The identification of transforming genes in human tumor cells has been made possible by DNA mediated gene transfer techniques. To date, it has been possible to show that most of these transforming genes are activated cellular analogues of the ras oncogene family. To better understand the relationship between these oncogenes and other human genes, we have determined their chromosomal localization by analyzing human rodent somatic cell hybrids with molecularly cloned human proto-oncogene probes. It was possible to assign N-ras to chromosome 1 and regionally localize c-K-ras-1 and c-K-ras-2 to human chromosomes 6pter-q13 and 12q, respectively. These results along with previous studies demonstrate the highly dispersed nature of ras genes in the human genome. Previous reports indicated that the c-myb gene also resides on chromosome 6. It has been possible to sublocalize c-myb to the long arm of chromosome 6 (q15-q21). The non-random aberrations in chromosomes 1, 6 and 12 that occur in certain human tumors suggest possible etiologic involvement of ras and/or myb oncogenes in such tumors.
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http://dx.doi.org/10.1093/nar/11.23.8221 | DOI Listing |
Plant Signal Behav
December 2025
Technology Center, China Tobacco Jiangsu Industrial Co, Ltd, Nanjing, China.
Nuclear Factor Y (NF-Y) represents a group of transcription factors commonly present in higher eukaryotes, typically consisting of three subunits: NF-YA, NF-YB, and NF-YC. They play crucial roles in the embryonic development, photosynthesis, flowering, abiotic stress responses, and other essential processes in plants. To better understand the genome-wide NF-Y domain-containing proteins, the protein physicochemical properties, chromosomal localization, synteny, phylogenetic relationships, genomic structure, promoter -elements, and protein interaction network of NtNF-Ys in tobacco ( L.
View Article and Find Full Text PDFTransl Cancer Res
December 2024
Medical College of Qinghai University, Xining, China.
Background: Chromosome segregation 1 like () overexpression can promote proliferation and migration in cancer. In previous study, we found that CSE1L expression was higher in gastric cancer (GC) tissues compared to normal tissues. However, the biological function and molecular mechanism of CSE1L in GC remains unclear.
View Article and Find Full Text PDFAm J Surg Pathol
January 2025
Bioinformatics Core Facility, Lyda Hill Department of Bioinformatics, Department of Pathology University of Texas Southwestern Medical Center, Dallas, TX.
The cholangioblastic variant of intrahepatic cholangiocarcinoma is a distinctive neoplasm that typically affects young women without underlying liver disease. Morphologically, it demonstrates solid, trabecular, and tubulocystic architecture, biphasic small cell-large cell cytology, and immunoreactivity for inhibin, neuroendocrine markers, and biliary but not hepatocellular markers. In 2021, our group identified a characteristic NIPBL::NACC1 gene fusion in cholangioblastic cholangiocarcinoma, and since then ~20 genetically confirmed cases have been reported in the literature.
View Article and Find Full Text PDFChromosome Res
January 2025
Saint-Petersburg State University, Saint-Petersburg, Russia.
Danio rerio, commonly known as zebrafish, is an established model organism for the developmental and cell biology studies. Although significant progress has been made in the analysis of the D. rerio genome, cytogenetic studies face challenges due to the unclear identification of chromosomes.
View Article and Find Full Text PDFNeurol Genet
February 2025
Department of Neurology and Neurosurgery, McGill University, Montreal, Canada.
In the late 1800s, Nikolaus Friedreich first described "degenerative atrophy of the posterior columns of the spinal cord," noting its connection to progressive ataxia, sensory loss, and muscle weakness, now recognized as Friedreich ataxia (FRDA). Renewed interest in the disease in the 1970s and 80s by the Quebec Cooperative Group and by Anita Harding led to the development of clinical diagnostic criteria and insights into associated biochemical abnormalities, although the primary defect remained unknown. In 1988, Susan Chamberlain mapped FRDA's location on chromosome 9.
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