Isolated trisomy 11 in de novo acute myeloid leukemia

Krum, Everson Augusto; Hamed, Tatiane; Yamamoto, Masahiro; Chauffaille, Maria de Lourdes Lopes Ferrari

doi:10.1590/s1516-84842008000300016

Cited by 1 publication

(1 citation statement)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Basically, both chromosome 7 and 11 contain genes that are involved in the tumor progression such as EGFR , HGF , HOX , BRAF , PAFAH1B2 , FLI1 , and ETS1 [ 30 – 35 ], in particular LAMB1 , MET , MMP1 , CCND1 , ORAOV1 , FADD , PPFIA1 , and CTTN genes which related to HNSCC [ 36 – 38 ]. In addition, the gain of chromosome 7 was predominantly found in colorectal cancer, glioblastoma, and renal cell carcinoma [ 32 , 39 , 40 ], and the gain of chromosome 11 was reported in ovarian cancer and myeloid leukemia [ 41 , 42 ]. This suggests that the gain of both chromosome 7 and 11 have significance in carcinogenesis, when compared to other chromosomes in numerical aberration.…”

Section: Discussionmentioning

confidence: 99%

Genomic Alteration in Head and Neck Squamous Cell Carcinoma (HNSCC) Cell Lines Inferred from Karyotyping, Molecular Cytogenetics, and Array Comparative Genomic Hybridization

et al. 2016

View full text Add to dashboard Cite

Genomic alteration in head and neck squamous cell carcinoma (HNSCC) was studied in two cell line pairs (HN30-HN31 and HN4-HN12) using conventional C-banding, multiplex fluorescence in situ hybridization (M-FISH), and array comparative genomic hybridization (array CGH). HN30 and HN4 were derived from primary lesions in the pharynx and base of tongue, respectively, and HN31 and HN12 were derived from lymph-node metastatic lesions belonging to the same patients. Gain of chromosome 1, 7, and 11 were shared in almost all cell lines. Hierarchical clustering revealed that HN31 was closely related to HN4, which shared eight chromosome alteration cases. Large C-positive heterochromatins were found in the centromeric region of chromosome 9 in HN31 and HN4, which suggests complex structural amplification of the repetitive sequence. Array CGH revealed amplification of 7p22.3p11.2, 8q11.23q12.1, and 14q32.33 in all cell lines involved with tumorigenesis and inflammation genes. The amplification of 2p21 (SIX3), 11p15.5 (H19), and 11q21q22.3 (MAML2, PGR, TRPC6, and MMP family) regions, and deletion of 9p23 (PTPRD) and 16q23.1 (WWOX) regions were identified in HN31 and HN12. Interestingly, partial loss of PTPRD (9p23) and WWOX (16q23.1) genes was identified in HN31 and HN12, and the level of gene expression tended to be the down-regulation of PTPRD, with no detectable expression of the WWOX gene. This suggests that the scarcity of PTPRD and WWOX genes might have played an important role in progression of HNSCC, and could be considered as a target for cancer therapy or a biomarker in molecular pathology.

show abstract