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Questions and Answers
What is a primary characteristic that differentiates benign tumors from malignant tumors?
What is a primary characteristic that differentiates benign tumors from malignant tumors?
What diagnostic approach utilizes the examination of small tissue samples for cancer diagnosis?
What diagnostic approach utilizes the examination of small tissue samples for cancer diagnosis?
Which tumor marker is associated with prostate cancer?
Which tumor marker is associated with prostate cancer?
In the TNM staging system, what does 'N' represent?
In the TNM staging system, what does 'N' represent?
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Which grading scale indicates increasing levels of anaplasia?
Which grading scale indicates increasing levels of anaplasia?
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What is the purpose of molecular analyses in cancer diagnosis?
What is the purpose of molecular analyses in cancer diagnosis?
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Which of the following best describes tumor-associated antigens?
Which of the following best describes tumor-associated antigens?
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What is the main function of immunohistochemistry in cancer diagnostics?
What is the main function of immunohistochemistry in cancer diagnostics?
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What characteristic do neoplasms exhibit in relation to normal growth factors?
What characteristic do neoplasms exhibit in relation to normal growth factors?
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Which statement accurately describes the epidemiology of cancer?
Which statement accurately describes the epidemiology of cancer?
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How do balanced translocations contribute to cancer development?
How do balanced translocations contribute to cancer development?
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Which of the following describes the typical nature of familial cancers?
Which of the following describes the typical nature of familial cancers?
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Which mechanism can lead to the insensitivity of tumor cells to growth-inhibitory signals?
Which mechanism can lead to the insensitivity of tumor cells to growth-inhibitory signals?
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What is primarily affected in tumor cells during the process of deletions?
What is primarily affected in tumor cells during the process of deletions?
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What role do miRNAs play in the context of carcinogenesis?
What role do miRNAs play in the context of carcinogenesis?
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What type of mutations may contribute to malignancy in tumor cells?
What type of mutations may contribute to malignancy in tumor cells?
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What is required for tumor development in the case of tumor suppressor genes?
What is required for tumor development in the case of tumor suppressor genes?
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Which of the following describes malignant tumors?
Which of the following describes malignant tumors?
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Which term describes a benign tumor originating from glandular tissue?
Which term describes a benign tumor originating from glandular tissue?
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What is a characteristic feature of malignant tumors related to cell structure?
What is a characteristic feature of malignant tumors related to cell structure?
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Which mechanism describes how malignant tumors spread through the lymphatic system?
Which mechanism describes how malignant tumors spread through the lymphatic system?
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What role does HIF-1α play in tumors?
What role does HIF-1α play in tumors?
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What is the term for secondary implants of tumors that are discontinuous with the primary tumor?
What is the term for secondary implants of tumors that are discontinuous with the primary tumor?
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Which of the following is NOT a characteristic of benign tumors?
Which of the following is NOT a characteristic of benign tumors?
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Which type of tumor is derived from mesenchymal origin?
Which type of tumor is derived from mesenchymal origin?
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What is a common site for many tumors to metastasize due to the first capillary bed encountered?
What is a common site for many tumors to metastasize due to the first capillary bed encountered?
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What is a prominent feature of dysplasia in tumor pathology?
What is a prominent feature of dysplasia in tumor pathology?
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Which process is responsible for the degradation of extracellular matrix in tumor invasion?
Which process is responsible for the degradation of extracellular matrix in tumor invasion?
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In tumor nomenclature, what suffix is commonly used for benign tumors?
In tumor nomenclature, what suffix is commonly used for benign tumors?
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What factor contributes to the sustained angiogenesis observed in tumors?
What factor contributes to the sustained angiogenesis observed in tumors?
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Study Notes
Neoplasia
- A new growth or an abnormal outgrowing mass of tissue that is uncoordinated with the normal tissue.
- Continues to grow even after the original stimulus has ceased.
General Characteristics of Neoplasms
- Unresponsive to normal growth factor controls.
- Compete with normal tissues for metabolic resources.
