Allelotyping of acute myelogenous leukemia: loss of heterozygosity at 7q31.1 (D7S486) and q33-34 (D7S498, D7S505)

Koike, Michiaki; Tasaka, Taizo; Spira, Susanne; Tsuruoka, Nanae; Koeffler, H. Phillip

doi:10.1016/s0145-2126(98)00159-3

Cited by 41 publications

(35 citation statements)

References 22 publications

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“…For example, it was noted previously that chromosome arm 12p is frequently aberrant in childhood ALL, 14,15,47 as is 13q in childhood ALL and adult chronic lymphocytic leukemia. 14,[48][49][50] Furthermore, several of the loci detected in this study were previously implicated in the pathogenesis of AML, including deletion of 9q, 51 monosomy 7, partial deletions of 7q 23,[52][53][54][55] and 5q, and abnormalities of 3q. 1,25 Our finding of LOH on 5q and 3q in 2 patients without such abnormalities on cytogenetic analysis indicates that LOH analysis may be a more sensitive technique for identifying such patients with a poor prognosis.…”

Section: Discussionmentioning

confidence: 65%

Loss of heterozygosity in childhood de novo acute myelogenous leukemia

Sweetser

Chen

Blomberg

et al. 2001

Blood

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A genome-wide screening for loss of heterozygosity (LOH), a marker for possible involvement of tumor suppressor genes, was conducted in 53 children with de novo acute myelogenous leukemia (AML). A total of 177 highly polymorphic microsatellite repeat markers were used in locus-specific polymerase chain reactions. This comprehensive allelotyping employed flow-sorted cells from diagnostic samples and whole-genome amplification of DNA from small, highly purified samples. Nineteen regions of allelic loss in 17 patients (32%) were detected on chromosome arms 1q, 3q, 5q, 7q (n ‫؍‬ 2), 9q (n ‫؍‬ 4), 11p (n ‫؍‬ 2), 12p (n ‫؍‬ 3), 13q (n ‫؍‬ 2), 16q, 19q, and Y. The study revealed a degree of allelic loss underestimated by routine cytogenetic analysis, which failed to detect 9 of these LOH events. There was no evidence of LOH by intragenic markers for p53, Nf1, or CBFA2/ AML1. Most lymphocytes lacked the deletions, which were detected only in the leukemic myeloid blast population. Analysis of patients' clinical and biologic characteristics indicated that the presence of LOH was associated with a white blood cell count of 20 ؋ 10 9 /L or higher but was not correlated with a shorter overall survival. The relatively low rate of LOH observed in this study compared with find-

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Section: Discussionmentioning

confidence: 65%

Loss of heterozygosity in childhood de novo acute myelogenous leukemia

Sweetser

Chen

Blomberg

et al. 2001

Blood

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“…Acute myeloid leukemia and myelodysplastic syndrome, especially those that occur secondary to genotoxic chemotherapy, are associated with deletions on the 7q region ( Figure 4c), consistent with the existence on 7q of one or more tumor suppressor genes (TSG). To characterize the regions of loss, both FISH 43 and loss of heterozygosity studies [44][45][46][47][48] have been performed on cases of MDS and AML. These data have proven to be complex, with regions of loss commonly extending over a considerable portion of chromosome 7, from 7q21.3 to 7q33 and beyond.…”

Section: Leukemiamentioning

confidence: 99%

“…One region of loss, at 7q31.1, is commonly lost in other malignancies such as breast, prostate, colon, and ovary (reviewed in Ref. 45); ST7, a tumor suppressor gene, has recently been identified in prostate cancer and is located in this area. This is likely one contributory gene.…”

