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Questions and Answers
What is the main characteristic of benign tumors?
What is the main characteristic of benign tumors?
How do tumor suppressor genes contribute to tumor development?
How do tumor suppressor genes contribute to tumor development?
Which of the following terms describes the appearance of malignant tumors?
Which of the following terms describes the appearance of malignant tumors?
What does hyperchromasia in malignant tumors indicate?
What does hyperchromasia in malignant tumors indicate?
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Which of the following conditions is considered an acquired preneoplastic disorder?
Which of the following conditions is considered an acquired preneoplastic disorder?
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What suffix is typically used in the nomenclature of benign tumors?
What suffix is typically used in the nomenclature of benign tumors?
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Which feature is NOT characteristic of benign tumors?
Which feature is NOT characteristic of benign tumors?
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What best describes the loss of polarity in malignant tumors?
What best describes the loss of polarity in malignant tumors?
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Which of the following characteristics are NOT true about neoplasms?
Which of the following characteristics are NOT true about neoplasms?
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What is the typical genetic inheritance pattern associated with familial cancers?
What is the typical genetic inheritance pattern associated with familial cancers?
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Which of the following mutations contributes to carcinogenesis by altering signaling capacity?
Which of the following mutations contributes to carcinogenesis by altering signaling capacity?
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How does miRNA overexpression contribute to cancer development?
How does miRNA overexpression contribute to cancer development?
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Which of the following is a known factor that can contribute to an increased risk of cancer development?
Which of the following is a known factor that can contribute to an increased risk of cancer development?
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What is a common feature of sporadic cancers compared to familial cancers?
What is a common feature of sporadic cancers compared to familial cancers?
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Which genetic alteration typically results in increased expression of oncogenes?
Which genetic alteration typically results in increased expression of oncogenes?
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Which of the following statements accurately reflects the role of endocrine signals in neoplasm growth?
Which of the following statements accurately reflects the role of endocrine signals in neoplasm growth?
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What is the primary feature that characterizes the process of dysplasia in tissues?
What is the primary feature that characterizes the process of dysplasia in tissues?
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Which mechanism is NOT typically associated with the metastatic spread of sarcomas?
Which mechanism is NOT typically associated with the metastatic spread of sarcomas?
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In the invasion of the extracellular matrix (ECM), what is the first step that tumor cells undergo?
In the invasion of the extracellular matrix (ECM), what is the first step that tumor cells undergo?
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What triggers the process of angiogenesis in tumors?
What triggers the process of angiogenesis in tumors?
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During the intravasation process, what is the primary action of tumor cells involving the blood vessel's basement membrane?
During the intravasation process, what is the primary action of tumor cells involving the blood vessel's basement membrane?
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Which of the following is a hallmark of malignancy related to tissue invasion?
Which of the following is a hallmark of malignancy related to tissue invasion?
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What component plays a significant role in the degradation of the extracellular matrix (ECM) during tumor invasion?
What component plays a significant role in the degradation of the extracellular matrix (ECM) during tumor invasion?
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What is the final step in the invasion process of tumor cells through the ECM?
What is the final step in the invasion process of tumor cells through the ECM?
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What is the primary role of proteolytic enzymes secreted by tumor and stromal cells in the context of tumor progression?
What is the primary role of proteolytic enzymes secreted by tumor and stromal cells in the context of tumor progression?
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Which factor is primarily associated with the organ tropism observed in some tumors?
Which factor is primarily associated with the organ tropism observed in some tumors?
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How can benign tumors be differentiated from malignant tumors?
How can benign tumors be differentiated from malignant tumors?
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Which sampling approach is NOT commonly used for tumor diagnosis?
Which sampling approach is NOT commonly used for tumor diagnosis?
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What is the significance of tumor markers such as PSA in cancer management?
What is the significance of tumor markers such as PSA in cancer management?
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Teratomas are characterized by which of the following features?
Teratomas are characterized by which of the following features?
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What factor does not help in differentiating between malignant and benign tumors?
What factor does not help in differentiating between malignant and benign tumors?
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Which of these cancer types is NOT classified as a carcinoma?
Which of these cancer types is NOT classified as a carcinoma?
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Study Notes
Neoplasia
- A new growth or abnormal mass of tissue that grows uncoordinated with normal tissue and persists after the stimulus that caused it has ended.
- Have degree of autonomy steadily increasing in size regardless of their local environment and the nutritional status of the host.
General Characteristics of Neoplasms
- Unresponsive to normal growth factors that control cell division.
- Compete with normal cells and tissues for their metabolic needs.
- Require endocrine stimulatory signals for their growth.
Epidemiology of Cancer
- Incidence varies with age, race, geographic factors, and genetic backgrounds.
- Most common at the two extremes of age.
- Geographic variation arises from different environmental exposures.
- Most are sporadic, but some are familial.
- Familial cancers tend to be bilateral and arise earlier in life than their sporadic counterparts.
