Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 191: What is the term for the study of neoplastic growths?

A. Tetralogy
B. Anaplasia
C. Oncology (Correct Answer)
D. Neoplasia

Explanation: **Explanation:** **Correct Answer: C. Oncology** The term **Oncology** is derived from the Greek word *oncos*, meaning "tumor," and *logos*, meaning "study." [1] In medical science, it refers to the specialized branch dedicated to the study, diagnosis, prevention, and treatment of tumors (neoplasms). While "neoplasia" describes the process of new growth, "oncology" is the formal name of the scientific discipline. [2] **Analysis of Incorrect Options:** * **A. Teratology:** This is the study of abnormal physiological development and congenital malformations (birth defects). It is unrelated to the study of tumors. * **B. Anaplasia:** This is a morphological hallmark of malignancy. It refers to a lack of differentiation, where cells lose their structural and functional characteristics, resembling primitive stem cells. It is a feature *within* a tumor, not the study of tumors. * **D. Neoplasia:** This literally means "new growth." [2] It refers to the pathological process of uncontrolled, uncoordinated, and autonomous cell proliferation. It is the condition itself, whereas oncology is the study of that condition. **High-Yield Clinical Pearls for NEET-PG:** * **Definition of Neoplasm (Willis):** "A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after cessation of the stimuli which evoked the change." [2] * **Parenchyma vs. Stroma:** All tumors have two basic components: the **parenchyma** (proliferating neoplastic cells) which determines biological behavior, and the **stroma** (connective tissue and blood vessels) which supports growth. [2] * **Desmoplasia:** Some tumors stimulate abundant collagenous stroma, making them hard or "scirrhous" (e.g., certain breast cancers). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 273-274. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 202-203.

Question 192: Cancer cells primarily derive energy from which metabolic process?

A. Glycolysis (Correct Answer)
B. Oxidative metabolism
C. Increased mitochondria
D. None of the above

Explanation: **Explanation:** The correct answer is **Glycolysis**. This phenomenon is known as the **Warburg Effect** (Aerobic Glycolysis) [1]. **1. Why Glycolysis is correct:** Even in the presence of ample oxygen, cancer cells shift their metabolism away from the energy-efficient oxidative phosphorylation toward **glycolysis**. While glycolysis produces significantly less ATP per glucose molecule (2 ATP vs. 36 ATP), it provides the rapidly dividing cell with metabolic intermediates (like carbon skeletons) necessary for the synthesis of nucleic acids, proteins, and lipids [1]. This metabolic reprogramming is triggered by signaling pathways such as **PI3K/AKT** and the upregulation of **HIF-1α** and **MYC** [1]. **2. Why the other options are incorrect:** * **B. Oxidative metabolism:** Although more efficient at generating ATP, oxidative phosphorylation does not provide the raw materials (biosynthetic precursors) required for rapid biomass doubling in malignant cells [1]. * **C. Increased mitochondria:** Cancer cells often exhibit altered mitochondrial function rather than an increase in number. In fact, the Warburg effect is characterized by a "shunting" of glucose away from the mitochondria. **3. High-Yield Clinical Pearls for NEET-PG:** * **PET Scanning:** The clinical application of the Warburg effect is **Positron Emission Tomography (PET)**. Patients are injected with **18-F-fluorodeoxyglucose (FDG)**, a glucose analog. Because cancer cells have an insatiable "glucose hunger" and overexpress GLUT transporters, they take up the FDG, allowing for the visualization of tumors. * **Key Driver:** The **TP53** gene normally promotes oxidative phosphorylation; its mutation in cancers further facilitates the switch to glycolysis. * **Autophagy:** In nutrient-deprived states, cancer cells may use autophagy to survive, but glycolysis remains their primary metabolic signature. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 308-310.

Question 193: Cowden syndrome is commonly associated with which of the following?

