechanisms for escaping immune surveillance, such as not expressing immunogenic antigens or secreting immunosuppressive molecules. The document discusses various tumor-associated antigens and oncofetal antigens. It also outlines approaches for tumor immunotherapy, including using cytokines and immunopotentiating agents to enhance anti-tumor immunity.
Immunotherapy utilizes the body's immune system to fight cancer by improving its ability to detect and kill cancer cells. Chimeric antigen receptors (CARs) are engineered receptors that are used to graft the specificity of a monoclonal antibody onto a T cell. CARs are under investigation as a cancer therapy using adoptive cell transfer. To produce CAR T cells, T cells are engineered using a virus-based gene delivery system containing packaging elements and a vector to transfer genetic material that encodes the CAR receptor structure. CAR T cell therapy shows promise but also risks toxicity that requires careful management. Ongoing research focuses on improving CAR specificity and controlling their activity in the body.
1) The document discusses cancer and the immune system, covering topics like tumor antigens, immune responses to tumors, and tumor escape mechanisms.
2) It provides an overview of tumor immunology, including how tumors evade the immune system through mechanisms like down-regulating class I MHC expression and antigen modulation.
3) The document also summarizes different immunotherapy approaches, such as treatments using cytokines, monoclonal antibodies, and vaccination strategies using isolated tumor peptides or transfected tumor cells.
Hallmarks of Cancer - Classical vs Metabolic approachSreepadmanabh M
The document summarizes the "Hallmarks of Cancer" proposed by Douglas Hanahan and Robert Weinberg in 2000. It identified six common traits or hallmarks that allow normal cells to transform into cancer cells: (1) self-sufficiency in growth signals, (2) insensitivity to anti-growth signals, (3) evading apoptosis, (4) limitless replicative potential, (5) sustained angiogenesis, and (6) tissue invasion and metastasis. In 2011, Hanahan proposed four additional hallmarks: deregulated metabolism, immune evasion, severe chromosomal abnormalities, and chronic inflammation inducing cancer. The document discusses evidence that a metabolic approach may provide further insights into understanding cancer.
immunology chapter 9 : activation of T lymphocytesprincesa_mera
1. T lymphocyte activation involves recognition of antigen peptides presented by MHC molecules on antigen presenting cells. This provides an initial activation signal that is enhanced by costimulatory molecules like B7 and CD28.
2. Upon activation, naive T cells proliferate extensively through clonal expansion, increasing the number of antigen-specific T cells by 100,000-fold. They also differentiate into effector T cell subsets.
3. The main effector T cell subsets are TH1 and TH2 cells, distinguished by their cytokine production. TH1 cells produce IFNγ and activate macrophages, while TH2 cells produce IL-4 and stimulate antibody class switching and eosinophil responses.
MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and affect multiple cellular processes. Dysregulation of miRNAs is common in cancer and can impact cancer hallmarks like sustained proliferation, evading growth suppression, resisting cell death, and activating invasion and metastasis. Certain miRNAs are considered oncogenes when their expression is increased in tumors, while others act as tumor suppressors when their expression is decreased. Altered miRNA expression and biogenesis machinery defects contribute to cancer development and progression. miRNAs also show potential as cancer biomarkers and therapeutic targets.
Cell within a tumor that possess the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor”.
“CSC can thus only be defined experimentally by their ability to recapitulate the generation of a continuously growing tumor”.
Metastatic cascade and Epithelial Mesenchymal TransitionShruti Dogra
This document provides an overview of cancer metastasis and the epithelial-mesenchymal transition (EMT) process. It discusses the metastatic cascade, which involves tumor cell invasion, intravasation into blood vessels, transport through circulation, extravasation and homing to distant sites, and formation of secondary tumors. EMT is described as a key step in metastasis that allows epithelial cells to detach from primary tumors and migrate. The molecular and cellular changes involved in EMT include loss of epithelial markers like E-cadherin and gain of mesenchymal markers. Transcription factors such as Snail, Slug, Twist, and ZEB play important roles in inducing EMT. Understanding metastasis and EMT can help develop strategies to prevent cancer spread
Tumor, Tumor immunology, cancer, hallmarks of cancer, carcinoma, lymphoma, metastasis, malignant, benign, angiogenesis, oncogenes and cancer induction, kuby detailed study quick revision, proto-oncogenes, tumor antigens, antibody, experiments for tumor antigens, methods for characterization of TSTA, Immunoediting, Current research n new approaches, monoclonal antibody
Therapeutic prospects in Cancer Immunotherapy.
