Podcast
Questions and Answers
What is the primary component of the basement membrane that tumor cells interact with during invasion?
What is the primary component of the basement membrane that tumor cells interact with during invasion?
Which of the following is NOT a function of adhesion molecules in tumor cells?
Which of the following is NOT a function of adhesion molecules in tumor cells?
What is the term for the process by which tumor cells escape from the primary tumor site and enter the bloodstream or lymphatic vessels?
What is the term for the process by which tumor cells escape from the primary tumor site and enter the bloodstream or lymphatic vessels?
Which of the following is a type of paracrine effector that promotes tumor cell motility?
Which of the following is a type of paracrine effector that promotes tumor cell motility?
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What is the term for the process by which tumor cells recruit blood vessels to the primary tumor site?
What is the term for the process by which tumor cells recruit blood vessels to the primary tumor site?
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Which of the following is NOT a component of the extracellular matrix?
Which of the following is NOT a component of the extracellular matrix?
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What is the term for the process by which tumor cells adhere to the endothelial lining of blood vessels during metastasis?
What is the term for the process by which tumor cells adhere to the endothelial lining of blood vessels during metastasis?
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Which of the following is a type of cell that can produce factors that promote tumor cell motility?
Which of the following is a type of cell that can produce factors that promote tumor cell motility?
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What is the primary mechanism by which tumor cells spread and grow?
What is the primary mechanism by which tumor cells spread and grow?
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Why are tumor cells vulnerable to destruction by immune cells?
Why are tumor cells vulnerable to destruction by immune cells?
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What is the outcome of tumor cells interacting with host immune cells?
What is the outcome of tumor cells interacting with host immune cells?
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Why is intravasation into vascular beds important for tumor cell spread?
Why is intravasation into vascular beds important for tumor cell spread?
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What is the role of extravasation in tumor cell spread?
What is the role of extravasation in tumor cell spread?
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How do tumor cells interact with host immune cells?
How do tumor cells interact with host immune cells?
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What is the outcome of tumor cells invading normal tissues?
What is the outcome of tumor cells invading normal tissues?
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Why is the primary tumor site important for tumor cell growth and spread?
Why is the primary tumor site important for tumor cell growth and spread?
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What is the likely outcome of having germ line mutations in BRCA2?
What is the likely outcome of having germ line mutations in BRCA2?
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What is the role of BRCA1 and BRCA2 in cancer development?
What is the role of BRCA1 and BRCA2 in cancer development?
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What is the characteristic of Hereditary Nonpolyposis Colon Cancer (HNPCC) syndrome?
What is the characteristic of Hereditary Nonpolyposis Colon Cancer (HNPCC) syndrome?
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What is the consequence of somatic mutations in DNA repair genes?
What is the consequence of somatic mutations in DNA repair genes?
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What is the role of DNA mismatch repair genes in cancer development?
What is the role of DNA mismatch repair genes in cancer development?
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What is the effect of inactivating BRCA1 and BRCA2 genes?
What is the effect of inactivating BRCA1 and BRCA2 genes?
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What is the relationship between germ line mutations in BRCA2 and cancer risk?
What is the relationship between germ line mutations in BRCA2 and cancer risk?
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What is the consequence of Tumor-Promoting Inflammation in cancer development?
What is the consequence of Tumor-Promoting Inflammation in cancer development?
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Which of the following checkpoint inhibitors is used to avoid immune destruction?
Which of the following checkpoint inhibitors is used to avoid immune destruction?
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What is the main function of BCL2 inhibitors in cancer treatment?
What is the main function of BCL2 inhibitors in cancer treatment?
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Which of the following signaling pathways is deregulated in cancer cells to promote growth?
Which of the following signaling pathways is deregulated in cancer cells to promote growth?
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What is the main function of MDM2 inhibitors in cancer treatment?
What is the main function of MDM2 inhibitors in cancer treatment?
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Which of the following is a hallmark of cancer?
Which of the following is a hallmark of cancer?
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What is the main function of PARP inhibitors in cancer treatment?
What is the main function of PARP inhibitors in cancer treatment?
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Which of the following is a type of inhibitor used to treat cancer?
Which of the following is a type of inhibitor used to treat cancer?
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What is the main function of VEGF inhibitors in cancer treatment?
What is the main function of VEGF inhibitors in cancer treatment?
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Which of the following is a hallmark of cancer that allows cancer cells to continue to grow and divide?
Which of the following is a hallmark of cancer that allows cancer cells to continue to grow and divide?
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What is the main function of anti-CTLA-4 in cancer treatment?
What is the main function of anti-CTLA-4 in cancer treatment?
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What role do paraneoplastic syndromes play in cancer patients?