- Have a degree of autonomy, steadily increasing in size regardless of the local environment or the nutritional status of the host.
- Require endocrine stimulatory signals for their growth.
Epidemiology of Cancer
- Incidence varies with age, race, geographic factors, and genetic backgrounds.
- Most common at the extremes of age (young children and elderly individuals).
- Geographic variation often results from different environmental exposures.
- Most cancers are sporadic, but some are familial.
- Hereditary predisposition can be autosomal dominant or autosomal recessive.
- Familial cancers tend to be bilateral and arise earlier in life than sporadic counterparts.
Acquired Preneoplastic Disorders
- Persistent regenerative cell replication (e.g., long-standing skin ulcer, hepatic cirrhosis).
- Hyperplastic and dysplastic proliferations (e.g., endometrial hyperplasia, dysplastic changes of the bronchus).
- Chronic atrophic gastritis.
- Chronic ulcerative colitis.
- Leukoplakia of the oral cavity.
- Villous adenomas of the colon.
Genetic Lesions in Cancer
- Tumor cells acquire mutations through several means, including point mutations and nonrandom chromosomal abnormalities.
- Balanced translocations contribute to carcinogenesis by overexpression of oncogenes or generation of novel fusion proteins with altered signaling capacity.
- Deletions frequently affect tumor suppressor genes, whereas gene amplification increases the expression of oncogenes.
- Overexpression of miRNAs can contribute to carcinogenesis by reducing the expression of tumor suppressors, while deletion or loss of expression of miRNAs can lead to overexpression of proto-oncogenes.
- Tumor suppressor genes and DNA repair genes can also be silenced by epigenetic changes.
Insensitivity to Growth Inhibitory Signals
- Tumor suppressor genes encode proteins that inhibit cellular proliferation by regulating the cell cycle.
- Both copies of the gene must be dysfunctional for tumor development to occur.
- Affected individuals inherit one defective (nonfunctional) copy of a tumor suppressor gene and lose the second one through somatic mutation in familial cases.
- Sporadic cases involve both copies being lost through somatic mutations.
Nomenclature of Benign Tumors
- Cell type of origin + suffix “-oma” (e.g., fibroma, chondroma, leiomyoma).
- According to cells of origin:
- Adenoma: glandular pattern.
- Papilloma: epithelial surfaces, producing microscopic or macroscopic finger-like structure.
- Polyp: mass projects above the mucosal surface to form a macroscopically visible structure.
- Cystadenomas: hollow cystic masses (in the ovary).
- Fibroadenoma of the breast and benign mixed tumor of salivary glands (pleomorphic adenoma): mixed cellular type.
Nomenclature of Malignant Tumors
- Mesenchymal origin → sarcomas (e.g., fibrosarcoma, chondrosarcoma, leiomyosarcoma).
- Epithelial origin (endo, meso, and ectoderm) → carcinomas (e.g., squamous cell carcinoma, adenocarcinoma).
- Two components (mesenchymal and epithelial) → Teratomas → divergent differentiation into all embryonic layers, commonly seen in the ovaries and testicles, being benign or malignant.
Malignant Tumors
- Pleomorphism: variation in size and shape.
- Hyperchromasia: Increased nuclear pigmentation.
- High nuclear/cytoplasmic (N/C) ratio.
- Giant cells may be formed containing several nuclei.
- Nuclear pleomorphism, with coarse and clumped chromatin.
- Numerous mitoses with atypical forms.
- Loss of polarity: cells fail to form a recognizable pattern of orientation.
- Dysplasia: loss in the uniformity of individual cells and their architectural orientation (partial or the entire thickness of the epithelium (carcinoma in situ).
Characteristics of Benign and Malignant Tumors
- Benign tumors resemble the tissue of origin and are well-differentiated; malignant tumors are poorly or completely undifferentiated (anaplastic).
- Benign tumors are slow-growing, while malignant tumors generally grow faster.
