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Relevant bibliographies by topics / Chromosome 3p

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Academic literature on the topic 'Chromosome 3p'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Chromosome 3p"

1

Dahiya, Rashmi, and Peter Ly. "Abstract A014: Modeling recurrent chromosomal alterations in renal cell carcinoma evolution." Cancer Research 83, no. 16_Supplement (2023): A014. http://dx.doi.org/10.1158/1538-7445.kidney23-a014.

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Abstract The loss of one copy of chromosome 3p represents an early truncal genetic event in the majority of clear cell renal cell carcinoma (ccRCC) tumors. Chromosome 3p loss can be initiated by chromothripsis, a process in which mis-segregated chromosomes entrapped within abnormal nuclear structures called micronuclei become pulverized into small genomic fragments. These fragments are then re-stitched together to form complex rearrangements that are accompanied by extensive segmental deletions that inactivate critical tumor suppressor genes located on chromosome 3p. Despite being a driver of

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2

Hötzel, Isidro, and William P. Cheevers. "A maedi–visna virus strain K1514 receptor gene is located in sheep chromosome 3p and the syntenic region of human chromosome 2." Journal of General Virology 83, no. 7 (2002): 1759–64. http://dx.doi.org/10.1099/0022-1317-83-7-1759.

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The maedi–visna lentivirus (MVV) induces encephalitis, interstitial pneumonia, arthritis and mastitis in sheep. While some MVV strains can enter cells of ruminant species only, others can enter cells from many species, including human, but not Chinese hamster cells. However, the identity of the receptor(s) used by MVV for entry is unknown. The MVV-K1514 receptor gene was localized in sheep and human chromosomes using hamster×sheep and hamster×human hybrid cell lines. Based on entry by a vector pseudotyped with the MVV-K1514 envelope, the MVV-K1514 receptor gene was mapped to sheep chromosome 3

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Journal, Baghdad Science. "Chromosomal aberrations and N-ras activation in human larynx carcinoma cell line Hep-2." Baghdad Science Journal 5, no. 3 (2008): 346–52. http://dx.doi.org/10.21123/bsj.5.3.346-352.

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In the present study, cytogenetic and molecular techniques were conducted to detect the chromosomal aneuploidy and the involvement of N and H genes in squamous larynx carcinoma cell line Hep-2.Our results showed that numerical and structural abnormalities were involved in larynx cancer Hep-2.The total number of chromosomes ranging from tripolyploidy in passage187to more than that in passage207.The more frequent chromosomes involved in numerical aberrations were chromosomes1,7,16,17 and 18. Structural chromosomal aberrations were also detected.Deletion of short arm was detected in chromosome 1(

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Al-Faisal, Abdul Hussain M., Amal M. Ali, and Nahi Y. Yassen. "Chromosomal aberrations and N-ras activation in human larynx carcinoma cell line Hep-2." Baghdad Science Journal 5, no. 3 (2008): 346–52. http://dx.doi.org/10.21123/bsj.2008.5.3.346-352.

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In the present study, cytogenetic and molecular techniques were conducted to detect the chromosomal aneuploidy and the involvement of N and H genes in squamous larynx carcinoma cell line Hep-2.Our results showed that numerical and structural abnormalities were involved in larynx cancer Hep-2.The total number of chromosomes ranging from tripolyploidy in passage187to more than that in passage207.The more frequent chromosomes involved in numerical aberrations were chromosomes1,7,16,17 and 18. Structural chromosomal aberrations were also detected.Deletion of short arm was detected in chromosome 1(

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5

Yang, Q., G. Yoshimura, I. Mori, T. Sakurai, and K. Kakudo. "Chromosome 3p and breast cancer." Journal of Human Genetics 47, no. 9 (2002): 453–59. http://dx.doi.org/10.1007/s100380200064.

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6

Riley, Jacquelyn D., Catherine M. Stefaniuk, Francine Erenberg, Angelika L. Erwin, Lauren Palange, and Caroline Astbury. "Chromosome 3p Inverted Duplication with Terminal Deletion: Second Postnatal Case Report with Additional Clinical Features." Case Reports in Genetics 2019 (July 25, 2019): 1–7. http://dx.doi.org/10.1155/2019/5384295.