Section: Leukemiamentioning

confidence: 99%

F-MuLV acceleration of myelomonocytic tumorigenesis in SV40 large T antigen transgenic mice is accompanied by retroviral insertion at Fli1 and a novel locus, Fim4

et al. 2002

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We describe here the development of a murine system for the identification of genes involved in myelomonocytic neoplasms. Transgenic C57BL/6J mice expressing SV40 early region under a myelomonocytic promoter develop histiocytic sarcomas with a latency of 167 days. We used retroviral proviral tagging to accelerate tumorigenesis and to uncover genetic changes that contribute to tumor development. Infection of transgenic mice with Friend murine leukemia virus (F-MuLV) shortened the latency of morbidity to 103 days (P Ͻ 0.001); this was associated with clonal proviral integrations in tumor DNA. As expected for F-MuLV, proviral insertions occurred at Fli1 in both transgenic and nontransgenic tumors. Four insertions were found at a novel locus, termed Fim4, on chromosome 6. This region is syntenic to human 7q32, a region that is commonly deleted in human myelodysplastic syndrome and acute myeloid leukemia. A murine BAC containing Fim4 was sequenced and analyzed, and while there was significant human-mouse homology in the area of the insertions, no candidate gene has been identified. Thus we have established a system to identify genes involved in myelomonocytic tumors, and have used it to identify Fim4, a new common site of proviral insertion. Study of this locus may provide insight into genes involved in AML-associated 7q32 deletions in humans.

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“…However, the mechanism of the process of multistage carcinogenesis is still not well understood [5][6][7][8][9][10][11][12] . Recently, a number of cytogenetic and molecular genetic studies have revealed that LOH on the long arm of chromosome 7 occurs frequently in many types of primary cancers including nasopharyngeal, gastric, breast, ovarian, and oral carcinomas, and investigators have identified the most common site of LOH as 7q31-32, implying the existence of at least one multi-tissue tumor suppressor gene (TSG) at this locus [13][14][15][16][17][18][19][20][21][22] . Based on these findings, in our previous studies, we have cloned a novel tumor related gene from this common deletion region in 7q31-32 by positional candidate cloning strategy, we named it NAG6, and its GenBank accession number was AF156971.…”

Section: Introductionmentioning

confidence: 99%

Expression of tumor related gene NAG6 in gastric cancer and restriction fragment length polymorphism analysis

Zhang¹,

Sheng²,

Wang³

et al. 2004

WJG

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AIM: NAG6 gene is a novel tumor related gene identified recently. This study was designed to examine the expression of this gene in gastric cancer and corresponding normal tissues, and to investigate its role in the occurrence and development of gastric cancer, also to study if the genetic structure of NAG6 was altered in gastric cancer. METHODS:Reverse transcription-polymerase chain reaction (RT-PCR), Northern blot analysis and dot hybridization were used to compare the expression level of NAG6 gene in 42 cases of gastric cancer tissues with their corresponding normal tissues of the same patients respectively. In addition, restriction fragment length polymorphism (RFLP) analysis was adopted to study if the genetic structure of NAG6 was altered in gastric carcinomas. RESULTS:The expression of NAG6 in 57.1% gastric cancer tissues (25/42) was absent by RT-PCR analysis. The downregulation rate of NAG6 in gastric cancer tissues was significantly higher than that in corresponding normal tissues (P<0.01). However no correlation between the downregulation of NAG6 and lymph-node and/or distance metastasis was found in this study (P>0.05). Dot hybridization confirmed the results of RT-PCR. Furthermore, the results of EcoRI RFLP analysis of NAG6 gene demonstrated that 3 of 7 cases of gastric cancer showed loss of 5 kb fragment in comparison with their corresponding normal tissues.

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Allelotyping of acute myelogenous leukemia: loss of heterozygosity at 7q31.1 (D7S486) and q33-34 (D7S498, D7S505)

Cited by 41 publications

References 22 publications

Loss of heterozygosity in childhood de novo acute myelogenous leukemia

Loss of heterozygosity in childhood de novo acute myelogenous leukemia

F-MuLV acceleration of myelomonocytic tumorigenesis in SV40 large T antigen transgenic mice is accompanied by retroviral insertion at Fli1 and a novel locus, Fim4

Expression of tumor related gene NAG6 in gastric cancer and restriction fragment length polymorphism analysis

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