A. Renal cell carcinoma
B. Thymic carcinoid
C. Cerebellar haemangioblastoma
D. Hamartoma (Correct Answer)

Explanation: **Explanation:** **Cowden Syndrome** is an autosomal dominant disorder caused by a germline mutation in the **PTEN gene** (a tumor suppressor gene on chromosome 10q23) [1]. PTEN normally inhibits the PI3K/AKT pathway; its loss leads to uncontrolled cell proliferation and survival. 1. **Why Hamartoma is correct:** The hallmark of Cowden syndrome is the development of multiple **hamartomas** (disorganized but benign growths) across various organs [1]. These typically manifest as **trichilemmomas** (skin), oral papillomas, and gastrointestinal polyps [1]. While these lesions are benign, patients have a significantly increased risk of malignancies, particularly **breast, thyroid (follicular), and endometrial carcinomas.** 2. **Why other options are incorrect:** * **Renal cell carcinoma:** Primarily associated with **Von Hippel-Lindau (VHL)** syndrome or Birt-Hogg-Dubé syndrome. * **Thymic carcinoid:** Classically associated with **Multiple Endocrine Neoplasia Type 1 (MEN1)** [2]. * **Cerebellar haemangioblastoma:** This is a pathognomonic feature of **Von Hippel-Lindau (VHL)** syndrome, along with retinal angiomas. **High-Yield Clinical Pearls for NEET-PG:** * **Lhermitte-Duclos disease:** A rare, slow-growing gangliocytoma of the cerebellum; it is considered a pathognomonic CNS manifestation of Cowden syndrome. * **PTEN Hamartoma Tumor Syndrome (PHTS):** This umbrella term includes Cowden syndrome, [1] Bannayan-Riley-Ruvalcaba syndrome, and Proteus syndrome. * **Most common malignancy:** Breast cancer is the most frequent cancer in Cowden syndrome (up to 85% lifetime risk). * **Thyroid involvement:** Usually presents as benign adenomas or **Follicular carcinoma** (rarely papillary, never medullary). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 813. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1139-1140.

Question 194: Which syndrome is associated with an increased risk of leukemia?

A. Plummer-Vinson syndrome
B. Klinefelter syndrome (Correct Answer)
C. Sturge-Weber syndrome
D. Multiple hamartoma

Explanation: **Explanation:** **Correct Option: B. Klinefelter Syndrome (47, XXY)** Klinefelter syndrome is a chromosomal disorder characterized by an extra X chromosome in males [1]. It is associated with a significantly increased risk of certain malignancies, most notably **Germ Cell Tumors (specifically mediastinal extragonadal GCTs)** and **Breast Cancer** (20 times higher risk than normal males). Crucially, for NEET-PG, it is also linked to an increased incidence of **Acute Myeloid Leukemia (AML)** and other hematological malignancies. The underlying mechanism is thought to involve genetic instability and hormonal imbalances associated with the extra X chromosome. **Incorrect Options:** * **A. Plummer-Vinson Syndrome:** Characterized by the triad of iron deficiency anemia, esophageal webs, and glossitis. It is a precursor to **Squamous Cell Carcinoma of the esophagus** and pharynx, not leukemia. * **C. Sturge-Weber Syndrome:** A phakomatosis (neurocutaneous disorder) characterized by port-wine stains and leptomeningeal angiomas. It is not traditionally associated with an increased risk of systemic malignancies like leukemia. * **D. Multiple Hamartoma (Cowden Syndrome):** Caused by a mutation in the **PTEN gene**. It increases the risk of breast, thyroid (follicular), and endometrial cancers, but not leukemia. **High-Yield Clinical Pearls for NEET-PG:** * **Down Syndrome (Trisomy 21)** is the most common chromosomal disorder associated with leukemia (AMKL/M7 before age 3, ALL after age 3) [1]. * Other genetic conditions with high leukemia risk: **Fanconi Anemia**, **Bloom Syndrome**, and **Ataxia-Telangiectasia** (all involve DNA repair defects). * In Klinefelter syndrome, the most common cause of death is actually cardiovascular disease, but the classic "cancer association" tested is **Mediastinal Germ Cell Tumors**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 92-93.

