Relevant bibliographies by topics / Tumour suppressor genes; Breast cancer

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Tumour suppressor genes; Breast cancer'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Tumour suppressor genes; Breast cancer"

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Børresen-Dale, A. L. "Tumour suppressor genes in breast cancer." European Journal of Cancer 34 (September 1998): S37. http://dx.doi.org/10.1016/s0959-8049(98)80137-8.

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S Patil, Priya, Jaydeep N Pol, and Ashalata D Patil. "ROLE OF TUMOUR SUPPRESSOR GENE P53 IN TRIPLE NEGATIVE BREAST CANCER." International Journal of Anatomy and Research 5, no. 4.2 (November 1, 2017): 4585–89. http://dx.doi.org/10.16965/ijar.2017.402.

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Lai, Dulcie, Stacy Visser-Grieve, and Xiaolong Yang. "Tumour suppressor genes in chemotherapeutic drug response." Bioscience Reports 32, no. 4 (April 23, 2012): 361–74. http://dx.doi.org/10.1042/bsr20110125.

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Since cancer is one of the leading causes of death worldwide, there is an urgent need to find better treatments. Currently, the use of chemotherapeutics remains the predominant option for cancer therapy. However, one of the major obstacles for successful cancer therapy using these chemotherapeutics is that patients often do not respond or eventually develop resistance after initial treatment. Therefore identification of genes involved in chemotherapeutic response is critical for predicting tumour response and treating drug-resistant cancer patients. A group of genes commonly lost or inactivated are tumour suppressor genes, which can promote the initiation and progression of cancer through regulation of various biological processes such as cell proliferation, cell death and cell migration/invasion. Recently, mounting evidence suggests that these tumour suppressor genes also play a very important role in the response of cancers to a variety of chemotherapeutic drugs. In the present review, we will provide a comprehensive overview on how major tumour suppressor genes [Rb (retinoblastoma), p53 family, cyclin-dependent kinase inhibitors, BRCA1 (breast-cancer susceptibility gene 1), PTEN (phosphatase and tensin homologue deleted on chromosome 10), Hippo pathway, etc.] are involved in chemotherapeutic drug response and discuss their applications in predicting the clinical outcome of chemotherapy for cancer patients. We also propose that tumour suppressor genes are critical chemotherapeutic targets for the successful treatment of drug-resistant cancer patients in future applications.
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Försti, Asta, Qianren Jin, Lena Sundqvist, Magnus Söderberg, and Kari Hemminki. "Use of Monozygotic Twins in Search for Breast Cancer Susceptibility Loci." Twin Research 4, no. 4 (August 1, 2001): 251–59. http://dx.doi.org/10.1375/twin.4.4.251.

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AbstractWe have used Swedish monozygotic twins concordant for breast cancer to study genetic changes associated with the development of breast cancer. Because loss of heterozygosity (LOH) at a specific genomic region may reflect the presence of a tumour suppressor gene, loss of the same allele in both of the twins concordant for breast cancer may pinpoint a tumour suppressor gene that confers a strong predisposition to breast cancer. DNA samples extracted from the matched tumour and normal tissues of nine twin pairs were analysed for allelic imbalance using a set of microsatellite markers on chromosomes 1, 13, 16 and 17, containing loci with known tumour suppressor genes. The two main regions, where more twin pairs than expected had lost the same allele, were located at 16qtel, including markers D16S393, D16S305 and D16S413, and at 17p13, distal to the p53 locus. Our results show that the monozygotic twin model can be used to suggest candidate regions of potential tumour suppressor genes, even with a limited number of twin pairs.
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Buchholz, Thomas A., Michael M. Weil, Michael D. Story, Eric A. Strom, William A. Brock, and Marsha D. McNeese. "Tumor suppressor genes and breast cancer." Radiation Oncology Investigations 7, no. 2 (1999): 55–65. http://dx.doi.org/10.1002/(sici)1520-6823(1999)7:2<55::aid-roi1>3.0.co;2-#.

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Oliveira, Andre M., Jeffrey S. Ross, and Jonathan A. Fletcher. "Tumor Suppressor Genes in Breast Cancer." Pathology Patterns Reviews 124, suppl_1 (December 1, 2005): S16—S28. http://dx.doi.org/10.1309/5xw3l8lu445qwgqr.

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Wijshake, Tobias, Zhongju Zou, Beibei Chen, Lin Zhong, Guanghua Xiao, Yang Xie, John G. Doench, Lynda Bennett, and Beth Levine. "Tumor-suppressor function of Beclin 1 in breast cancer cells requires E-cadherin." Proceedings of the National Academy of Sciences 118, no. 5 (January 25, 2021): e2020478118. http://dx.doi.org/10.1073/pnas.2020478118.