What role do paraneoplastic syndromes play in cancer patients?
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How does the activation of macrophages relate to tumor necrosis?
How does the activation of macrophages relate to tumor necrosis?
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What is the significance of grading tumors?
What is the significance of grading tumors?
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What is a common outcome of the release of free fatty acids in cancer progression?
What is a common outcome of the release of free fatty acids in cancer progression?
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What is the significance of cytokines in assessing cancer stage?
What is the significance of cytokines in assessing cancer stage?
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Why are clinical and radiologic studies important in tumor evaluation?
Why are clinical and radiologic studies important in tumor evaluation?
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What is one reason tumor grades are considered more informative than tumor stages?
What is one reason tumor grades are considered more informative than tumor stages?
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What is an implication of cytokine action in relation to tumor cells?
What is an implication of cytokine action in relation to tumor cells?
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Tumor cells are resistant to destruction by immune cells.
Tumor cells are resistant to destruction by immune cells.
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Tumor cells grow rapidly in the primary tumor site due to the suppression by resident immune cells.
Tumor cells grow rapidly in the primary tumor site due to the suppression by resident immune cells.
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Extravasation into vascular beds is a crucial step for tumor cell motility.
Extravasation into vascular beds is a crucial step for tumor cell motility.
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Intravasation into vascular beds is a process that occurs only in late-stage tumors.
Intravasation into vascular beds is a process that occurs only in late-stage tumors.
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Tumor cells always grow rapidly in the primary tumor site without any suppression by immune cells.
Tumor cells always grow rapidly in the primary tumor site without any suppression by immune cells.
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The primary tumor site is not important for tumor cell growth and spread.
The primary tumor site is not important for tumor cell growth and spread.
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Tumor cells can escape from immune cells only through intravasation into vascular beds.
Tumor cells can escape from immune cells only through intravasation into vascular beds.
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Tumor cells are always supported by stromal support in the primary tumor site.
Tumor cells are always supported by stromal support in the primary tumor site.
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Extravasation of tumor cells into vascular beds is a process that occurs only in late-stage tumors.
Extravasation of tumor cells into vascular beds is a process that occurs only in late-stage tumors.
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Tumor cells always grow rapidly in the primary tumor site without any suppression by immune cells.
Tumor cells always grow rapidly in the primary tumor site without any suppression by immune cells.
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Intravasation into vascular beds is essential for tumor cell motility.
Intravasation into vascular beds is essential for tumor cell motility.
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Tumor cells are always supported by stromal support in the primary tumor site.
Tumor cells are always supported by stromal support in the primary tumor site.
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Adhesion molecules are involved in the process of extravasation of tumor cells into vascular beds.
Adhesion molecules are involved in the process of extravasation of tumor cells into vascular beds.
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Metastatic tumors always form in distant organs with similar tissue structure to the primary tumor site.
Metastatic tumors always form in distant organs with similar tissue structure to the primary tumor site.
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The primary tumor site is not important for tumor cell growth and spread.
The primary tumor site is not important for tumor cell growth and spread.
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Tumor cells can escape from immune cells only through intravasation into vascular beds.
Tumor cells can escape from immune cells only through intravasation into vascular beds.
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The host immune system is always capable of destroying tumors.
The host immune system is always capable of destroying tumors.
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Tumor cells can only spread through the lymphatic vessels.
Tumor cells can only spread through the lymphatic vessels.
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The primary tumor site is not important for tumor cell growth and spread.
The primary tumor site is not important for tumor cell growth and spread.
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Immune cells always support tumor cell growth and spread.
Immune cells always support tumor cell growth and spread.
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Tumor cells can only evade immune cells through intravasation into vascular beds.
Tumor cells can only evade immune cells through intravasation into vascular beds.
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Tumor cells grow rapidly in the primary tumor site due to the suppression by resident immune cells.
Tumor cells grow rapidly in the primary tumor site due to the suppression by resident immune cells.
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Extravasation into vascular beds is a process that occurs only in late-stage tumors.
Extravasation into vascular beds is a process that occurs only in late-stage tumors.
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Tumor cells are resistant to destruction by immune cells due to their genetic mutations.
Tumor cells are resistant to destruction by immune cells due to their genetic mutations.
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Activation of BAX/BAK may be stimulated by antiangiogenic factors.
Activation of BAX/BAK may be stimulated by antiangiogenic factors.
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Cytokines produced by macrophages are involved in the promotion of tumor angiogenesis.
Cytokines produced by macrophages are involved in the promotion of tumor angiogenesis.
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BCL-2 and its relatives are known to inhibit apoptosis in tumor cells.
BCL-2 and its relatives are known to inhibit apoptosis in tumor cells.