Interleukins for Renal Cell Carcinoma.
BCG for Bladder Cancer.
Vaccination Strategies: Oncolytic virus for melanoma, Dendritic Cell therapy for CA Prostate.
Immune Checkpoint inhibitors. PD1 and PD L1 inhibitors.
Adoptive Cell Therpay. CAR T Cell Therapy
Clinical efficacy. Costs.
The immune system plays an important role in tumor immunity by recognizing and destroying tumor cells. However, tumors have developed several mechanisms to evade the immune system. Tumors express a variety of tumor antigens that can elicit an immune response, but they often downregulate antigen expression or lose antigenicity over time. Additionally, tumors employ immunosuppressive strategies like increasing immunosuppressive cytokines or reducing co-stimulatory molecules to avoid immune detection and destruction. While immune surveillance exists, tumors have found ways to circumvent it through immune escape mechanisms.
The document discusses immuno-oncology and the relationship between cancer and the immune system. It provides an overview of topics that will be covered in an upcoming webinar, including advances in immuno-oncology for different cancer types and combination immunotherapy approaches. The document then reviews key topics in more depth, including how immuno-oncology focuses on improving the body's immune response against cancer and recent immunotherapy approvals. It also discusses how cancer can evade the immune system and strategies for cancer immunotherapy, such as manipulating co-stimulatory signals, enhancing antigen presenting cells, and using cytokines, monoclonal antibodies, and cancer vaccines.
This document summarizes a case study on using exosomes for cancer therapy. Key points include:
1) Exosomes were loaded with the anticancer drug paclitaxel (PTX) using incubation, electroporation, or sonication methods. Sonication provided the greatest drug loading capacity and stability.
2) Loaded exosomes (exoPTX) accumulated more in drug-resistant cancer cells than free drug. ExoPTX also overcame P-glycoprotein mediated drug resistance.
3) In mouse studies, exoPTX treatment significantly inhibited lung metastasis growth compared to free drug or control treatments.
4) The results suggest that exosome carriers can deliver
The document discusses advances in genomic sequencing technology and its potential to revolutionize cancer treatment. James Hadfield of Cancer Research UK describes how sequencing costs have plummeted from $3 billion for the first human genome to $1,000 per genome today. Next-generation sequencing is enabling analysis of cancer genomes and monitoring of tumor evolution during treatment. Hadfield argues that personalized cancer genomic medicine, using sequencing to tailor treatments to individual patients' tumor mutations, should be implemented as quickly as possible, as it represents the most significant change in cancer care since chemotherapy.
The document discusses criteria for evaluating genomic tests, including whether the test is clinically meaningful, how it was validated, reliability, practicality, and cost-effectiveness. It emphasizes that tests must provide value beyond traditional measures and require multiple studies as evidence. Genomic tests are developed through a process similar to drug development, starting with initial studies to develop relevant profiles which are then validated in additional studies with prospective design. Sources of variability must be rigorously controlled and clinical context is important.
The document describes the Center of Cancer Nanotechnology Excellence (CCNE) at the University of Maryland. CCNEs link physical scientists and engineers working at the nanoscale with cancer biologists and oncologists to enable multi-disciplinary research on cancer-oriented nanotechnology. The Maryland CCNE will focus on pancreatic and lung cancer, with projects including targeted drug delivery using silicon nanotubes, surfactant nanovesicles, and magnetic particles. The center will have cores for translational research, bioinformatics, and analytical characterization. It will evaluate vitamin-targeted nanoparticles for chemotherapy delivery, having shown riboflavin receptors are upregulated in breast cancer cells and may enable targeted delivery.
Contains the speakers details of the 23rd International Conference on Cancer Research and Pharmacology.
For more details, visit: https://cancer.cmesociety.com/
Dr. Kyla Grimshaw is presenting on using cell-based assays in cancer drug development. She discusses Horizon Discovery's services including isogenic cell lines for target validation, modeling the tumor microenvironment, and high-throughput screening platforms. Key applications of cell-based assays addressed are target validation, patient stratification, determining optimal assay conditions, and evaluating combination therapies. Recent developments include endogenous reporter cell lines and patient-derived xenograft models.
