<prompt> C Myc on chromosome 8 is seen in:Burkitts lymphomaFollicular lymphomaMantle cell lymphomaBody cavity lymphoma  <response>: Ana-A-Burkitts lymphomaRef: Robbins Pathologic Basis of Disease, 8th edition, Pg: 259 589Explanation:BURKITT LYMPHOMAThere are three clinical types:African endemic Burkin lymphoma,Sporadic nonendemic Burkitt lymphomaAggressive lymphomas associated with HIV.These 3 types are histologically identical.MorphologyThe tumor exhibits a high mitotic index and contains numerous apoptotic cells, the nuclear remnants of which are phagocytosed by interspersed benign macrophages.These phagocytes have abundant clear cytoplasm, creating a characteristic starry sky pattern.ImmunophenotypeThese are tumors of mature B cellsIt expresses surface IgM, CD 19. CD20, CD 10, and BCL6. a phenotype consistent with a germinal center B-cell origin.Unlike other tumors of germinal center origin, this does not express anti-apoptotic protein BCL2.Molecular PathogenesisAll forms of Burkitt lymphoma are associated with translocations of the c-MYC gene on chromosome 8.The translocation partner is usually the IgH locus but may also be the Ig g or y light-chain loci., All endemic tumors are latently infected with EBV, which is also present in about 25 of HIV- associated tumors and 15 to 20 of sporadic cases.Clinical FeaturesEndemic Burkitt lymphoma often presents as a mass involving the mandible and shows an unusual predilection for involvement of abdominal viscera, particularly the kidneys, ovaries, and adrenal glands.Sporadic Burkitt lymphoma most often appears as a mass involving the ileocecum and peritoneum.Burkitt lymphoma is very aggressive but responds well to intensive chemotherapy. See table belowTable of Q. 10 Selected Oncogenes, Their Mode of Activation, and Associated Human TumorsCategoryProtooncogeneMode of ActivationAssociated Human TumorGROWTH FACTORSPDGF-j3 chainSIS official name PBGFBOverexpressionAstrocytomaOsteosarcomaFibroblast growth factorsHST1OverexpressionStomach cancerINT2 official name FGF3AmplificationBladder cancerBreast cancerMelanomaTGF-aTGFAOverexpressionAstrocytomasHepatocellular carcinomasHGFHGFOverexpressionThyroid cancerGROWTH FACTOR RECEPTORSEGF-receptor familyER8B1 EGFR, ERRB2OverexpressionSquamous cell carcinoma of the lung,GliomasFMS-like tyrosine kinase 3FL 73AmplificationBreast and ovarian cancersReceptor forneurotrophicfactorsRETPoint mutationLeukemia Point mutationMultiple endocrine neoplasia 2A and B, familial medullary thyroid carcinomasPDGF receptorPDGFRBOverexpression,translocationGliomas, leukemiasReceptor for stem cell steelfactorKITPoint mutationGastrointestinal stromal tumors GIST Seminomas LeukemiasPROTEINS INVOLVED IN SIGNAL TRANSDUCTIONGTP-bin dingKRASPoint mutationColon, lung, and pancreatic tumorsHRASPoint mutationBladder and kidney tumorsNRASPoint mutationMelanomas, hematologic malignanciesNonreceptor tyrosine kinaseABLTranslocationChronic myeloid leukemiaAcute 1ympboblastic leukemiaRAS signal transductionBRAFPoint mutationMelanomasWNT signal transductionb-cateninPoint mutationHepatoblastomas,Overexpressionhepatocellular carcinomaNUCLEAR-REGULATORY PROTEranscriptionalActivatorsC-MYCTranslocationBurkitt lymphomaN-WCAmplificationNeuroblastoma, small-cell carcinoma of the lungL-MYCAmplificationSmall-cell carcinoma of the lungCELL CYCLE REGULATORSCyclinsCyclin DTranslocationMantle cell lymphomaAmplificationBreast and esophageal cancersCyclin EOverexpressionBreast cancerCyclin-dependent kinaseCDK4Amplification or point mutationGlioblastoma, melanoma, sarcoma 