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Tumor-associated macrophages exclusively aid in immune defense against cancer cells.
Tumor-associated macrophages exclusively aid in immune defense against cancer cells.
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Mitochondrial factors released by tumors can influence proangiogenic activity.
Mitochondrial factors released by tumors can influence proangiogenic activity.
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Proangiogenic factors are primarily produced by normal resident cells in the tissue.
Proangiogenic factors are primarily produced by normal resident cells in the tissue.
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The activation of stromal cells is essential for the progression of tumor angiogenesis.
The activation of stromal cells is essential for the progression of tumor angiogenesis.
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The role of proapoptotic proteins is to promote cell survival in tumors.
The role of proapoptotic proteins is to promote cell survival in tumors.
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The presence of functional CD8+ T cells is a strong predictor of cancer survival.
The presence of functional CD8+ T cells is a strong predictor of cancer survival.
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The immune system is always capable of recognizing and eliminating nascent cancers.
The immune system is always capable of recognizing and eliminating nascent cancers.
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The "immunoscore", which quantifies the immune cell infiltration in a tumor, has no predictive value for cancer survival.
The "immunoscore", which quantifies the immune cell infiltration in a tumor, has no predictive value for cancer survival.
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The presence of "invisible" tumors that are not detectable by the immune system is a common occurrence.
The presence of "invisible" tumors that are not detectable by the immune system is a common occurrence.
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The understanding of immune evasion mechanisms has led to a revolution in cancer therapy, with the development of "immunotherapies".
The understanding of immune evasion mechanisms has led to a revolution in cancer therapy, with the development of "immunotherapies".
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The exact role of immune cells, like macrophages and NK cells, in cancer progression is well understood.
The exact role of immune cells, like macrophages and NK cells, in cancer progression is well understood.
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What is the significance of receptors on the surface of tumor cells in regards to metastatic behavior?
What is the significance of receptors on the surface of tumor cells in regards to metastatic behavior?
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How do adhesion molecules contribute to the extravasation of tumor cells?
How do adhesion molecules contribute to the extravasation of tumor cells?
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What is the role of the microenvironment in supporting the growth and spread of tumor cells?
What is the role of the microenvironment in supporting the growth and spread of tumor cells?
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How do tumor cells interact with the stroma to promote their growth and invasion?
How do tumor cells interact with the stroma to promote their growth and invasion?
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What is the significance of the deposit of tumor cells in secondary tissues?
What is the significance of the deposit of tumor cells in secondary tissues?
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How do tumor cells modulate the immune response to promote their growth and survival?
How do tumor cells modulate the immune response to promote their growth and survival?
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What is the role of chemokines in promoting the migration and invasion of tumor cells?
What is the role of chemokines in promoting the migration and invasion of tumor cells?
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How do tumor cells interact with the extracellular matrix to promote their growth and invasion?
How do tumor cells interact with the extracellular matrix to promote their growth and invasion?
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What is the role of CD28 in the process of costimulation?
What is the role of CD28 in the process of costimulation?
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How do checkpoint inhibitors like CTLA-4 and PD-1 affect T cell activation?
How do checkpoint inhibitors like CTLA-4 and PD-1 affect T cell activation?
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What is the role of dendritic cells in presenting antigens to T cells?
What is the role of dendritic cells in presenting antigens to T cells?
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What is the outcome of T cells interacting with tumor cells in the absence of costimulation?
What is the outcome of T cells interacting with tumor cells in the absence of costimulation?
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What is the purpose of anti-CTLA-4 therapy in cancer treatment?
What is the purpose of anti-CTLA-4 therapy in cancer treatment?
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How do PD-1 ligands on tumor cells affect T cell activation?
How do PD-1 ligands on tumor cells affect T cell activation?
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What is the role of primed cytotoxic T cells in anti-tumor immunity?
What is the role of primed cytotoxic T cells in anti-tumor immunity?
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How do tumor cells evade immune detection?
How do tumor cells evade immune detection?
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What is the purpose of anti-PD-1 therapy in cancer treatment?
What is the purpose of anti-PD-1 therapy in cancer treatment?
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How do T cells recognize and kill tumor cells?
How do T cells recognize and kill tumor cells?
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How do checkpoint inhibitors, such as anti-CTLA-4 and anti-PD-1/PD-L1, contribute to cancer treatment?
How do checkpoint inhibitors, such as anti-CTLA-4 and anti-PD-1/PD-L1, contribute to cancer treatment?
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What is the role of MDM2 inhibitors in cancer treatment, and how do they relate to the function of p53?
What is the role of MDM2 inhibitors in cancer treatment, and how do they relate to the function of p53?
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Describe the role of BCL2 inhibitors in cancer treatment, and how they relate to the regulation of apoptosis.