Richard Carvajal discusses navigating treatment options for uveal melanoma, focusing on immunotherapeutic strategies. He outlines several systemic treatment approaches including genetic, epigenetic, and immunological targeting. Checkpoint blockade with ipilimumab and nivolumab has shown some efficacy in uveal melanoma but responses are lower than in cutaneous melanoma potentially due to lower tumor mutation burden and PD-L1 expression. Adoptive T cell therapy clinical trials have also shown responses. Ipilimumab and nivolumab are being studied in the adjuvant and metastatic settings. Additional immunotherapies including T cell redirecting therapies targeting gp100 are in clinical trials. Combination strategies may be necessary to improve outcomes for
This document outlines the basic steps in cancer research. It discusses how cancer cells differ from normal cells by invading surrounding tissues and spreading to other sites. There are different types of cancer like oral, liver, and skin cancer. Cancer research involves epidemiology, prediction, prevention, early detection, diagnosis, prognosis, and treatment methods like surgery, chemotherapy, radiation, and immunotherapy. Research goes through different phases from students to professors and uses various skills, methods, and readouts to analyze effects on tumors and immune responses in vitro, ex vivo, and in vivo using animal tumor models. The overall goal is to translate findings from preclinical research in the lab through clinical trials to benefit patients.
This document discusses cancer immunotherapy. It begins by describing tumor antigens that can be recognized by the immune system, such as tumor-specific antigens, tumor-associated antigens, and antigens from oncogenic viruses. It then discusses how tumors evade the immune system and various approaches to immunotherapy, including active immunotherapies using vaccines made of tumor cells, purified antigens, or antigen-loaded dendritic cells. Passive immunotherapies discussed include adoptive cellular therapy, monoclonal antibodies, and immunotoxins. Clinical trials and effectiveness of different immunotherapies are also summarized.
Next-Generation Sequencing Clinical Research Milestones InfographicQIAGEN
DNA mutations have been implicated in several diseases, particularly cancer. NGS presents an ideal technology to efficiently profile the multitude of mutations in a high throughput manner. In 2001 the first draft of human genome was published. Since then many major milestones have been reached. Do you know when PIK3CA was identified in colon cancer? When was Olaparib for ovarian cancer treatment? This infographic traces the major clinical research milestones starting from the first draft of the human genome.
This document discusses next-generation sequencing (NGS) and its role in cancer research. It begins with an introduction to NGS technology and applications. The speaker then discusses how NGS can help with cancer research by identifying new cancer genes and mutations, assisting with diagnosis and targeted therapies, and enabling patient stratification. The need for NGS is explained by discussing cancer genetics, statistics on cancer incidence, and the need to identify driver mutations and develop personalized treatments. Qiagen offers an end-to-end NGS workflow and solutions including sample preparation, target enrichment, library preparation, sequencing, and data analysis. Their targeted gene panels and analysis software provide a streamlined sample-to-result experience for cancer research.
Radiation-induced collateral damage-impact on metastasisLynn Feys
Here are the key points about chemotherapy for TNBC:
- Chemotherapy is the main systemic treatment for TNBC due to the lack of targeted therapies.
- Anthracycline- and taxane-based regimens such as AC-T (doxorubicin + cyclophosphamide followed by paclitaxel) are considered standard.
- Platinum salts like cisplatin may be added for patients with BRCA1 mutations which confer sensitivity.
- Dose-dense regimens with shorter intervals between cycles can improve outcomes compared to conventional schedules.
- Neoadjuvant chemotherapy is often used to shrink large tumors before surgery and predict response to treatment. Achieving a pathologic complete
Advances in Oncolytic Virotherapy - Creative BiolabsCreative-Biolabs
Oncolytic virotherapy, an innovative approach leverages the natural ability of viruses to infect and kill tumor cells, offering a beacon of hope for patients battling cancer. Our journey through this domain uncovers the mechanisms of action of oncolytic viruses, explores representative examples, discusses strategic modifications and combinations with other therapies, addresses challenges, and reviews the clinical status of this cutting-edge treatment.
