Delineation of a 6 cM commonly deleted region in childhood acute lymphoblastic leukemia on the 6q chromosomal arm

Abstract

Deletion of the long arm of human chromosome 6 in acute lymband; 14 a second study that surveyed 2655 ALLs with abnorphoblastic leukemia (ALL) has been shown by cytogenetic mal karyotype identified two putative regions in 6q15-21 and studies in 4-11% of cases. To characterize further the region 6q22-27; 1 finally, FISH analysis of six cases of childhood ALL of deletion and to precisely establish its frequency, we studied with 6q deletions found that the commonly deleted region loss of heterozygozity (LOH) in 120 children with ALL using contained a marker located in 6q16.3. 27 polymorphic markers located from the 6q14-15 chromosomal band to the telomere. LOH was detected in eight patients. AThe aim of the present study was to delineate precisely the single region of LOH, flanked distally by D6S1594 and proxicritical region(s) that is (are) deleted on the 6q chromosomal mally by D6S301 was detected. These DNA markers are separarm in order to further localize the TSG(s) involved in this ated by 6 cM and are approximately located at the 6q21-22 tumor type. For this purpose, we searched for LOH in blasts band. Our present results delineate a region that is likely to from 120 children with ALL using highly informative microsatcontain a tumor-suppressor gene involved in a subset of childellite markers. This approach also permitted us to establish the hood ALLs.

Cytogenetic abnormalities and clinical correlations in peripheral T‐cell lymphoma

“…The frequent loss of 6q21 in PTCL, as well as other diseases, such as childhood ALL, suggests the presence of a tumor suppressor gene which may contribute to the development of malignancy (Gérard et al, 1997). In this study, the region of genetic loss most common to all three PTCL subgroups clustered at 6q21.…”

Suppression of tumorigenicity in human ovarian cancer cell lines is controlled by a 2 cM fragment in chromosomal region 6q24-q25

“…This suggests that its role in tumor suppression is not restricted to tumors of ovarian origin, but may be important for a large variety of di erent cancer types. Indeed, deletions or losses of heterozygosity a ecting chromosome 6 were reported in cancers from a large number of di erent organs including carcinomas of the breast (Devilee et al, 1991;Sheng et al, 1996), endometrium (Tibiletti et al, 1997), and prostate (Cooney et al, 1996), as well as in small cell lung carcinomas (Merlo et al, 1994), lymphomas and leukemias (Gerard et al, 1997;Menasce et al, 1994), and melanomas (Walker et al, 1994).…”

PA26, a novel target of the p53 tumor suppressor and member of the GADD family of DNA damage and growth arrest inducible genes

“…Deletions in this region have been described in non-Hodgkin lymphoma (Ot et al, 1993;Johansson et al, 1995), acute lymphoblastic leukemia (Gerard et al, 1997) bladder carcinoma (Brown et al, 1994), ovarian (Pejovic, 1995;Orphanos et al, 1995a) and mammary carcinomas (Orphanos et al, 1995b;Sheng et al, 1996;Noviello et al, 1996) and squamous cell carcinomas of the head and neck (Rao et al, 1994), indicating the presence of one or more tumorsuppressor genes. This possibility is supported by chromosome transfer experiments (Negrini et al, 1994;Sandhu et al, 1996;Morelli et al, 1997) which seem to suggest that the putative tumor suppressor gene in 6q21 may be functioning as a senescence gene.…”