Describe the role of BCL2 inhibitors in cancer treatment, and how they relate to the regulation of apoptosis.
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What is the significance of the EGFR signaling pathway in cancer cells, and how do its inhibitors contribute to cancer treatment?
What is the significance of the EGFR signaling pathway in cancer cells, and how do its inhibitors contribute to cancer treatment?
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How do PARP inhibitors contribute to cancer treatment, and what is their relationship to DNA repair mechanisms?
How do PARP inhibitors contribute to cancer treatment, and what is their relationship to DNA repair mechanisms?
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What is the role of VEGF inhibitors in cancer treatment, and how do they relate to angiogenesis?
What is the role of VEGF inhibitors in cancer treatment, and how do they relate to angiogenesis?
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Describe the relationship between tumor-promoting inflammation and cancer development.
Describe the relationship between tumor-promoting inflammation and cancer development.
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What is the significance of sustaining proliferative signaling in cancer cells, and how do its inhibitors contribute to cancer treatment?
What is the significance of sustaining proliferative signaling in cancer cells, and how do its inhibitors contribute to cancer treatment?
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How do inhibitors of genome instability and mutation contribute to cancer treatment, and what is their relationship to DNA repair mechanisms?
How do inhibitors of genome instability and mutation contribute to cancer treatment, and what is their relationship to DNA repair mechanisms?
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Describe the role of evading growth suppressors in cancer development, and how do its inhibitors contribute to cancer treatment?
Describe the role of evading growth suppressors in cancer development, and how do its inhibitors contribute to cancer treatment?
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Explain how defects in DNA repair systems, specifically homologous recombination repair, contribute to the development of cancer, using the examples of BRCA1 and BRCA2.
Explain how defects in DNA repair systems, specifically homologous recombination repair, contribute to the development of cancer, using the examples of BRCA1 and BRCA2.
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Describe the role of germline mutations in DNA repair genes, such as BRCA1 and BRCA2, in the predisposition to cancer.
Describe the role of germline mutations in DNA repair genes, such as BRCA1 and BRCA2, in the predisposition to cancer.
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Explain the link between defective homologous recombination repair and the increased risk of breast cancer.
Explain the link between defective homologous recombination repair and the increased risk of breast cancer.
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Why are defects in DNA repair pathways, such as homologous recombination, a significant factor in cancer development? Discuss the role of these pathways in maintaining genomic integrity.
Why are defects in DNA repair pathways, such as homologous recombination, a significant factor in cancer development? Discuss the role of these pathways in maintaining genomic integrity.
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What is the relationship between DNA repair defects and the development of cancer syndromes, such as hereditary breast and ovarian cancer syndrome? How do these syndromes differ from sporadic cancers?
What is the relationship between DNA repair defects and the development of cancer syndromes, such as hereditary breast and ovarian cancer syndrome? How do these syndromes differ from sporadic cancers?
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How do defects in DNA repair systems contribute to the development of a higher risk of ovarian carcinoma and other cancers?
How do defects in DNA repair systems contribute to the development of a higher risk of ovarian carcinoma and other cancers?
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Discuss the impact of DNA repair defects on the development of both inherited and sporadic cancers. Explain how these defects contribute to the accumulation of mutations and tumorigenesis.
Discuss the impact of DNA repair defects on the development of both inherited and sporadic cancers. Explain how these defects contribute to the accumulation of mutations and tumorigenesis.
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Why are women with BRCA1 mutations at a higher risk of developing both breast and ovarian cancer? Discuss the underlying mechanism and the role of these genes in DNA repair.
Why are women with BRCA1 mutations at a higher risk of developing both breast and ovarian cancer? Discuss the underlying mechanism and the role of these genes in DNA repair.
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What mechanism is associated with Cushing syndrome in small cell lung carcinoma?
What mechanism is associated with Cushing syndrome in small cell lung carcinoma?
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Which neoplasm is commonly associated with hypercalcemia?
Which neoplasm is commonly associated with hypercalcemia?
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What is one immunologic mechanism related to myasthenia associated with lung carcinoma?
What is one immunologic mechanism related to myasthenia associated with lung carcinoma?
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What substance is commonly secreted in relation to the Trousseau phenomenon?
What substance is commonly secreted in relation to the Trousseau phenomenon?
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Which tumor type is associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
Which tumor type is associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
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Name a neoplasm associated with hypoglycemia due to insulin-like substances.
Name a neoplasm associated with hypoglycemia due to insulin-like substances.
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What dermatologic disorder is linked to gastric carcinoma?
What dermatologic disorder is linked to gastric carcinoma?
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What immunologic mechanism is associated with red cell aplasia and thymoma?