Proteogenomic analysis of human colon cancer reveals new therapeutic opportun...Gul Muneer
We performed the first proteogenomic study on a prospectively collected colon cancer cohort. Comparative proteomic and phosphoproteomic analysis of paired tumor and normal adjacent tissues produced a catalog of colon cancer-associated proteins and phosphosites, including known and putative new biomarkers, drug targets, and cancer/testis antigens. Proteogenomic integration not only prioritized genomically inferred targets, such as copy-number drivers and mutation-derived neoantigens, but also yielded novel findings. Phosphoproteomics data associated Rb phosphorylation with increased proliferation and decreased apoptosis in colon cancer, which explains why this classical tumor suppressor is amplified in colon tumors and suggests a rationale for targeting Rb phosphorylation in colon cancer. Proteomics identified an association between decreased CD8 T cell infiltration and increased glycolysis in microsatellite instability-high (MSI-H) tumors, suggesting glycolysis as a potential target to overcome the resistance of MSI-H tumors to immune checkpoint blockade. Proteogenomics presents new avenues for biological discoveries and therapeutic development.
The document describes the EpiTect Methyl II PCR Array System for analyzing DNA methylation. It provides an overview of the system which enables pathway or disease-focused profiling of regional DNA methylation using optimized kits, assays, and data analysis templates. The system offers a complete solution for DNA methylation analysis from sample isolation through data analysis. Key advantages include its ability to simultaneously analyze methylation of many genes, compatibility with standard qPCR instruments, and generation of results comparable to bisulfite sequencing but with higher throughput and without the need for bisulfite conversion.
Identifying novel and druggable targets in a triple negative breast cancer ce...Thermo Fisher Scientific
In this study, we developed a CRISPR/Cas9-based high throughput loss-of-function screen for identifying target genes responsible for the tumor proliferation and growth in TNBC. Our initial focus was to identify essential kinases in MDA-MB-231 cell line using the Invitrogen™ LentiArray™ Human Kinase CRISPR Library, which targets 840 kinases with up to 4 different gRNAs per protein kinase for complete gene knockout. This functional screen identified over 90 protein kinases that are essential for cell viability and cell proliferation. Ten of these hits (CDK1, CDK2, CDK8, CDK10, CDK11A, CDK19, CDK19, CDC7, EPHA2 and WEE1) are well-known targets validated in the literature. Currently, we are in the process validating the novel hits through target gene sequencing, western blotting and target specific small molecule kinase inhibitors.
Cancer is caused by genetic and epigenetic changes that alter the cell genome. Cancer bioinformatics analyzes DNA, RNA, and protein sequences to better understand cancer mechanisms. It utilizes databases like CGAP, HCGP, and caBIG that integrate gene expression data from millions of tumor and normal tissues to determine cancer expression patterns. Methods in cancer bioinformatics include genomics to study whole genome changes, transcriptomics to analyze all gene transcripts, and proteomics to study protein expression, modifications, and interactions, with the goal of discovering new cancer diagnostics and therapeutics.
The document summarizes research using chick embryo models to study cancer metastasis. It describes several advantages of the chick embryo model, including its ability to support rapid growth of xenografted human tumor cells. Several chick embryo cancer models are outlined, including models for spontaneous metastasis, analyzing tumor cell interactions with vasculature, and studying invasion and extravasation. Examples are given of studies using these models to analyze tumor growth and metastasis of various cancer cell lines and effects of potential therapeutics.
Oncolytic Virus Therapy Development - Creative BiolabsCreative-Biolabs
Oncolytic virotherapy is cancer treatment using a native or reprogrammed virus that has the potential to targeting and killing cancerous cell. Taking advantage of the OncoVirapy™ platform, Creative Biolabs provides customized, standardized, and reliable and high-quality oncolytic virus therapy development services for clients globally.
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.
Styles of Scientific Reasoning, Scientific Practices and Argument in Science ...Elsa von Licy
The document discusses various topics related to scientific reasoning, practices, and argumentation including different styles of scientific thinking, features of scientific knowledge, and teaching and learning science. It provides examples of "crazy ideas" in science that are now accepted, examines the role of argument in science, and outlines the scientific practices and central questions of science. It also discusses developing models, planning investigations, analyzing data, and constructing explanations as key scientific practices.