Question 195: Presence of more than two germ cell layers in a tumor is called:

A. Dysgerminoma
B. Teratoma (Correct Answer)
C. Theca cell tumor
D. Seminoma

Explanation: ### Explanation **Correct Answer: B. Teratoma** **Concept:** A **Teratoma** is a germ cell tumor composed of tissues derived from more than one germ cell layer—and frequently all three: **ectoderm** (e.g., skin, brain tissue), **mesoderm** (e.g., muscle, fat, bone), and **endoderm** (e.g., gut epithelium, thyroid tissue) [1]. These tumors arise from totipotent germ cells that have the capacity to differentiate into any cell type found in the adult body [2]. They are classified as **mature** (well-differentiated/benign), **immature** (containing fetal-like tissue/malignant), or **monodermal** (specialized, e.g., Struma ovarii) [3]. **Analysis of Incorrect Options:** * **A & D. Dysgerminoma / Seminoma:** These are "germinomas"—tumors composed of primordial germ cells that have **not** undergone differentiation [4]. They consist of a uniform population of cells and do not form tissues from multiple germ layers. Dysgerminoma is the female equivalent of the male Seminoma [5]. * **C. Theca cell tumor:** This is a **sex cord-stromal tumor**, not a germ cell tumor. It is typically functional (estrogen-producing) and composed of spindle-shaped cells resembling theca cells of the ovarian follicle. **NEET-PG High-Yield Pearls:** * **Most common site:** The ovary (usually mature cystic teratoma/dermoid cyst) and the testis [1]. * **Sacrococcygeal Teratoma:** The most common germ cell tumor in childhood/neonates. * **Struma Ovarii:** A specialized monodermal teratoma composed entirely of mature thyroid tissue; it can cause hyperthyroidism [3]. * **Malignant Transformation:** Rarely, a mature element in a teratoma can undergo malignant change (e.g., Squamous Cell Carcinoma arising in a dermoid cyst) [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 480-481. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1033-1034. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, p. 1034. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 979-980. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1140-1141.

Question 196: Which of the following cancers is least associated with genetic and familial causes?

A. Ovarian
B. Prostate
C. Lung (Correct Answer)
D. Breast

Explanation: **Explanation:** The correct answer is **Lung Cancer**. In oncology, cancers are broadly categorized based on their primary drivers: environmental/lifestyle factors versus genetic/hereditary predispositions. **Why Lung Cancer is the correct answer:** Lung cancer is overwhelmingly associated with **environmental carcinogens**, specifically tobacco smoke (responsible for ~80-90% of cases) [1], [2], radon, and asbestos exposure [3], [4]. While certain genetic polymorphisms (e.g., in the *CHRNA3* gene) can influence nicotine addiction or susceptibility, the vast majority of lung cancers are sporadic and lack a strong familial inheritance pattern compared to the other options. **Analysis of Incorrect Options:** * **Breast Cancer:** Approximately 5–10% of cases are strictly hereditary. Mutations in **BRCA1 and BRCA2** significantly increase lifetime risk (up to 80%). Other syndromes like Li-Fraumeni (*TP53*) also play a role. * **Ovarian Cancer:** This has the strongest genetic link among the options. Up to **15–20%** of epithelial ovarian cancers are associated with germline mutations, primarily **BRCA1/2** and Lynch Syndrome (HNPCC). * **Prostate Cancer:** Family history is a major risk factor. Men with a first-degree relative affected have double the risk. Specific susceptibility genes include **HOXB13** and *BRCA2*. **NEET-PG High-Yield Pearls:** * **Most common genetic cause of cancer:** Mutations in the **TP53** tumor suppressor gene (found in >50% of all human tumors). * **Li-Fraumeni Syndrome:** Characterized by germline *TP53* mutations leading to "SBLA" syndrome (Sarcoma, Breast, Leukemia, Adrenal gland cancers). * **Lynch Syndrome (HNPCC):** Associated with *MSH2/MLH1* mutations; increases risk of Colon, Endometrial, and Ovarian cancers. * **Retinoblastoma:** The classic model for the "Two-Hit Hypothesis" (Knudson's hypothesis) regarding tumor suppressor genes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 331-332. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 719-720. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 286. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 221-222.

Question 197: In which of the following malignancies is histological grade a good prognostic indicator?

