PMID- 15193435 OWN - NLM STAT- MEDLINE DCOM- 20040727 LR - 20171116 IS - 0165-4608 (Print) IS - 0165-4608 (Linking) VI - 152 IP - 1 DP - 2004 Jul 1 TI - The role of fluorescence in situ hybridization (FISH) for monitoring hematologic malignancies with BCR/ABL or ETO/AML1 rearrangement: a comparative study with FISH and G-banding on 919 consecutive specimens of hematologic malignancies. PG - 1-7 AB - Fluorescence in situ hybridization (FISH) can detect minor genetic changes that cytogenetic analysis may miss; however, there are few reports on the kinds of genetic changes that show large discrepancies between results obtained with FISH versus G-banding techniques. To investigate genetic changes that tend to be detected with FISH only, we compared the results of cytogenetic study and FISH analysis in 919 consecutive specimens from 304 patients with hematologic malignancies, covering most of the frequent genetic changes by using 18 types of FISH probes. The genetic changes with especially large discrepancy rates at diagnosis were del(7q) (20.0%), PML/RARA (17.6%), and trisomy 21 (12.5%) and, at follow-up, BCR/ABL (28.2%) and AML1/ETO (24.4%); the latter two showed only small discrepancies at diagnosis (4.7 and 4.8%, respectively). The overall discrepancy rate was 6.0% at diagnosis and 11.9% at follow-up, indicating generally greater discrepancy rates at follow-up. In all but one of the cases with discrepant results, G-banding missed the corresponding chromosomal abnormalities revealed with FISH. Considered by type of leukemia, the discrepancy rate at follow-up was higher in acute biphenoptypic leukemia (38%) and acute lymphoblastic leukemia (24.5%) than in acute myelogenous leukemia (10.6%). Given these results, all patients with known genetic changes should have FISH analysis in follow-up, for an accurate assessment of the likelihood of complete remission or recurrence. If this is not practical, then at a minimum FISH analysis should be done in follow-up for patients with genetic changes of BCR/ABL and AML1/ETO seen at diagnosis. FAU - Lee, Dong Young AU - Lee DY AD - Department of Clinical Pathology, Seoul National University College of Medicine, 28 Yongon-dong Chongno-gu, Seoul 110-744, Republic of Korea. FAU - Cho, Han Ik AU - Cho HI FAU - Kang, Yoon Hee AU - Kang YH FAU - Yun, Sung Soo AU - Yun SS FAU - Park, Sun Yang AU - Park SY FAU - Lee, Yun Song AU - Lee YS FAU - Kim, Youngsoo AU - Kim Y FAU - Lee, Dong Soon AU - Lee DS LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Cancer Genet Cytogenet JT - Cancer genetics and cytogenetics JID - 7909240 RN - 0 (AML1-ETO fusion protein, human) RN - 0 (Core Binding Factor Alpha 2 Subunit) RN - 0 (Oncogene Proteins, Fusion) RN - 0 (RUNX1 Translocation Partner 1 Protein) RN - 0 (Transcription Factors) RN - EC 2.7.10.2 (Fusion Proteins, bcr-abl) SB - IM MH - Adolescent MH - Adult MH - Aged MH - Aged, 80 and over MH - Child MH - Child, Preschool MH - Chromosome Aberrations MH - *Chromosome Banding MH - Core Binding Factor Alpha 2 Subunit MH - Female MH - Fusion Proteins, bcr-abl/*genetics MH - *Gene Rearrangement MH - Hematologic Neoplasms/diagnosis/*genetics MH - Humans MH - In Situ Hybridization, Fluorescence MH - Infant MH - Male MH - Middle Aged MH - Oncogene Proteins, Fusion/*genetics MH - RUNX1 Translocation Partner 1 Protein MH - Transcription Factors/*genetics EDAT- 2004/06/15 05:00 MHDA- 2004/07/28 05:00 CRDT- 2004/06/15 05:00 PHST- 2003/07/08 00:00 [received] PHST- 2003/09/15 00:00 [revised] PHST- 2003/09/16 00:00 [accepted] PHST- 2004/06/15 05:00 [pubmed] PHST- 2004/07/28 05:00 [medline] PHST- 2004/06/15 05:00 [entrez] AID - S0165460803004199 [pii] AID - 10.1016/j.cancergencyto.2003.09.014 [doi] PST - ppublish SO - Cancer Genet Cytogenet. 2004 Jul 1;152(1):1-7. doi: 10.1016/j.cancergencyto.2003.09.014.