Anti-philosophy rejects traditional philosophy and logic, instead embracing creativity, spirituality, and personality. It considers philosophy to be dead, kept alive artificially by analytic philosophers. The document criticizes how philosophy is currently taught and argues it has become unproductive, replacing original aims with nonsense. Anti-philosophy's goal is not to destroy philosophy but to transform its current state and avoid fundamentalism in philosophy and science.
There is no_such_thing_as_a_social_science_introElsa von Licy
This document provides an introduction and overview of the arguments made in the book "There is No Such Thing as Social Science". It begins by stating the provocative title and questioning whether the authors will take it back or qualify their position.
It then outlines three ways the term "social science" could be used - referring to a scientific spirit of inquiry, a shared scientific method, or reducibility to natural sciences. The authors argue against the latter two, methodological and substantive reductionism.
The introduction discusses how opponents may accuse the authors of being a priori or anti-reductionist, but argues that those defending social science are actually being dogmatic by insisting it must follow a scientific model. It frames the debate as being
2. Sample & Assay Technologies
Cancer & Inflammation Webinar Outline
Inflammation – brief overview
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Introduction: Inflammation
Definition: a protective tissue response to tissue damage or microbes, which serves to
destroy, dilute, or wall off both the injurious agent and the injured tissues.
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Microbes/Infection
Tissue Damage
Acute Inflammation
Infection Clearance
Tissue Homeostasis
Epigenetic
Changes
mRNA
Changes
Cytokines & Chemokines
Signaling Pathways
Immune system composition
Chronic Inflammation
Pre-cancer & Cancer
Chronic Inflammatory Diseases
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‘TLR in Inflammation’ webinar
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‘TLR in Inflammation’ webinar
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Cancer & Inflammation Webinar Outline
Inflammation – brief overview
Cancer
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Cancer
“Cancer is the result of uncontrolled growth of a given cell type that occurs together
with the invasion of surrounding tissue and the spread of malignant cells.”
Karin & Greten (2005) Nature Reviews Immunology (5): 749
Three Mechanistic phases
Initiation
Genomic alterations
(DNA Damage)
(DNA mutations)
Promotion
Proliferation & Growth
Progression
Invasion & Metastasis
Inflammation
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13. Sample & Assay Technologies
Link between Cancer & Inflammation
Bacteria, viruses, chemicals, chronic inflammation
Malignancy
Inflammatory Stimulus
Bladder cancer
Schistosomiasis
Gastric lymphoma
H. pylori-induced gastritis
MALT lymphoma
H. pylori
Hepatocellular carcinoma
HBV, HCV
Kaposi’s sarcoma
HHV8
Bronchial carcinoma
Silica, Asbestos
Mesothelioma
Asbestos
Ovarian cancer
Endometriosis
Colorectal cancer
IBD
Esophageal cancer
Barrett’s metaplasia
Papillary thyroid carcinoma
Thyroiditis
Prostate cancer
Prostatitis
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Cancer & Inflammation Webinar Outline
Inflammation – brief overview
Cancer
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Inflammation in cancer initiation
Injury
Inflammation
Cytokines
ROS, RNI
(Extracellular)
ROS, RNI
(Intracellular)
Base excision repair
DNA damage
DNA mutations
Tumor Initiation
(DNA damage)
Epigenetic Changes
Adapted from Grivennikov et al, Cell 2010
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16. Sample & Assay Technologies
Inflammation in cancer initiation
Injury
Inflammation
Cytokines
ROS, RNI
(Extracellular)
ROS, RNI
(Intracellular)
Base excision repair
DNA damage
DNA mutations
Tumor Initiation
(DNA damage)
Epigenetic Changes
Adapted from Grivennikov et al, Cell 2010
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Inflammation in cancer initiation
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18. Sample & Assay Technologies
Inflammation in cancer initiation
Increased tumor multiplicity in mice experiencing DNA damage
after inflammation
Azoxymethane: colonic carcinogen
Aag+/+
Aag (Alkyladenine DNA glycosylase):
Base excision repair enzyme
Aag-/-
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18
19. Sample & Assay Technologies
Inflammation in cancer initiation
Accumulation of Nitrotyrosine in both strains
Nitrotyrosine has been identified as an indicator of cell damage and inflammation,
as well as an indicator of exposure to NO. Repeated cycles of DSS treatment
leads to positive nitrotyrosine staining in colons of treated animals. Similar
staining intensity is detected for both Aag+/+ and Aag-/- colons.