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Distal deletions and duplications of 3p are individually well-characterized chromosome abnormalities. Here, we report an inverted duplication of 3p with an adjacent terminal 3p deletion in a 17-month-old girl who had prenatal intrauterine growth restriction and cardiac defects. Other findings included hemangiomas, neutropenia, umbilical hernia, hypotonia, gross motor delay, microcephaly, and ptosis. Family history was noncontributory. Microarray analysis revealed a 5.37 Mb deletion of chromosome bands 3p26.1 to 3p26.3 and a 13.68 Mb duplication of 3p24.3 to 3p26.1. FISH analysis confirmed that

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Tarkan-Argüden, Yelda, Seniha Hacihanefioglu, Gül Öngen, Müzeyyen Erk, and Asim Cenani. "3p Abnormalities in Peripheral Lymphocytes in Small Cell Lung Cancer." Tumori Journal 95, no. 4 (2009): 535–37. http://dx.doi.org/10.1177/030089160909500423.

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3p abnormalities are the most frequent chromosome abnormalities in small cell lung cancer (SCLC). To date these abnormalities have only been observed in cells derived from tumor tissues. It is thought that cancer-related chromosome abnormalities in peripheral lymphocytes could help to predict cancer development, prognosis, and future metastasis. We report clonal and nonclonal 3p abnormalities in the peripheral lymphocytes of two patients with SCLC. A standard T-lymphocyte culture method and GTL banding technique were applied to the samples, and various clonal and nonclonal chromosome 3 abnorma

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Grebe, Stefan K. G., Bryan McIver, Ian D. Hay, et al. "Frequent Loss of Heterozygosity on Chromosomes 3p and 17p without VHL or p53 Mutations Suggests Involvement of Unidentified Tumor Suppressor Genes in Follicular Thyroid Carcinoma1." Journal of Clinical Endocrinology & Metabolism 82, no. 11 (1997): 3684–91. http://dx.doi.org/10.1210/jcem.82.11.4352.

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Follicular thyroid carcinoma (FTC) exhibits frequent loss of heterozygosity (LOH) on chromosomes 10q and 3p, suggesting involvement of tumor suppressor genes. We screened 14 FTC (10 Hurthle cell carcinomas and 4 nonoxyphilic FTC), 14 papillary thyroid carcinomas, and 7 follicular adenomas for LOH on chromosome arms 1p, 3p, 3q, 10p, 10q, 11p, 11q, 13q, 17p, and 17q. LOH was more frequent in FTC than in follicular adenoma or papillary thyroid carcinoma. In FTC, rates of LOH on 3p (86%), 17p (72%), and 10q (57%) were higher than the average rate of LOH (33%; P &lt; 0.05). Most frequently invo

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Mallick, Samyukta, and Alison M. Taylor. "Abstract 1414: The role of chromosome arm 3p and human papillomavirus on proliferation, differentiation, and metastasis in squamous cancers." Cancer Research 83, no. 7_Supplement (2023): 1414. http://dx.doi.org/10.1158/1538-7445.am2023-1414.

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Abstract Squamous Cell Carcinoma (SCC) is an aggressive form of cancer that develops in the mucosal epithelium of the digestive and respiratory tracts as well as on the skin. Two major risk factors for development of SCC are carcinogen exposures, such as alcohol and tobacco, and Human Papillomavirus (HPV) infection. Viral- and carcinogen-driven SCCs have differential responses to radiation, chemotherapy, and immunotherapy, with HPV+ SCCs responding better to these treatments than HPV- carcinomas. Analysis of aneuploidy patterns of genomic samples from The Cancer Genome Atlas (TCGA) have shown

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Zhang, G. L., and K. L. Xu. "Loss of heterozygosity at chromosome 3p in epithelial ovarian cancer in China." International Journal of Gynecologic Cancer 12, no. 2 (2002): 198–201. http://dx.doi.org/10.1136/ijgc-00009577-200203000-00010.

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The aim of this investigation was to determine the relationship between 3p loss of heterozygosity (LOH) and the pathogenesis of ovarian cancer. Fifty cases of epithelial ovarian tumor, including 40 cases with malignant tumors and 10 cases with benign tumors, were examined by polymerase chain reaction (PCR) with D3s1228 and D3s1038 microsatellite polymorphism markers at 3p. Thirty-two of the 40 cases (80%) with ovarian cancer showed LOH at 3p14 or 3p25, but only 1 of 10 cases (10.0%) with benign ovarian tumor showed 3p LOH. Among them, 24 cases (60.0%) had LOH at 3p14 and 16 cases (40.0%) at 3p

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Dissertations / Theses on the topic "Chromosome 3p"

1

Liu, Jian. "Deletion mapping of human 3P in major epithelial malignancies and fine localization of candidate tumor suppressor genes /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-577-8/.