A. Melanoma
B. Soft tissue sarcoma (Correct Answer)
C. Renal cell carcinoma
D. Lung cancer

Explanation: **Explanation:** In oncology, **grading** (histological assessment of differentiation) and **staging** (extent of spread) are the two primary prognostic tools [1]. While staging is generally the most important indicator for most cancers, **Soft Tissue Sarcomas (STS)** are a classic exception where histological grade is the single most important prognostic factor for predicting metastasis and overall survival [2]. **1. Why Soft Tissue Sarcoma is Correct:** The French Federation of Cancer Centers Sarcoma Group (FNCLCC) grading system is the gold standard for STS. It evaluates three parameters: **tumor differentiation, mitotic count, and necrosis.** Because sarcomas of the same stage can behave very differently based on their cellular aggressiveness, the grade dictates the clinical management and the likelihood of distant spread [2]. **2. Why Other Options are Incorrect:** * **Melanoma:** The most important prognostic indicator is **Breslow’s Thickness** (vertical depth of invasion in mm), which is a component of staging, not grading. * **Renal Cell Carcinoma (RCC):** While the Fuhrman or ISUP grade is used, the **TNM Stage** (especially vascular invasion into the renal vein) is a much stronger predictor of outcome. * **Lung Cancer:** Prognosis is almost entirely dependent on the **TNM Stage** at the time of diagnosis and the specific molecular/genetic mutations (e.g., EGFR, ALK) rather than the histological grade. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of Thumb:** Staging is generally more important than grading for most solid tumors [1]. * **Exceptions:** Grade is superior in **Soft Tissue Sarcoma, Transitional Cell Carcinoma (Bladder), and Astrocytomas.** * **Breslow Thickness** is the most important prognostic factor for Melanoma (replaces the older Clark’s Level). * **Gleason Scoring** is the specific grading system used for Prostate Cancer. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 254-255. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1224-1226.

Question 198: A 63-year-old woman discovers a lump in her right breast. Mammography confirms the presence of a suspicious mass, and a needle core biopsy reveals that the mass is cancerous with amplification of the Her-2/neu oncogene. What kind of protein is the gene product of Her-2/neu?

A. GTPase
B. GTPase-activating protein
C. Nuclear transcription factor
D. Receptor tyrosine kinase (Correct Answer)

Explanation: **Explanation:** The **HER-2/neu** (also known as **ERBB2**) gene is a proto-oncogene located on chromosome 17 [1]. It encodes a 185-kDa transmembrane glycoprotein that belongs to the **Epidermal Growth Factor Receptor (EGFR) family** [2]. **1. Why the Correct Answer is Right:** The HER-2/neu protein functions as a **Receptor Tyrosine Kinase (RTK)** [2]. Unlike other members of its family, it does not have a specific ligand-binding domain; instead, it remains in an "active" conformation, ready to heterodimerize with other EGFR members. Amplification of this gene (seen in ~15–25% of breast cancers) leads to protein overexpression, resulting in constitutive tyrosine kinase activity [1]. This triggers downstream signaling pathways (like MAPK and PI3K/AKT) that drive uncontrolled cell proliferation and survival. **2. Why Incorrect Options are Wrong:** * **GTPase:** This describes the **RAS** family of oncogenes (e.g., KRAS, HRAS). RAS proteins act as molecular switches, cycling between active GTP-bound and inactive GDP-bound states. * **GTPase-activating protein (GAP):** These are regulatory proteins (like **Neurofibromin 1**) that catalyze the hydrolysis of GTP to GDP, acting as tumor suppressors. * **Nuclear transcription factor:** This describes oncogenes like **MYC** (C-MYC, N-MYC, L-MYC). These proteins bind to DNA to regulate the expression of genes involved in the cell cycle. **Clinical Pearls for NEET-PG:** * **Targeted Therapy:** Trastuzumab (Herceptin) is a monoclonal antibody specifically targeting the HER-2 receptor [1]. * **Prognosis:** HER-2 amplification is traditionally associated with a more aggressive clinical course but serves as a vital **predictive marker** for response to targeted therapy [1]. * **Testing:** Evaluated via Immunohistochemistry (IHC) for protein expression or FISH for gene amplification [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1068. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 292.

Question 199: Orphan Annie-eye nuclei are seen in which of the following conditions?

A. Papillary carcinoma of thyroid (Correct Answer)
B. Medullary carcinoma of thyroid
C. Anaplastic carcinoma of thyroid
D. Follicular carcinoma of thyroid

