General Pathology MCQs: Cancer, Tumors & OmpathStudy

General Pathology MCQs --- Q1. A 52-year-old woman undergoes thyroidectomy for a well-circumscribed, encapsulated thyroid nodule. Histology shows uniform follicles resembling normal thyroid architecture. Most accurate designation? a. Papillary carcinoma b. Follicular adenoma c. Follicular carcinoma d. Medullary carcinoma e. Anaplastic carcinoma Answer: b A well-circumscribed, encapsulated nodule with normal-appearing follicular architecture and no invasion is the definition of a benign follicular adenoma. Follicular carcinoma requires demonstrated capsular/vascular invasion, which isn't described here. --- Q2. A 65-year-old man has a firm sigmoid colon mass. Colonoscopy shows an ulcerated lesion with irregular borders. Biopsy demonstrates invasion through the muscularis propria. Which histological feature most strongly distinguishes this lesion as malignant rather than benign? a. High mitotic activity b. Cellular pleomorphism c. Invasion through basement membrane d. Increased nuclear-to-cytoplasmic ratio e. Hyperchromatic nuclei Answer: c Invasion through the basement membrane (breaching normal tissue boundaries) is the defining structural criterion of malignancy — the other features (mitoses, pleomorphism, N:C ratio, hyperchromasia) can also be seen in some benign or dysplastic lesions. --- Q3. A 45-year-old woman develops chronic myeloid leukemia (CML). Cytogenetic analysis reveals a reciprocal translocation between chromosomes 9 and 22. The resultant fusion gene codes for a protein with which abnormal activity? a. Constitutive receptor tyrosine kinase activation b. Constitutive non-receptor tyrosine kinase activation c. Constitutive growth factor secretion d. Impaired mismatch repair function e. Impaired apoptosis via caspase inhibition Answer: b The t(9;22) Philadelphia chromosome creates the BCR-ABL fusion gene, encoding a constitutively active non-receptor (cytoplasmic) tyrosine kinase — the molecular target of imatinib. --- Q4. A 33-year-old woman with breast cancer is found to have HER2/neu gene amplification. Which of the following best describes the mechanism by which HER2/neu promotes oncogenesis? a. Mutated GTP-binding protein leading to persistent signaling b. Overexpressed growth factor receptor causing increased proliferative signaling c. Viral oncoprotein binding to p53 and RB proteins d. Point mutation in tyrosine kinase domain leading to constitutive activation e. Chromosomal translocation producing fusion transcription factor Answer: b HER2/neu (ERBB2) amplification leads to overexpression of a normal (not mutated) growth factor receptor, driving excessive downstream proliferative signaling — the basis for trastuzumab therapy. --- Q5. A 28-year-old man presents with bilateral retinoblastomas. Genetic analysis reveals a germline mutation in one allele of the RB gene, followed by somatic loss of the second allele. This exemplifies which principle? a. Knudson's two-hit hypothesis b. Haploinsufficiency c. Dominant-negative mutation d. Loss-of-function mutation in an oncogene e. Epigenetic silencing Answer: a This is the textbook description of Knudson's two-hit hypothesis for tumour suppressor genes — an inherited first hit plus an acquired somatic second hit. --- Q6. A 62-year-old man with chronic hepatitis B develops hepatocellular carcinoma. Molecular studies reveal inactivation of p53. Which of the following best describes the normal role of p53 in preventing tumor development? a. Phosphorylation of RB to permit cell cycle progression b. Induction of angiogenesis through VEGF c. Repair of DNA by mismatch repair system d. Induction of apoptosis in cells with irreparable DNA damage e. Activation of telomerase to maintain genomic stability Answer: d p53 is the "guardian of the genome" — its central protective role is triggering cell-cycle arrest and, if DNA damage is irreparable, apoptosis. It does not itself perform DNA repair, activate telomerase, or induce angiogenesis. --- Q7. A point mutation in the RAS gene that locks it in an active GTP-bound state results in which cellular effect? a. Loss of apoptosis b. Continuous cell proliferation independent of growth factors c. Genomic instability d. Impaired angiogenesis e. Increased immune recognition Answer: b RAS normally cycles between active (GTP-bound) and inactive (GDP-bound) states, transmitting growth signals only transiently. A mutation locking it "on" causes continuous downstream MAPK signaling and proliferation, independent of upstream growth factor receptor activation. --- Q8. The ERBB2 (HER2/neu) oncogene contributes to tumorigenesis primarily by: a. Enhancing DNA repair b. Overexpression of a growth factor receptor c. Inactivating p53 d. Promoting epithelial–mesenchymal transition e. Decreasing MHC class I expression Answer: b Reinforces Q4 — amplification/overexpression of this receptor tyrosine kinase is the core oncogenic mechanism. --- Q9. Autocrine stimulation of growth factor receptors is best exemplified by: a. Glioblastom