- Some acquired diseases, known as preneoplastic disorders, are associated with an increased risk for development of cancer.
Genetic Lesions in Cancer
- Tumor cells acquire mutations through 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 may be silenced by epigenetic changes, which involve reversible, heritable changes in gene expression that occur not by mutation but by methylation of the promoter.
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.
- In familial predisposition, affected persons inherit one defective copy of a tumor suppressor gene and lose the second one through somatic mutation.
- In sporadic cases, both copies are lost through somatic mutations.
Benign Tumors
- Resemble their normal cells of origin morphologically and functionally.
- Well differentiated cells.
- Mitoses are very scanty in number and are of normal configuration.
- Grow slowly, localized, and do not infiltrate.
Acquired Preneoplastic Disorders
- Persistent regenerative cell replication, e.g. long-standing skin ulcer and hepatic cirrhosis.
- Hyperplastic and dysplastic proliferations, e.g. endometrial hyperplasia and dysplastic changes of the bronchus.
- Chronic atrophic gastritis.
- Chronic ulcerative colitis.
- Leukoplakia of the oral cavity.
- Villous adenomas of the colon.
Nomenclature of Benign Tumors
- Cell type from which the tumor arises + suffix "-oma", e.g. fibroma, chondroma, leiomyoma.
- According to cells of origin, e.g.:
- Adenoma: glandular pattern
- Papilloma: epithelial surfaces, producing microscopic or macroscopic finger-like structure
- Polyp: mass that 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 type
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).
- Rapidly growing tumor with progressive infiltration, invasion, destruction, and penetration of the surrounding tissue.
- Metastasis: secondary implants discontinuous with the primary tumor.
Pathways of Metastasis
- Seeding within body cavities.
- Lymphatic spread, typical for carcinomas.
- Hematogenous spread for sarcomas, but carcinomas also metastasize by this route.
- The liver and lungs are the most common secondary sites.
Mechanisms of Local And Distant Spread
- Invasion of ECM: reach to the basement membrane, then invade the interstitial connective tissue and then penetrate the blood vessels’ basement membrane; As four stages:
- Detachment of tumor cells from each other by loss of surface E-cadherins.
- Attachment of tumor cells to matrix components.
- Degradation of ECM by production and induction of fibroblasts to produce proteases, especially metalloproteinases including gelatinases, collagenases and stromelysins.
- Migration of tumor cells by cell-derived cytokines, cleavage products of matrix components and some growth factors.
Vascular Dissemination
- Intravasation: by degradation of blood vessels’ basement membrane, forming tumor emboli by aggregation with leukocytes and platelets, hiding tumor cells from the immune system.
- Extravasation of free tumor cells involves adhesion to the endothelium followed by transgression through the basement membrane by a similar mechanism to intravasation.
Development of Sustained Angiogenesis
- Vascularization of tumors is essential for their growth and is controlled by the balance between angiogenic and antiangiogenic factors that are produced by tumor and stromal cells.
- Hypoxia triggers angiogenesis through the actions of HIF-1α on the transcription of the pro-angiogenic factor VEGF.
- Many factors regulate angiogenesis; for example, p53 induces synthesis of the angiogenesis inhibitor.
Ability to Invade Tissues
- Cell–cell contacts are lost by the inactivation of E-adherin through a variety of pathways.
- Basement membrane and interstitial matrix degradation is mediated by proteolytic enzymes secreted by tumor cells and stromal cells, such as MMPs.
- Proteolytic enzymes also release growth factors sequestered in the ECM and generate chemotactic and angiogenic fragments from cleavage of ECM glycoproteins.
- 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, probably due to activation of adhesion or chemokine receptors whose ligands are expressed by endothelial cells at the metastatic site.
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) e.g. Teratomas → divergent differentiation into all embryonic layers, commonly seen in the ovaries and testicles, being benign or malignant.
Characteristics of Benign and Malignant Tumors
- Benign and malignant tumors can be distinguished from one another based on the degree of differentiation, rate of growth, local invasiveness, and distant spread.
- Benign tumors resemble the tissue of origin and are well differentiated; malignant tumors are poorly or completely undifferentiated (anaplastic).
- Benign tumors are slow-growing, whereas 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, whereas malignant tumors are locally invasive and metastasize to distant sites.
Laboratory Diagnosis of Cancer
- Several sampling approaches exist for the diagnosis of tumors, including excision, biopsy, fine-needle aspiration, and cytologic smears.
- Immunohistochemistry and flow cytometry studies help in the diagnosis and classification of tumors, because distinct protein expression patterns define different entities.
- Proteins released by tumors into the serum (tumor markers), such as PSA, can be used to screen populations for cancer and to monitor for recurrence after treatment.
- Molecular analyses are used to determine diagnosis, prognosis, the detection of minimal residual disease, and the diagnosis of hereditary predisposition to cancer.
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