c-Ha-ras1 is not deleted in aniridia-Wilms' tumour association.

摘要: Non-random tumour-specific chromosomal abnormalities have been observed in cells of many different human tumours. In Wilms' tumour (WT) and retinoblastoma, a deletion occurs germinally or somatically has considered an important step development. One class potential cellular transforming genes comprises the homologues highly oncogenic retroviruses. A remarkable concordance between location oncogenes breakpoints involved acquired translocations is becoming apparent various cancers: c-mos, c-myc c-abl are located at that occur acute myeloblastic leukaemia, Burkitt's lymphoma chronic myelocytic leukaemia respectively. Thus when oncogene c-Ha-ras1 was localized to short arm chromosome 11 (refs 6-8; region 11p11 leads p15 not 11p13 as stated ref. 5), it proposed possible aetiological agent aniridia-WT association (AWTA) results from (although gene recently isolated WT cell line (G401) shown be homologous either c-Ha-ras c-Ki-ras9). We now looked for rearrangement DNA four subjects with del(11p13)-associated predisposition tumour, aniridia, genitourinary mental retardation. report here no case deleted, we further refined its 11p15.1 11p15.5. On basis enzyme studies direct dosage determination beta-globin neoplastic non-neoplastic tissues one patient, conclude normal counterpart 11p cannot account development tumour.