Carcinogenesis
All mutations that lead to carcinogenesis are either due to exogenous agents or endogenous products of cell metabolism
What our notes say
- All mutations that lead to carcinogenesis are either due to exogenous agents or endogenous products of cell metabolism (Oncopathology MCQs: Test Your Knowledge on Cancer Pathology)
- A lethal genetic mutation is required for carcinogenesis to occur (Oncopathology MCQs: Test Your Knowledge on Cancer Pathology)
- Core principle: genetic damage is the foundation of carcinogenesis. (Genetic Disorders Pathology Crash Course: Exam Revision Notes)
- E6 and E7 are the primary oncoproteins — most important for understanding HPV carcinogenesis (EXAM: Bacteriophages, Laboratory Diagnosis, HPV & Parvovirus B19)
- Carcinogenesis – the overall multi-step process by which normal cells become cancerous (Medical Virology: Hepatitis, Viral Carcinogenesis & Oncogenic Viruses)
- Oncogenic Viruses — mechanisms of viral carcinogenesis, key oncogenic viruses, associated malignancies (EXAM: Hepatitis Viruses, Oncogenic Viruses, Paramyxoviruses & Arboviruses)
Study material on Carcinogenesis
- Medical Virology: Hepatitis, Viral Carcinogenesis & Oncogenic Viruses
- Oncopathology MCQs: Test Your Knowledge on Cancer Pathology
- ONCOPATHOLOGY - 30 KEY SHORT ANSWER QUESTIONS Hallmarks 1,2 & 3
- Genetic Disorders Pathology Crash Course: Exam Revision Notes
- Hallmarks of Cancer: Molecular Basis, Cell Cycle & Oncogenes
- ONCOPATHOLOGY MCQ EXAMINATION HAllmarks of Cancer 1,2 &3
- Oncopathology Hallmarks of Cancer MCQs
Practice questions on Carcinogenesis
An experiment is designed to study the genetics of cancer. The study will link the appearance of cancer to specific gene abnormalities. Which of the following forms of cell molecular analysis is most useful to identify gene alterations involved in carcinogenesis?
- Florescence in situ hybridization
- Flow cytometry
- Immunohistochemistry
- Single nucleotide polymorphisms
- Tumor marker expression
Answer: D. SNPs can be analyzed to find alterations present in cancer cells. One could analyze multiple histologically similar cancers to determine what gene(s) alteration(s) such as deletions and amplifications may underlie carcinogenesis. Using millions of SNPs can produce a virtual karyotype down to the gene level. ---
The 'field effect' in lung carcinogenesis means
- The tumor spreads through the air spaces
- Diffuse injury to the airway mucosa by carcinogens predisposes to multiple tumors
- The tumor stays confined to one lobe
- Radiation therapy field
Answer: B. The 'field effect' or 'field cancerization' describes how the entire respiratory tract is exposed to carcinogens (like smoke), leading to multiple independent genetic mutations. ---
In the multistep carcinogenesis model of colon cancer, which genetic alteration typically occurs FIRST?
- Loss of TP53
- Inactivation of APC
- Activation of KRAS
- Loss of tumor suppressor on 18q
Answer: B. The adenoma-carcinoma sequence in colon cancer typically begins with APC inactivation, followed by KRAS activation, then loss of 18q tumor suppressors, and finally TP53 loss. ---
The concept that metastatic potential may be an intrinsic property developed early in carcinogenesis challenges which traditional view?
- That angiogenesis is required for metastasis
- That metastasis requires stochastic generation of metastatic subclones late in tumor progression
- That cancer cells must invade the ECM
- That p53 mutations occur in cancer
Answer: B. Gene expression profiling suggests some tumors acquire metastatic signatures early during carcinogenesis, not just through late-stage random mutations generating metastatic subclones. ---
HPV oncoprotein E7 drives cervical carcinogenesis primarily by
- Upregulating apoptotic signalling pathways
- Activating the PTEN tumour suppressor gene
- Integrating into the host mitochondrial genome
- Inactivating the Rb tumour suppressor protein
Answer: D. E7 binds and inactivates Rb, promoting uncontrolled cell cycle progression. E6 targets p53. ---
What fundamental process in carcinogenesis involves failure of growth inhibition?
- Enhanced apoptosis
- Insensitivity to growth inhibitory signals
- Increased differentiation
- Reduced mutation rate
- Usually mediated by non-specific mechanisms
Answer: B. Failure of growth inhibition (insensitivity to growth inhibitory signals) is fundamental in carcinogenesis. Disruption of tumor suppressor genes renders cells refractory to growth inhibition and mimics growth-promoting effects.