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Pathology General 638393cf

Gastric carcinoma is associated with all EXCEPT ?

A
Inactivation of p53
B
Over expression of C-erb
C
Over expression of C-met
D
Activation of RAS
High-Yield Explanation
Ans. is 'd' Activation of RAS In the course of multi-step stomach carcinogenesis, various genetic and epigenetic alterations of oncogenes, tumor-suppressor genes, DNA repair genes, cell cycle regulators and cell adhesion molecules are involved. Genetic alteration in gastric cancer include: Intestinal type gastric cancer: K-ras mutation, APC mutation, pS2 methylation, HMLH1 methylation, p I ema methylation, p 73 deletion and C-erb B-2 amplification. Diffuse type gastric caner: CDH I gene (E-Cadherin) mutation, K-sam amplification. For both type: Telomerase reduction (telomerase shoening), hTE expression, genetic instability, overexpression of the cyclin E & CDC25B & E2F I genes,p53 mutations, reduced expression, CD44 aberrabont transcripts, and amplification of the C-met Cyclin E genes. Coming to question: All the given four genetic alterations may be associated with stomach cancer. However among the given options K-ras is best answer as it is associated with gastric cancer in minimum percentage (amongst given options): Source: Textbook of mechanism of carcinogenesis and cancer prevention K-ras mutation -4 <10% p53 mutation 30-60% C-erb B-2 amplifcation --> 20% C-met amplifciation --> 20%

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