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20. Sample & Assay Technologies
Inflammation in cancer initiation
Oncogenic mutations are increased in mice lacking base
excision repair enzymes after inflammation
LCM
PCR Amplification
Sequencing
Gene: Ctnnb1 (β Catenin 1)
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21. Sample & Assay Technologies
Inflammation in cancer initiation
Conclusions
Inflammatory conditions
RNOS
Base excision repair
Oncogenic mutations
Tumor growth
Title, Location, Date
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Cancer & Inflammation Webinar Outline
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QIAGEN tools for cancer & inflammation
qBiomarker Somatic Mutation PCR Arrays & Assays
Analyze Somatic Mutations by Real-time PCR
Profile 85 different
mutations on one array
(372 mutations on one
384 array)
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and reaction
performance
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QIAGEN tools for cancer & inflammation
qBiomarker Somatic Mutation PCR Arrays & Assays
Focused Content
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QIAGEN tools for cancer & inflammation
qBiomarker Somatic Mutation PCR Arrays & Assays
Focused Content
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QIAGEN tools for cancer & inflammation
qBiomarker Somatic Mutation PCR Arrays & Assays
Focused Content
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QIAGEN tools for cancer & inflammation
qBiomarker Somatic Mutation PCR Arrays & Assays
Complete Workflow
Sample
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Customer support group:
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Cancer & Inflammation Webinar Outline
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Cancer
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Inflammation in cancer promotion
Title, Location, Date
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30. Sample & Assay Technologies
Inflammation in cancer promotion
Mdr2-KO mice develop hepatocellular carcinoma on the
background of chronic hepatitis (inflammatory condition)
Arrowheads indicate tumors
H&E staining
Title, Location, Date
30
31. Sample & Assay Technologies
Inflammation in cancer promotion
NFkB activation is involved in Mdr2-KO hepatocarcinogenesis
NFkB Nuclear staining
TNFa leads to NFkB activation (red = Kupffer cells; yellow = hepatocytes)
NFkB activation is seen predominantly adjacent to
inflamed portal tracts, NOT in all neoplastic
hepatocytes, suggesting an inflamed phenomenon.
(blue = bile epithelium; yellow = hepatocytes)
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31
32. Sample & Assay Technologies
Inflammation in cancer promotion
NSAID treatment decreased inflammation
2.5 month old mice
10-day ibuprofen treatment
MPO staining
Decreased neutrophils
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33. Sample & Assay Technologies
Inflammation in cancer promotion
TNFa drives NFkB activation
Treatment with anti-TNFa decreased
NFkB nuclear staining (activation)
Source of TNFa is the non-hepatocyte fraction of the liver
H: hepatocyte fraction
R: non-hepatocyte fraction
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34. Sample & Assay Technologies
Inflammation in cancer promotion
NFkB is critical for tumor promotion
Generate DKO mice to directly assess the role of NFkB in hepatocarcinogenesis
∆N-IκBhep
Mdr2 KO
X
NFkB inactivated in hepatocytes
(Dox-activated NFkB)
Double mutant (DM)
Mdr2-/- ∆N-IκBhep
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34
35. Sample & Assay Technologies
Inflammation in cancer promotion
NFkB is dispensable for early stages of HCC development
4 month old mice
No change in inflammation
7 month old mice
No change in dysplasia
Title, Location, Date
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36. Sample & Assay Technologies
Inflammation in cancer promotion
NFkB is critical for tumor promotion
Inactivation of NFkB in
hepatocytes results in decreased
tumor volume
NFkB activated in hepatocytes
Title, Location, Date
36
37. Sample & Assay Technologies
Inflammation in cancer promotion