Explanation: **Explanation:** **Orphan Annie-eye nuclei** are the pathognomonic histological hallmark of **Papillary Thyroid Carcinoma (PTC)** [1]. These nuclei appear large and optically clear (empty) with peripheral chromatin condensation, resembling the eyes of the comic strip character "Little Orphan Annie" [2]. This appearance is an artifact of formal fixation due to finely dispersed chromatin. **Why Option A is correct:** PTC is the most common thyroid malignancy [3]. Diagnosis is based on characteristic nuclear features, even in the absence of papillary architecture: 1. **Orphan Annie-eye nuclei:** Optically clear/ground-glass appearance. 2. **Nuclear Grooves:** Longitudinal invaginations of the nuclear membrane. 3. **Pseudo-inclusions:** Cytoplasmic invaginations into the nucleus. 4. **Psammoma bodies:** Laminated calcifications (seen in ~50% of cases). **Why other options are incorrect:** * **Medullary Carcinoma (B):** Derived from parafollicular C-cells; characterized by amyloid stroma (Congo Red positive) and "salt and pepper" chromatin [2]. * **Anaplastic Carcinoma (C):** Highly aggressive; shows pleomorphic giant cells, spindle cells, and frequent mitoses, but lacks specific PTC nuclear features [2]. * **Follicular Carcinoma (D):** Distinguished by capsular or vascular invasion; nuclei are typically hyperchromatic and lack the "clearing" seen in PTC. **High-Yield Clinical Pearls for NEET-PG:** * **Most common risk factor:** Ionizing radiation [3]. * **Genetic mutations:** *BRAF* mutation (most common, associated with classical PTC) and *RET/PTC* rearrangements. * **Prognosis:** Excellent, typically spreads via lymphatics [2]. * **Cytology:** Orphan Annie-eye nuclei are **NOT** seen on FNAC (as it is a fixation artifact); they are only seen on permanent paraffin sections. FNAC focuses on nuclear grooves and inclusions [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1099. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 429-430. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1098-1099.

Question 200: Von Hippel-Lindau (VHL) syndrome is most commonly associated with which carcinoma?

A. Lung carcinoma
B. Renal cell carcinoma (Correct Answer)
C. Endometrial carcinoma
D. Hepatocellular carcinoma

Explanation: **Explanation:** **Von Hippel-Lindau (VHL) syndrome** is an autosomal dominant hereditary cancer syndrome caused by a germline mutation in the **VHL tumor suppressor gene** located on **chromosome 3p25**. **Why Renal Cell Carcinoma (RCC) is correct:** The VHL protein normally acts as part of a ubiquitin ligase complex that targets **Hypoxia-Inducible Factor 1α (HIF-1α)** for degradation. In VHL syndrome, the loss of this protein leads to the constitutive stabilization of HIF-1α, which triggers the overexpression of growth factors like VEGF and PDGF. This "pseudo-hypoxia" state drives angiogenesis and cell proliferation, specifically predisposing patients to **Clear Cell Renal Cell Carcinoma** [1]. Approximately 70% of VHL patients develop RCC, often bilaterally and multicentrically. **Why other options are incorrect:** * **Lung Carcinoma:** Primarily associated with smoking or mutations in EGFR/ALK; not a component of the VHL spectrum. * **Endometrial Carcinoma:** Linked to Lynch Syndrome (HNPCC) and Cowden Syndrome (PTEN mutation), but not VHL. * **Hepatocellular Carcinoma:** Associated with Chronic Hepatitis (B/C) and Cirrhosis; VHL is associated with liver cysts, but rarely malignancy. **High-Yield Clinical Pearls for NEET-PG:** * **VHL Manifestations (mnemonic: HARP):** **H**emangioblastomas (Cerebellum/Retina), **A**ngiomatosis, **R**CC (Clear cell type), and **P**heochromocytoma. * **Pancreatic involvement:** Serous cystadenomas and Neuroendocrine tumors (NETs). * **Epididymal papillary cystadenomas** are a highly specific finding. * **Genetics:** Follows the "Knudson Two-Hit Hypothesis" (one inherited mutation, one acquired somatic mutation). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-959.

Practice by Chapter

Nomenclature and Classification of Tumors

Practice Questions

Characteristics of Benign and Malignant Neoplasms

Practice Questions

Molecular Basis of Cancer

Practice Questions

Carcinogenesis and Carcinogens

Practice Questions

Tumor Progression and Metastasis

Practice Questions

Tumor Markers

Practice Questions

Paraneoplastic Syndromes

Practice Questions

Genetic Basis of Cancer

Practice Questions

Tumor Immunity

Practice Questions

Cancer Epidemiology and Prevention

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Neoplasia — MCQs

Neoplasia — MCQs

On this page

Practice by Chapter

Want unlimited practice?