ABSTRACT
Two members of the KOX gene family, ZNF23 (KOX16) and ZNF32 (KOX30), have been mapped by in situ hybridization to chromosome regions 16q22 and 10q23-q24, respectively. The map location of ZNF23 and ZNF32 placed these zinc finger protein genes near to chromosome loci that, under certain in vitro conditions, are expressed as fragile sites (FRA16B, FRA16C) and (FRA10D, FRA10A, FRA10B and FRA10E). Human zinc finger gene ZNF32 maps to a chromosome region on 10q23-24 in which deletions have been observed associated with malignant lymphoma on 10q22-23 and with carcinoma of the prostate on 10q24. ZNF23 is located on 16q22 in a chromosomal region that has been involved in chromosome alterations characteristic of acute myeloid leukemia. A second Kox zinc finger gene (ZNF19/KOX12) was recently mapped to the same chromosome region on human chromosome 16q22. In the analogous murine position, the murine zinc finger genes Zfp-1 and Zfp-4 are found in the syntenic 16q region of mouse chromosome 8. Thus, ZNF19 and ZNF23 might be members of an evolutionarily conserved zinc finger gene cluster located on human chromosome 16q22.
Subject(s)
Chromosomes, Human, Pair 10 , Chromosomes, Human, Pair 16 , DNA-Binding Proteins/genetics , Zinc Fingers/genetics , Chromosome Fragile Sites , Chromosome Fragility , Chromosome Mapping , Humans , In Situ Hybridization , Molecular Sequence Data , Multigene FamilyABSTRACT
Using a combination of banding techniques, we examined two atypical 21;22 translocations, 46,XX or XY,t(21;22)(p11;q11). In situ chromosomal hybridization of a probe for the constant region of the lambda light chain locus demonstrated that the 22q11 breakpoints of both rearrangements were proximal to the C lambda gene cluster. These studies permitted us to distinguish the 22q11 breakpoints of these translocations from the breakpoint of the 22q--chromosome of chronic myelogenous leukemia.
Subject(s)
Chromosomes, Human, 21-22 and Y , Immunoglobulin Light Chains/genetics , Immunoglobulin lambda-Chains/genetics , Translocation, Genetic , Chromosome Banding , Chromosome Mapping , Female , Genes , Humans , Karyotyping , Lymphocytes/cytology , Nucleic Acid HybridizationABSTRACT
A human diploid fibroblast cell line has been established from the lung tissue of a male fetus. This has been characterized and frozen away in large quantity. A smaller quantity of fibroblastlike cells from skin has also been established, partially characterized, and placed in frozen storage from the same fetus. This project is in support of the National Institute on Aging research in general cell biology. The present lines designated IMR-91 lung and IMR-91 skin complement the previous human diploid fibroblast culture (IMR-90) established from a female fetus. The lack of random inactivation of one of the two X chromosomes in the present male line reduces the genetic heterogeneity inherent in the female line.
Subject(s)
Cell Line , Fetus , Lung/cytology , Skin/cytology , Cell Division , Cell Survival , Clone Cells/cytology , Diploidy , Fibroblasts/cytology , HLA Antigens/analysis , Humans , Karyotyping , Male , Mitotic IndexSubject(s)
Chromosome Deletion , Chromosome Inversion , Chromosome Mapping , Mutation , Cells, Cultured , Chromosome Banding , Humans , New JerseyABSTRACT
The incidence of chromosomal aberrations in banded karyotypes and of sister-chromatid exchanges (SCEs) was determined in the lymphocytes of survivors of childhood cancer as 2 parameters which are pertinent in assessing the genetic damage induced by chemotherapy. The proportion of cells with chromosome breakage or structural rearrangement-type aberration was 1 cell in 67 in a control group of 8 untreated cancer patients and 2 parents of cancer patients, 1 cell in 8 in 12 patients currently on therapy, and 1 cell in 50 in 17 patients sampled 6 months to 35 years post-treatment. The range of mean SCE levels per cell was 4.5-6.5 in the untreated cancer patients, 4.0-9.6 in non-cancer controls, 3.3-33.7 in patients on therapy, and 4.6-9.7 in post-therapy survivors. Considerably variability was observed between individuals with both SCE and breakage assays but therapy-induced increases in SCEs were not necessarily correlated with increased levels of aberrations arising from chromosomal breakage.
