Chapter 079. Cancer Genetics (Part 8)

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Table 79-3 Representative Oncogenes at Chromosomal Translocations Gene (Chromosome) Translocation Malignancy ABL BCR (22q11) (9q34.1)– (9;22)(q34;q11) Chronic myelogenous leukemia ATF1 EWS (22q12) (12q13)– (12;22)(q13;q12) Malignant melanoma of soft parts (MMSP) BCL1 IgH (14q32) (11q13.3)– (11;14)(q13;q32) Mantle lymphoma cell BCL2 IgH (14q32) (18q21.3)– (14;18)(q32;q21) Follicular lymphoma FLI1 EWS (22q12) (11q24)– (11;22)(q24;q12) Ewing's sarcoma LCK TCRB (7q35) (1p34)– (1;7)(p34;q35) T lymphocytic (ALL) cell acute leukemia MYC (14q32) (8q24)–IgH (8;14)(q24;q32) Burkitt's B cell ALL lymphoma, WT1 EWS (22q12) (11p13)– (11;22)(p13;q12) Desmoplastic small round cell tumor (DSRCT) PAX3 (2q35)– (2;13)(q35;q14) Alveolar FKHR/ALV(13q14) rhabdomyosarcoma PAX7 (1p36)– (1;13)(p36;q14) Alveolar rhabdomyosarcoma KHR/ALV(13q14) RET (10q11.2) ...

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Chapter 079. Cancer Genetics (Part 8) Table 79-3 Representative Oncogenes at Chromosomal Translocations Gene Translocation Malignancy (Chromosome) ABL (9q34.1)– (9;22)(q34;q11) Chronic myelogenous BCR (22q11) leukemia ATF1 (12q13)– (12;22)(q13;q12) Malignant melanoma EWS (22q12) of soft parts (MMSP)
BCL1 (11q13.3)– (11;14)(q13;q32) Mantle cell IgH (14q32) lymphoma BCL2 (18q21.3)– (14;18)(q32;q21) Follicular lymphoma IgH (14q32) FLI1 (11q24)– (11;22)(q24;q12) Ewing's sarcoma EWS (22q12) LCK (1p34)– (1;7)(p34;q35) T cell acute TCRB (7q35) lymphocytic leukemia (ALL) MYC (8q24)–IgH (8;14)(q24;q32) Burkitt's lymphoma, (14q32) B cell ALL WT1 (11p13)– (11;22)(p13;q12) Desmoplastic small EWS (22q12) round cell tumor (DSRCT) PAX3 (2q35)– (2;13)(q35;q14) Alveolar
FKHR/ALV(13q14) rhabdomyosarcoma PAX7 (1p36)– (1;13)(p36;q14) Alveolar KHR/ALV(13q14) rhabdomyosarcoma RET (10q11.2) (10;17)(q11.2;q23) Papillary thyroid carcinomas Source: From R Hesketh: The Oncogene and Tumour Suppressor Gene Facts Book, 2d ed. San Diego, Academic Press, 1997; with permission. The first reproducible chromosome abnormality detected in human malignancy was the Philadelphia chromosome detected in CML. This cytogenetic abnormality is generated by reciprocal translocation involving the ABL oncogene, a tyrosine kinase on chromosome 9, being placed in proximity to the BCR (breakpoint cluster region) on chromosome 22. Figure 79-7 illustrates the generation of the translocation and its protein product. The consequence of expression of the BCR-ABL gene product is the activation of signal transduction pathways leading to cell growth independent of normal external signals. Imatinib, a drug that specifically blocks the activity of BCR-ABL has shown remarkable
efficacy with little toxicity in patients with CML. Knowledge of genetic alterations in cancer can lead to mechanism-based design and development of cancer drugs. Figure 79-7 Specific translocation seen in chronic myelogenous leukemia (CML) . The Philadelphia chromosome (Ph) is derived from a reciprocal translocation between chromosomes 9 and 22 with the breakpoint joining the sequences of the ABL oncogene with the BCR gene. The fusion of these DNA sequences allows the generation of an entirely novel fusion protein with modified
function. (Courtesy of ER Fearon and KR Cho.)