What immunologic mechanism is associated with red cell aplasia and thymoma?
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Which tumor type can lead to polycythemia due to increased erythropoietin production?
Which tumor type can lead to polycythemia due to increased erythropoietin production?
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Which two types of neoplasms commonly exhibit immunologic disorders of the central nervous system?
Which two types of neoplasms commonly exhibit immunologic disorders of the central nervous system?
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However, ___________ angiogenesis has not been as extensively studied as or gnostic anymore; presumably, subordinate cones of or
However, ___________ angiogenesis has not been as extensively studied as or gnostic anymore; presumably, subordinate cones of or
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As discussed previously in the context of cellular aging (see Chapter 1), most normal ___________ cells can double 60 to 70 times, after which blood vessels emerge, thereby sedating the need for
As discussed previously in the context of cellular aging (see Chapter 1), most normal ___________ cells can double 60 to 70 times, after which blood vessels emerge, thereby sedating the need for
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Cells those the ability to divide and enter ___________, thereby preventing the need for
Cells those the ability to divide and enter ___________, thereby preventing the need for
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Blocking _______ or CTLA-4 with antibodies leads to primed CTL capable of killing tumor cells.
Blocking _______ or CTLA-4 with antibodies leads to primed CTL capable of killing tumor cells.
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This phenomenon is neo ___________ due to progressive shortening of telomeres at the ends of chromosomes.
This phenomenon is neo ___________ due to progressive shortening of telomeres at the ends of chromosomes.
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Dendritic cells present tumor _______-MHC to CD8+ T cells.
Dendritic cells present tumor _______-MHC to CD8+ T cells.
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The consequences of telomere shortening, when pronounced, are ___________.
The consequences of telomere shortening, when pronounced, are ___________.
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CTLA-4 is a molecule that inhibits the activity of _______ cells.
CTLA-4 is a molecule that inhibits the activity of _______ cells.
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CD28 is a _______ molecule that activates T cells.
CD28 is a _______ molecule that activates T cells.
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Invasion and ___________ are the most critical aspects of cancer progression.
Invasion and ___________ are the most critical aspects of cancer progression.
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Anti-PD-1 therapy leads to the killing of _______ cells.
Anti-PD-1 therapy leads to the killing of _______ cells.
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Tumor cells interact with the host ___________ cells, leading to the destruction of tumor cells.
Tumor cells interact with the host ___________ cells, leading to the destruction of tumor cells.
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The primary tumor site is important for tumor cell ___________ and spread.
The primary tumor site is important for tumor cell ___________ and spread.
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In the absence of _______ , CD8+ T cells are inhibited.
In the absence of _______ , CD8+ T cells are inhibited.
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PD-1 ligand is expressed on _______ cells.
PD-1 ligand is expressed on _______ cells.
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CD8+ CTL granules contain molecules that kill _______ cells.
CD8+ CTL granules contain molecules that kill _______ cells.
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Blocking PD-1 or CTLA-4 can lead to the activation of _______ cells.
Blocking PD-1 or CTLA-4 can lead to the activation of _______ cells.
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Anti-CTLA-4 therapy leads to the activation of _______ cells.
Anti-CTLA-4 therapy leads to the activation of _______ cells.
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In many patients, loss of ______ has been associated with poor outcome.
In many patients, loss of ______ has been associated with poor outcome.
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[Blank] and quality of immune responses are often correlated with cancer outcome.
[Blank] and quality of immune responses are often correlated with cancer outcome.
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Upregulation of ______ genes are more typical of mesenchymal cells.
Upregulation of ______ genes are more typical of mesenchymal cells.
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There is an increased incidence of certain cancers in ______ deficiency states.
There is an increased incidence of certain cancers in ______ deficiency states.
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Recent studies have shown that therapies that simulate ______ are effective against certain cancers.
Recent studies have shown that therapies that simulate ______ are effective against certain cancers.
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EMT is often accompanied by ______ of the basement membrane.
EMT is often accompanied by ______ of the basement membrane.
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Tumor cells often acquire ______ changes, leading to a more invasive phenotype.
Tumor cells often acquire ______ changes, leading to a more invasive phenotype.
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EMT is characterized by the loss of ______ and the gain of mesenchymal traits.
EMT is characterized by the loss of ______ and the gain of mesenchymal traits.
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However, ______ patients
However, ______ patients
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These genes are unstable and ______ or decrease in
These genes are unstable and ______ or decrease in
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HNPCC syndrome accounts for only 2% to 4% of all ______ cancers, but MSI can be detected in about 15% of sporadic cancers.
HNPCC syndrome accounts for only 2% to 4% of all ______ cancers, but MSI can be detected in about 15% of sporadic cancers.
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In this respect, they resemble ______ genes.