- Benign tumors are well-circumscribed and have a capsule; malignant tumors are poorly circumscribed and invade the surrounding normal tissues.
- Benign tumors remain localized to the site of origin; malignant tumors are locally invasive and metastasize to distant sites.
Mechanisms of Local and Distant Spread
- Invasion of Extracellular Matrix (ECM):
- Tumor cells detach from each other due to loss of surface E-cadherins.
- Attachment to matrix components.
- ECM Degradation: Production and induction of fibroblasts to produce proteases, especially metalloproteinases, including gelatinases, collagenases, and stromelysins.
- Migration of tumor cells through cytokines, cleavage products of matrix components, and growth factors.
- Vascular Dissemination:
- Intravasation: degradation of blood vessels' basement membrane, forming tumor emboli (aggregation with leukocytes and platelets).
- Extravasation: adhesion to the endothelium followed by transgression through the basement membrane by a similar mechanism to intravasation.
Development of Sustained Angiogenesis
- Angiogenesis is essential for tumor growth and is controlled by the balance between angiogenic and antiangiogenic factors produced by tumor and stromal cells.
- Hypoxia triggers angiogenesis through the actions of HIF-1α on the transcription of the pro-angiogenic factor VEGF.
- p53 induces synthesis of the angiogenesis inhibitor TSP-1.
Invasion of Tissues
- Occurs in four steps: loosening of cell–cell contacts, degradation of ECM, attachment to novel ECM components, and migration of tumor cells.
- Cell–cell contacts are lost by the inactivation of E-cadherin through various pathways.
- Basement membrane and interstitial matrix degradation is mediated by proteolytic enzymes secreted by tumor cells and stromal cells, such as MMPs.
- Proteolytic enzymes release growth factors sequestered in the ECM and generate chemotactic and angiogenic fragments from cleavage of ECM glycoproteins.
Metastasis
- The metastatic site of many tumors can be predicted by the location of the primary tumor.
- Many tumors arrest in the first capillary bed they encounter (lung and liver, most commonly).
- Some tumors show organ tropism, possibly due to activation of adhesion or chemokine receptors whose ligands are expressed by endothelial cells at the metastatic site.
Laboratory Diagnosis of Cancer
- Sampling approaches: excision, biopsy, fine-needle aspiration, and cytologic smears.
- Immunohistochemistry and flow cytometry studies help in diagnosis and classification based on protein expression patterns.
- Tumor markers (proteins released by tumors into serum), such as PSA, are used for screening populations for cancer and monitoring for recurrence after treatment.
- Molecular analyses are used to determine diagnosis, prognosis, detection of minimal residual disease, and diagnosis of hereditary predisposition to cancer.
- Molecular profiling by cDNA arrays and sequencing can determine expression of large segments of the genome and catalog all of the mutations in the tumor genome, useful for treatment and prognostication.
Tumor Antigens (Tumor Markers)
- Tumor-specific antigens: unique antigens for tumors.
- Tumor-associated antigens: shared by normal untransformed cells.
- Examples of tumor markers include:
- MAGE-1 (melanoma-associated antigen-1)
- CA-125 and CA-119 (pancreatic and breast cancer)
- Prostate-specific antigen (PSA)
- Alpha-fetoprotein (AFP) in hepatocellular carcinoma
- Carcinoembryonic (CEA) antigen in colorectal carcinomas.
Grading and Staging
- Grading: based on cytological differentiation of tumor cells and the number of mitoses within the tumor. Graded I, II, III, or IV in order of increasing anaplasia.
- Staging is based on:
- The size of the primary lesion.
- Extent of spread to regional lymph nodes.
- Presence or absence of metastases.
- TNM staging system:
- T: Tumor size.
- N: Lymph node metastases.
- M: Distant metastases.
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Description
This quiz covers the fundamental concepts of neoplasia, including its characteristics and growth patterns. It also explores the epidemiology of cancer, examining how age, race, and genetic factors influence cancer incidence. Test your knowledge on these critical aspects of cancer biology.