NFkB inhibition results in suppression of anti-apoptotic factors
Increased hepatocyte apoptosis in DM mice
(DM mice & KO + anti-TNF = inactivation of
NFkB in hepatocytes)
Liver protein extracts from KO mice
Inactivation of NFkB decreased the expression
of anti-apoptotic genes
Title, Location, Date
37
38. Sample & Assay Technologies
Inflammation in cancer promotion
Conclusions
Inflammatory stimulus (Mdr2 KO)
Inflammatory cytokine (TNFa)
NFkB activation
Modulation of gene expression
Tumor growth
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Increased survival
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Cancer & Inflammation Webinar Outline
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QIAGEN tools for cancer & inflammation
RT2 Profiler PCR Arrays & Assays
Analyze gene expression by Real-time PCR
Profile 84 different
genes on one array
(370 genes on one 384
array)
Appropriate controls
for data normalization,
sample quality, and
reaction performance
Focus on your
questions and papers
http://sabiosciences.com/PCRArrayPlate.php
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41. Sample & Assay Technologies
QIAGEN tools for cancer & inflammation
RT2 Profiler PCR Arrays & Assays
Focused Content
Array
Species
NFkB Pathway
Human/Mouse/Rat
NFkB Targets
Human/Mouse/Rat
Apoptosis
Human/Mouse/Rat
TNF Pathway
Human/Mouse/Rat
Others (>140)
Varies
Array
Species
IL6/STAT3 Pathway
Human/Mouse/Rat
JAK/STAT Pathway
Human/Mouse/Rat
Inflammatory responses Human/Mouse/Rat
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42. Sample & Assay Technologies
QIAGEN tools for cancer & inflammation
RT2 Profiler PCR Arrays & Assays
Complete Workflow
Sample
Isolation &
Preparation
Assay
Set-up &
Analysis
Customer support group:
1-888-503-3187
support@SABiosciences.com
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43. Sample & Assay Technologies
Cancer & Inflammation Webinar Outline
Inflammation – brief overview
Cancer
Inflammation in Cancer Initiation
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Inflammation in Cancer Promotion
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Inflammation in Cancer Progression
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44. Sample & Assay Technologies
Inflammation in cancer progression
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45. Sample & Assay Technologies
Inflammation in cancer progression
TAMs and CSF-1
Tumor-associated macrophages (TAMs) populate most solid tumors.
TAMs are associated with poor prognosis.
Colony-stimulating factor (CSF-1) is a regulator of the proliferation, differentiation, and
survival of macrophages.
CSF-1 expression is prevalent in invasive tumor cells.
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46. Sample & Assay Technologies
Inflammation in cancer progression
Generate DM mice to directly assess the role of CSF-1 in cancer progression
CSF1op
MMTV-PyMT
X
CSF1 null recessive mutation
(CSF-1 not expressed)
Double mutant (DM)
PyMT-CSF1op
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46
47. Sample & Assay Technologies
Inflammation in cancer progression
Growth and size of primary mammary tumors are not altered in
absence of CSF-1
CSF-1
No CSF-1
Title, Location, Date
47
48. Sample & Assay Technologies
Inflammation in cancer progression
Metastasis of mammary tumors is decreased in absence of
CSF-1
CSF-1
No CSF-1
Title, Location, Date
48
49. Sample & Assay Technologies
Inflammation in cancer progression
Progression of mammary tumors is decreased in absence of
CSF-1
CSF-1
Title, Location, Date
No CSF-1
49
50. Sample & Assay Technologies
Inflammation in cancer progression
Presence of TAMs is decreased in absence of CSF-1
CSF-1
No CSF-1
+/op
op/op
7-wk mice
(F4/80 staining)
19-20-wk mice
(F4/80 staining)
Title, Location, Date
50
51. Sample & Assay Technologies
Inflammation in cancer progression
Conclusions
Development of primary tumor
Growth of primary tumor
Recruitment of TAMs to primary tumor
Metastasis of primary tumor to distant sites
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51
52. Sample & Assay Technologies
Inflammation in cancer progression
There is a correlation between TAM abundance and poor prognosis.