In this respect, they resemble ______ genes.
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Tumors, producing enzymes that enhance ______ tumor invasion and
Tumors, producing enzymes that enhance ______ tumor invasion and
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Tumors, producing enzymes that enhance local tumor invasion and ______ metastasis.
Tumors, producing enzymes that enhance local tumor invasion and ______ metastasis.
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Benign and malignant tumors may cause local and systemic problems through a variety of direct and indirect ______.
Benign and malignant tumors may cause local and systemic problems through a variety of direct and indirect ______.
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The ______ or by the elaboration of hormones indigenous to the tissue of origin of the tumor
The ______ or by the elaboration of hormones indigenous to the tissue of origin of the tumor
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They may be the earliest manifestation of an occult neoplasm and their clinical recognition is important for several ______.
They may be the earliest manifestation of an occult neoplasm and their clinical recognition is important for several ______.
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Anamorphic location is a crucial determinant of the local, "space-occupying" ______ of both benign and malignant tumors.
Anamorphic location is a crucial determinant of the local, "space-occupying" ______ of both benign and malignant tumors.
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Therapies approved for use or in advanced clinical ______ are listed.
Therapies approved for use or in advanced clinical ______ are listed.
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The hallmarks of cancer: the next ______.
The hallmarks of cancer: the next ______.
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Therapeutic targeting of hallmarks of ______.
Therapeutic targeting of hallmarks of ______.
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They appear in 10% to 15% of cancer ______.
They appear in 10% to 15% of cancer ______.
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Match the following cancer-related processes with their correct descriptions:
Match the following cancer-related processes with their correct descriptions:
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Match the following factors related to tumor cell spread with their impact:
Match the following factors related to tumor cell spread with their impact:
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Match the following types of tumors with their characteristics:
Match the following types of tumors with their characteristics:
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Match the following concepts related to tumor cells with their correct explanations:
Match the following concepts related to tumor cells with their correct explanations:
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Match the following challenges faced by tumor cells with their outcomes:
Match the following challenges faced by tumor cells with their outcomes:
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Match the following tumor cell characteristics with their implications:
Match the following tumor cell characteristics with their implications:
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Match the following phenomena related to tumor expansion with their effects:
Match the following phenomena related to tumor expansion with their effects:
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Match the following cellular interactions with their consequences on tumor proliferation:
Match the following cellular interactions with their consequences on tumor proliferation:
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Match the following terms with their descriptions related to tumor angiogenesis:
Match the following terms with their descriptions related to tumor angiogenesis:
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Match the following pathways with their roles in apoptosis and angiogenesis:
Match the following pathways with their roles in apoptosis and angiogenesis:
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Match the following effects with their corresponding mechanisms in tumor biology:
Match the following effects with their corresponding mechanisms in tumor biology:
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Match the following conditions with their effects on tumor growth:
Match the following conditions with their effects on tumor growth:
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Match the following substances with their effects on angiogenesis and apoptosis:
Match the following substances with their effects on angiogenesis and apoptosis:
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Match the following roles with the corresponding molecules involved in tumor processes:
Match the following roles with the corresponding molecules involved in tumor processes:
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Match the following tumor-related phenomena with their implications:
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Match the following factors with their contributions to tumor angiogenesis:
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Match the following cancer treatment strategies with their primary action:
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Match the following tumor characteristics with their description:
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Match the following types of inhibitors with their target:
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Match the following signaling pathways with their roles in cancer:
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Match the following cancer hallmarks with their meanings:
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Match the following tumor suppressor roles with their functions:
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Match the following immune checkpoint inhibitors with their mechanism of action:
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Match the following tumors with their characteristic immune evasion mechanisms:
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Match the following checkpoint blockade effects with their consequences:
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Match the following tumor types with their association to immune checkpoint inhibitors:
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Match the following immune regulatory mechanisms with their roles:
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Match the following terms related to immune response in tumors with their definitions:
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Match the following immune reactions with their targets in cancer therapy:
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Match the following effects of tumors with their descriptions:
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Match the following processes with their effects on tumor cells:
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Study Notes
Tumor Biology and Metastasis
- Cleavage products of the extracellular matrix components, such as collagen and laminin, and certain growth factors contribute to tumor cell behavior.
- Tumor and stroma cells produce proteases that facilitate the invasive potential of cells through the basement membrane.
Vascular Dissemination and Tumor Cell Homing
- Tumor cells frequently evade local sites of origin to infiltrate blood circulation or lymphatics, leading to systemic spread.
- Intravasation refers to the process where tumor cells enter the bloodstream or lymphatic system, driven by various factors, which can occur even in small cancers.
- Circulating tumor cells are susceptible to destruction by immune cells during their journey through the bloodstream.
