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Prevalence of common fusion transcripts in acute lymphoblastic leukemia: A report of 304 cases
Author(s) -
Chopra Anita,
Soni Sushant,
Verma Deepak,
Kumar Dev,
Dwivedi Rahul,
Vishwanathan Anjali,
Vishwakama Garima,
Bakhshi Sameer,
Seth Rachna,
Gogia Ajay,
Kumar Lalit,
Kumar Rajive
Publication year - 2015
Publication title -
asia‐pacific journal of clinical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 29
eISSN - 1743-7563
pISSN - 1743-7555
DOI - 10.1111/ajco.12400
Subject(s) - immunophenotyping , incidence (geometry) , medicine , fusion transcript , breakpoint cluster region , minimal residual disease , fusion gene , lymphoblastic leukemia , pediatrics , leukemia , oncology , gastroenterology , immunology , biology , flow cytometry , genetics , gene , receptor , physics , optics
Aim Information about fusion transcripts in acute lymphoblastic leukemia (ALL) is used to risk‐stratify patients, decide on the treatment and to detect minimal residual disease. This study was conducted to determine the frequency of common fusion transcripts BCR‐ABL , TEL‐AML1 , MLL‐AF4 and E2A‐PBX1 for B ‐ ALL and SIL‐TAL1 for T ‐ ALL as seen at a tertiary care center in I ndia. Methods Up to 304 new cases of ALL (271 B ‐ ALL and 33 T ‐ ALL ) diagnosed on morphology, cytochemistry and immunophenotyping were studied. All were screened for the common fusion transcripts by RT‐PCR . Results Both our B ‐ (218/271; 80.4%) and T ‐ ALL (26/33; 78.8%) patients were largely children. In the B ‐ ALL children, BCR‐ABL was detected in 26/218 (11.9%), E2A‐PBX1 in 13/218 (5.9%), TEL‐AML1 in 16/218 (7.3%) and MLL‐AF4 in 3/218 (1.4%) patients. Adult B ‐ ALL cases had BCR‐ABL in 15/53 (28.3%) and E2A‐PBX in 2/53 (3.8%); however, no other fusion transcript was detected. SIL‐TAL1 was found in four of 26 pediatric (15%) and zero of 7 adult T ‐ ALL cases. Conclusion The higher incidence of BCR‐ABL and lower incidence of TEL‐AML 1 in our ALL patients, both in children and adults as compared with the W est, suggests that patients in I ndia may be biologically different. This difference may explain at least in part the higher relapse rate and poorer outcome in our B ‐ ALL cases.