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Phipps, Maude Elvira. "The physical mapping of chromosome 3p25-26 : a region involved in Von Hippel-Lindau disease and chromosome 3p deletion syndrome." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336776.

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Manderson, Emily Noelle. "Characterization of Chromosome 3 anomalies and 3p genes implicated in human epithelial ovarian cancer." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84290.

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Cytogenetic, loss of heterozygosity (LOH) and midrocell-mediated chromosome transfer (MMCT) analyses of epithelial ovarian cancer (EOC) have provided evidence for the role of genes on the short arm of chromosome 3 (3p) in the development of this disease. LOH analysis of ovarian tumors performed in the laboratory of Dr. Tonin identified two minimal regions of deletion (MRD) at 3p25--p26 and 3p24, and a third region extending from 3p14 to the centromere. Based on this study, I hypothesized that there are at least three tumor suppressor genes (TSG)s on the 3p arm that function in suppressi

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Lee, Man-yan, and 李敏茵. "Analysis on chromosome 3p in smokers and non-smokers with non-small cell lung carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31226231.

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Lee, Man-yan. "Analysis on chromosome 3p in smokers and non-smokers with non-small cell lung carcinoma /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25335224.

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Birch, Ashley. "Transcriptome, genomic and gentle analyses of chromosome 3p genes implicated as tumour suppressors in ovarian cancer." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110457.

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Numerical and structural aberrations of chromosome (chr) 3 have been frequently reported in epithelial ovarian cancer (EOC), with non-random losses of 3p consistently observed by karyotype and comparative genomic hybridization analyses. These losses are reported to involve several 3p loci, implying the presence of multiple tumour suppressor genes (TSGs) relevant to the progression of EOC. Both loss of heterozygosity (LOH) analyses of EOC samples and functional complementation assays of chr3 into EOC cell lines support this position. The hypothesis of this thesis states that there is at least o

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Cody, Neal A. L. 1980. "Physical and functional evidence in support of candidate chromosome 3p tumour suppressor genes implicated in epithelial ovarian cancer." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115662.

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Epithelial ovarian cancer (EOC) is difficult to detect in early stage disease, resulting in a high mortality rate. The molecular events underlying EOC development remain largely unknown. Chromosome 3 exhibits frequent deletions and rearrangements in EOC by cytogenetic analysis. In addition, loss of heterozygosity (LOH) mapping of matched ovarian tumour and constitutional DNA samples exhibits specific regions of chromosome 3 loss involving distinct regions: 3p25-p26, 3p24 and a region proximal to 3p14. Thus, chromosome 3p loss points to the location of tumour suppressor genes (TSG) implicated i

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8

Linne, Hannah Louise. "Investigating telomerase regulation in human breast cancer cells : a search for telomerase repressor sequences localised to chromosome 3P." Thesis, Brunel University, 2015. http://bura.brunel.ac.uk/handle/2438/11620.

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Cellular immortality is one of the ten hallmarks of human cancer and has been shown to be an essential prerequisite for malignant progression (Hanahan and Weinberg., 2011, Newbold et al., 1982, Newbold and Overell., 1983). In contrast, normal human somatic cells proliferate for a limited number of population doublings before entering permanent growth arrest known as replicative senescence. This is thought to be due to the progressive shortening of telomeric sequences with each round of cell division. Over 90% of human tumours, but not the majority of human somatic cells, have been found to exp

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9

Gu, Wen-Hui, and 古文慧. "Genomic alterations in cervical carcinoma:loss of heterozygosity on chromosomes 3p, 5p and p53 gene." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/25479985478281183348.

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Conference papers on the topic "Chromosome 3p"

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de Oliveira, Marcia Maria Costa, Luciane R. Cavalli, Cícero Andrade Urban, Rubens Silveira de Lima, Enilze Maria de Souza Fonseca Ribeiro, and Iglenir João Cavalli. "Abstract 2158: Loss of heterozygosity at chromosome 3p in ductal and lobular breast carcinomas." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2158.

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Reports on the topic "Chromosome 3p"

1

Drabkin, Harry. Isolation of a Breast Cancer Tumor Suppressor Gene from Chromosome 3P. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada391410.

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Drabkin, Harry A. Isolation of a Breast Cancer Tumor Suppressor Gene from Chromosome 3p. Defense Technical Information Center, 1998. http://dx.doi.org/10.21236/adb247843.

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