Interaction with Host Cells
- Tumor cells may grow poorly in foreign environments lacking critical support or may be inhibited by local immune cells.
- Genetic mutations, such as those in BRCA1 and BRCA2, heighten the risk of cancers including breast cancer due to compromised DNA repair mechanisms.
Tumor-Promoting Inflammation
- Chronic inflammation is identified as a key factor in the development of various cancers, including hereditary nonpolyposis colorectal cancer (HNPCC).
- DNA repair mechanisms are crucial for reversing DNA damage that can lead to tumor development.
Mechanisms of Tumorigenesis
- Checkpoint inhibitors, including anti-CTLA-4 and anti-PD-1/PD-L1, are pivotal in combating immune evasion by tumors.
- Growth suppressors and genes promoting cellular energetics play roles in sustaining tumor growth and signaling.
- Enabling metastatic traits involves inducing angiogenesis and resisting cell death through altered cellular responses.
Cancer Genetics and Mechanisms
- Tumor suppressor genes, including both copies of BRCA1 and BRCA2, must be inactivated for cancer to develop, implicating their importance in cell cycle regulation and DNA repair.
- Somatic mutations accumulate over time, contributing to the progression of various cancers, including carcinomas and lymphomas.
Paraneoplastic Syndromes
- Paraneoplastic syndromes emerge as complex symptom complexes that cannot be attributed merely to local tumor effects but indicate broader systemic impacts.
Prognostic Factors in Cancer
- Tumor stage, characterized by the extent of spread and aggressiveness, serves a critical role in determining patient prognosis and treatment strategies.
- Histopathological grading is essential for assessing cancer severity and guiding therapeutic interventions.
Tumor Angiogenesis and Related Mechanisms
- BAX/BAK activation is stimulated by proangiogenic factors released by tumor cells and inflammatory cells such as macrophages and stromal fibroblasts.
- Key anti-apoptotic proteins involved in tumor survival include BCL-2, BCL-XL, and MCL-1, often associated with the mitochondria.
- Tumor cells can release peptides that enhance angiogenic activity from surrounding stromal cells.
Tumor Cell Intravasation and Circulation
- Intravasation refers to tumor cells entering the bloodstream, occurring even from small cancers.
- Various factors can affect the metastatic potential of circulating tumor cells, including their vulnerability to destruction by immune cells.
- Adhesion to vascular beds and subsequent invasion of normal tissues is more complex for tumor cells than for normal cells.
Host Interaction and Immune Evasion
- Tumor cells grow well in the primary site but may lack crucial stromal support or be suppressed by resident immune cells.
- The expression of tissue-specific adhesion molecules and the production of specific chemokines by tumor cells play essential roles in extravasation and metastasis.
- Metastatic cells can create favorable or unfavorable microenvironments for tumor growth in new tissues.
Immune System Dynamics
- The immune system can recognize and destroy tumors, but some cancers evolve to evade or inhibit these immune responses.
- CD8+ T cells are significant predictors of outcomes in initiating nascent cancers, indicating a strong immune response.
- Cancer survival is linked to the ability of tumor cells to evade the host immune system or actively suppress it, known as the immunoscore.
Implications for Cancer Therapy
- Understanding tumor-immune interactions has led to advancements in immunotherapy, although the efficacy of different immune mechanisms remains an open question.
- A deeper comprehension of the behaviors of individual cancers in relation to the immune environment is crucial for developing effective treatments.
Extravasation and Metastasis
- Tumor cells express tissue-specific adhesion molecules for extravasation, allowing them to migrate from blood vessels into tissues.
- The production of specific chemokines in diverse tissues facilitates the homing of metastatic cancer cells, which express corresponding receptors.
- The presence of stroma can further support the growth of metastatic tumors by modifying the tissue environment.
Immune Checkpoints and Cancer
- Immune checkpoints such as PD-1 and CTLA-4 play crucial roles in regulating T cell activation.
- Blocking PD-1 or CTLA-4 with antibodies inhibits these checkpoints, potentially enhancing anti-tumor immunity.
- Dendritic cells present tumor peptides through MHC molecules, which is vital for T cell priming and activation.
DNA Repair and Cancer Risk
- Defective DNA repair mechanisms, particularly homologous recombination, are linked to oncogenic processes.
- Germline mutations in BRCA1 and BRCA2 genes significantly increase the risk of breast and ovarian cancers, with these mutations found in approximately 50% of familial breast cancers.
Cancer Treatment Mechanisms
- Checkpoint inhibitors (anti-CTLA-4, anti-PD-1/PD-L1) aim to avoid immune destruction of tumors.