However, it is not only the number of TAMs but also the cytokine-expression
profile of TAMs that might link inflammation with tumor progression
Balkwell et al. Cancer Cell 7; Mar 2005; 211
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QIAGEN tools for cancer & inflammation
ELISArray kits
Analyze Protein expression
Profile 12 different
analytes from 6
samples on one array
Appropriate controls
for reaction
performance
Also:
Mix-N-Match
Single-Analyte
Focus on your
questions and papers
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QIAGEN tools for cancer & inflammation
ELISArray kits
Focused Content
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Customer support group:
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Cancer & Inflammation Webinar Outline
Inflammation – brief overview
Cancer
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miRNA in cancer & inflammation
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61. Sample & Assay Technologies
miRNA in cancer & inflammation
Src activation induces transformation of normal cells
MCF10A cells (immortalized normal mammary epithelial cells)
Tamoxifen treatment
Activation of Src
Title, Location, Date
Transformation
61
62. Sample & Assay Technologies
miRNA in cancer & inflammation
Src-induced transformation is accompanied by an inflammatory
response mediated by NFkB
Title, Location, Date
62
63. Sample & Assay Technologies
miRNA in cancer & inflammation
Src-induced transformation is accompanied by increased
LIN28B and decreased Let-7a expression
Real-time PCR
Extract mRNA
SRC activation
Reverse transcribe to cDNA
NFkB activation
Screen 365 miRNAs
Increase LIN28B
Decrease Let-7a
Title, Location, Date
63
64. Sample & Assay Technologies
miRNA in cancer & inflammation
Let-7a and LIN28B regulate IL6 expression and activity during
Src-induced transformation
Increasing Let-7a levels decreases
IL6 levels
SRC activation
NFkB activation
Decreasing LIN28B levels decreases
IL6 levels
Increase LIN28B
Increase IL6
Decrease Let-7a
Title, Location, Date
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65. Sample & Assay Technologies
miRNA in cancer & inflammation
The IL6 signaling pathway, mediated through STAT3, regulates
Src-induced transformation
SRC activation
NFkB activation
Increase LIN28B
Increase IL6
Decrease Let-7a
Transformation
Title, Location, Date
65
66. Sample & Assay Technologies
miRNA in cancer & inflammation
Conclusions
Oncogene activation (Src)
NFkB activation
Modulation of miRNA expression
Inflammatory cytokine (IL6)
Transformation
Title, Location, Date
66
67. Sample & Assay Technologies
Cancer & Inflammation Webinar Outline
Inflammation – brief overview
Cancer
Inflammation in Cancer Initiation
qBiomarker Somatic Mutations System
Inflammation in Cancer Promotion
RT2 Profiler System
Inflammation in Cancer Progression
ELISArrays
miRNA in Cancer & Inflammation
miScript miRNA System
Promotions
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68. Sample & Assay Technologies
QIAGEN tools for cancer & inflammation
miScript miRNA PCR Arrays & Assays
Analyze miRNA expression by Real-time PCR
Profile 84 different
miRNAs on one array
(370 miRNAs on one
384 array)
Appropriate controls
for data normalization,
sample quality, and
reaction performance
Focus on your
questions and papers
http://sabiosciences.com/mirna.php
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69. Sample & Assay Technologies
QIAGEN tools for cancer & inflammation
miScript miRNA PCR Arrays & Assays
Focused Content
Screen ENTIRE miRNome
(ALL documented miRNAs)
http://sabiosciences.com/mirna_pcr_array.php
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70. Sample & Assay Technologies
QIAGEN tools for cancer & inflammation
miScript miRNA PCR Arrays & Assays
Complete Workflow
Sample
Isolation &
Preparation
Assay
Set-up &
Analysis
Customer support group:
1-888-503-3187
support@SABiosciences.com
Title, Location, Date
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71. Sample & Assay Technologies
QIAGEN tools for cancer & inflammation
Gene Expression
RT-PCR
Somatic mutations
Copy Number Variations & Alterations
Epigenetics
miRNA
DNA methylation
Histone modifications
Functional Studies
Reporter assays
siRNA/shRNA
Protein Expression
Cytokine & Chemokine levels
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Keep up to date: Follow Pathway focused biology on Facebook
Latest
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resources and
demos.
73. Sample & Assay Technologies
Cancer & Inflammation Webinar Outline
Inflammation – brief overview
Cancer
Inflammation in Cancer Initiation
qBiomarker Somatic Mutations System
Inflammation in Cancer Promotion
RT2 Profiler System
Inflammation in Cancer Progression
ELISArrays
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74. Sample & Assay Technologies
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