This is a real-world medical entrance exam question, please give the true answer based on the question and selection. Topic name: None, Subject name: Pathology
[{'content': 'Which of the following is known as the "guardian of the genome" - \nSelect and explain. \nA. p53, B. Mdm2, C. p14, D. ATM', 'role': 'user'}, {'content': "Answer: A \nExplanation: p53; Guardian of genome\n\np53 is a tumor suppressor gene.\np53 gene is located on chromosome 17.\np53 acts as molecular policeman that prevents the propagation of genetically damage cell.\np53 gene product, i.e. p53 protein is a DNA binding protein in the nucleus, when called into action, it controls the transcription of several other genes.\nThe ma 'or functional activities of the 53 rotein are cell c cle arrest and initiation of a o v.tosis in res onse to DNA damage.\nWhen there is DNA damage due to irradiation, UV light or mutagenic chemicals, there is rapid increase in p53 levels.\np53 causes -\n\nCell cycle arrest\n\n\np-53 induces transcription of p21, a CDK inhibitor.\np21 inhibit cyclin D-CDK-4 complex and there is arrest of cell cycle late in G1\xa0phase.\nThis allows time for DNA repair.\n\nDNA repair\n\np-53 also helps in DNA repair directly by inducing transcription of GADD 45 (growth arrest and DNA damage).\nGADD 45 encodes a protein that is involved in DNA repair.\nIf DNA damage is repaired successfully, p53 activate MDM-3 and this MDM-3 induce degradation of p-53 → Relieve in cell cycle block.\nIf DNA damage cannot be successfully repaired, p53 induces apoptosis by inducing the activation of apoptosis-inducing gene BAX.\nSo p53 prevents replication of cell with defective DNA → p53 functions as a critical gatekeeper against the formation of cancer.\nMutation in p53 leads to carcinogenesis because of loss of the above protective mechanism.\np-53 is the most common target for genetic alteration in human tumors: A little over 50% of human tumors\xa0contain mutation in this gene. \n(Note - Amongst oncogene RAS is involved most commonly).", 'role': 'assistant'}]