- Treatments targeting EGFR and BCL2 contribute to sustaining proliferative signaling and resisting apoptosis in cancer cells.
- VEGF signaling inhibitors can disrupt angiogenesis, essential for tumor growth.
Paraneoplastic Syndromes
- Endocrinopathies, including Cushing syndrome and hypercalcemia, are associated with various cancers, indicating a complex relationship between tumors and hormone regulation.
- Symptoms such as inappropriate ADH secretion (SIADH) and hypercalcemia may arise from tumor-derived substances that mimic hormone actions.
- Neurological disorders like myasthenia and dermatological conditions such as dermatomyositis can also be manifestations of underlying malignancies.
Hematological and Vascular Changes
- Tumors can induce hypercoagulability, leading to conditions like venous thrombosis, particularly noticeable in pancreatic cancer and other malignancies.
- Red cell aplasia and polycythemia can occur due to immunologic responses related to tumors, emphasizing the multifaceted nature of cancer effects on the body.
Angiogenesis and Tumor Progression
- Angiogenesis refers to the formation of new blood vessels, critical for tumor growth and metastasis.
- Normal human cells can double 60 to 70 times before senescence occurs, influenced by the availability of blood vessels.
- Senescence is associated with telomere shortening on chromosomes, impacting the ability of cells to divide.
- Loss of E-cadherin in many patients correlates to increased cell migration and aggressiveness of cancer.
Immune Responses and Cancer
- Tumors can vary immune responses, leading to changes in cell shape and mutations, worsening patient outcomes.
- Certain cancers often exhibit upregulation of genes associated with mesenchymal characteristics, promoting invasive behaviors.
- Immunologic changes in tumor environments are often referred to as epithelial-to-mesenchymal transition (EMT).
Therapeutic Targets
- Recent therapeutic agents stimulate T-cell responses and can enhance immune effectiveness.
- Drugs targeting PD-1 and CTLA-4 have been developed to inhibit cancer cells from evading immune detection.
Local Effects of Tumors
- Tumors can cause both local and systemic problems due to direct impact on surrounding tissues and production of hormones.
- Recognition of tumor anatomy is critical as it determines treatment approaches and potential surgical interventions.
- Benign and malignant tumors can create "space-occupying" effects, impacting normal organ function.
Genetic Mutations in Cancer
- Hereditary Non-Polyposis Colorectal Cancer (HNPCC) accounts for only 2% to 4% of colorectal cancers but is significant for its genetic implications.
- Microsatellite instability (MSI) can be observed in approximately 15% of sporadic cancers, indicating mutations that can lead to various cancer types.
- Recent advancements focus on targeting cancer hallmarks through approved therapies and ongoing clinical trials, enhancing overall survival rates.
Angiogenesis and Tumor Growth
- Angiogenesis is stimulated by factors like Caspase 3, which promotes the proliferation of endothelial cells and guides new blood vessel formation towards tumors.
- Tumor suppressors can balance processes to favor angiogenesis; for instance, p53 inhibits VEGF expression, preventing angiogenic stimulation.
- Loss of p53 in tumor cells creates an environment conducive to angiogenesis by allowing tumor cells to evade apoptosis.
Tumor Cell Intravasation
- Intravasation refers to the process by which tumor cells enter the bloodstream, which is facilitated by several factors that influence their metabolic potential.
- Tumor cells are vulnerable to destruction by immune cells during circulation, complicating their ability to adhere to vascular beds and invade normal tissues.
- The link between primary tumor growth and immune response is critical; resident immune cells can suppress tumor growth.
Tumor Immunity and Checkpoint Inhibitors
- Checkpoint inhibitors, such as anti-CTLA-4 and anti-PD-1/PD-L1, enhance T cell activation by blocking inhibitory signals, allowing CD8+ T cells to attack tumors.
- Tumor evasion strategies include avoiding immune destruction and reactivating growth suppressors like p53, using inhibitors that target pathways like MDM2.
Hallmarks of Cancer and Therapeutic Targets
- Major therapeutic approaches aim to counteract cancer hallmarks by targeting key cancer-related signaling pathways, such as EGFR and VEGF.
- Inhibitors of cellular proliferative signaling and apoptosis (e.g., BCL2 inhibitors) are being developed to disrupt cancer growth and metastasis.
Clinical Effects of Tumors
- Both benign and malignant tumors can cause local and systemic problems, affecting physiological processes through direct interaction and hormone elaboration.
- Recognition of the anatomical location of tumors is critical, as it determines the potential for complications and influences treatment strategies.
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Description
This quiz covers the role of extracellular matrix components and growth factors in tumor cell behavior, as well as vascular dissemination and tumor cell homing. It explores how tumor cells invade the basement membrane and evade local sites of origin to spread systemically.