BRIEF REPORT |
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Year : 2012 | Volume
: 18
| Issue : 1 | Page : 106-108 |
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Trisomy 8 in leukemia: A GCRI experience
Sonal R Bakshi1, Manisha M Brahmbhatt1, Pina J Trivedi1, Esha N Dalal1, Dharmesh M Patel1, Sejal S Purani1, Shilin N Shukla2, Pankaj M Shah2, Prabhudas S Patel1
1 Department of Cancer Biology, Cell Biology Division, The Gujarat Cancer and Research Institute, NCH Campus, Asarwa, Ahmedabad, Gujarat, India 2 Department of Medical Oncology, Cell Biology Division, The Gujarat Cancer and Research Institute, NCH Campus, Asarwa, Ahmedabad, Gujarat, India
Correspondence Address:
Prabhudas S Patel Department of Cancer Biology, Cell Biology Division, The Gujarat Cancer and Research Institute, NCH Campus, Asarwa, Ahmedabad - 380 016, Gujarat India
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DOI: 10.4103/0971-6866.96673
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Trisomy of chromosome 8 is frequently reported in myeloid lineage disorders and also detected in lymphoid neoplasms as well as solid tumors suggesting its role in neoplastic progression in general. It is likely to be a disease-modulating secondary event with underlying cryptic aberrations as it has been frequently reported in addition to known abnormalities contributing to clinical heterogeneity and modifying prognosis. Here, we share our findings of trisomy 8 in leukemia patients referred for diagnostic and prognostic cytogenetic assessment. Total 60 cases of trisomy 8, as a sole anomaly or in addition to other chromosomal aberrations, were reported (January 2005-September 2008). Unstimulated bone marrow or blood samples were cultured, followed by GTG banding and karyotyping as per the ISCN 2005. Patients with +8 were chronic myeloid leukemia (CML) (36), acute myeloid leukemia (AML) (17), and acute lymphoblastic leukemia (ALL) (7). In 7 patients, trisomy 8 was the sole anomaly, whereas in 6 patients +8 was in addition to normal clone, in 47 patients, the +8 was in addition to t(9;22), t(15;17), and others, including 3 with tetrasomy 8. Only one patient showed constitutional +8. The present study will form the basis of further cumulative studies to correlate potential differential effects of various karyotypic anomalies on disease progression and survival following a therapeutic regime. To unravel the role of extra 8 chromosome, constitutional chromosomal analysis and uniparental disomy will be considered. |
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