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Beclin 1, an autophagy and haploinsufficient tumor-suppressor protein, is frequently monoallelically deleted in breast and ovarian cancers. However, the precise mechanisms by which Beclin 1 inhibits tumor growth remain largely unknown. To address this question, we performed a genome-wide CRISPR/Cas9 screen in MCF7 breast cancer cells to identify genes whose loss of function reverse Beclin 1-dependent inhibition of cellular proliferation. Small guide RNAs targeting CDH1 and CTNNA1, tumor-suppressor genes that encode cadherin/catenin complex members E-cadherin and alpha-catenin, respectively, were highly enriched in the screen. CRISPR/Cas9-mediated knockout of CDH1 or CTNNA1 reversed Beclin 1-dependent suppression of breast cancer cell proliferation and anchorage-independent growth. Moreover, deletion of CDH1 or CTNNA1 inhibited the tumor-suppressor effects of Beclin 1 in breast cancer xenografts. Enforced Beclin 1 expression in MCF7 cells and tumor xenografts increased cell surface localization of E-cadherin and decreased expression of mesenchymal markers and beta-catenin/Wnt target genes. Furthermore, CRISPR/Cas9-mediated knockout of BECN1 and the autophagy class III phosphatidylinositol kinase complex 2 (PI3KC3-C2) gene, UVRAG, but not PI3KC3-C1–specific ATG14 or other autophagy genes ATG13, ATG5, or ATG7, resulted in decreased E-cadherin plasma membrane and increased cytoplasmic E-cadherin localization. Taken together, these data reveal previously unrecognized cooperation between Beclin 1 and E-cadherin–mediated tumor suppression in breast cancer cells.
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Tan, D. S. P., C. Marchiò, and J. S. Reis-Filho. "Hereditary breast cancer: from molecular pathology to tailored therapies." Journal of Clinical Pathology 61, no. 10 (August 4, 2008): 1073–82. http://dx.doi.org/10.1136/jcp.2008.057950.

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Hereditary breast cancer accounts for up to 5–10% of all breast carcinomas. Recent studies have demonstrated that mutations in two high-penetrance genes, namely BRCA1 and BRCA2, are responsible for about 16% of the familial risk of breast cancer. Even though subsequent studies have failed to find another high-penetrance breast cancer susceptibility gene, several genes that confer a moderate to low risk of breast cancer development have been identified; moreover, hereditary breast cancer can be part of multiple cancer syndromes. In this review we will focus on the hereditary breast carcinomas caused by mutations in BRCA1, BRCA2, Fanconi anaemia (FANC) genes, CHK2 and ATM tumour suppressor genes. We describe the hallmark histological features of these carcinomas compared with non-hereditary breast cancers and show how an accurate histopathological diagnosis may help improve the identification of patients to be screened for mutations. Finally, novel therapeutic approaches to treat patients with BRCA1 and BRCA2 germ line mutations, including cross-linking agents and PARP inhibitors, are discussed.
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Moerland, E., MH Breuning, CJ Cornelisse, and AM Cleton-Jansen. "Exclusion of BBC1 and CMAR as candidate breast tumour-suppressor genes." British Journal of Cancer 76, no. 12 (December 1997): 1550–53. http://dx.doi.org/10.1038/bjc.1997.594.

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Liang, Ying, Qi Lu, Wei Li, Dapeng Zhang, Fanglin Zhang, Qingping Zou, Lu Chen, et al. "Reactivation of tumour suppressor in breast cancer by enhancer switching through NamiRNA network." Nucleic Acids Research 49, no. 15 (July 30, 2021): 8556–72. http://dx.doi.org/10.1093/nar/gkab626.

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Abstract Dysfunction of Tumour Suppressor Genes (TSGs) is a common feature in carcinogenesis. Epigenetic abnormalities including DNA hypermethylation or aberrant histone modifications in promoter regions have been described for interpreting TSG inactivation. However, in many instances, how TSGs are silenced in tumours are largely unknown. Given that miRNA with low expression in tumours is another recognized signature, we hypothesize that low expression of miRNA may reduce the activity of TSG related enhancers and further lead to inactivation of TSG during cancer development. Here, we reported that low expression of miRNA in cancer as a recognized signature leads to loss of function of TSGs in breast cancer. In 157 paired breast cancer and adjacent normal samples, tumour suppressor gene GPER1 and miR-339 are both downregulated in Luminal A/B and Triple Negative Breast Cancer subtypes. Mechanistic investigations revealed that miR-339 upregulates GPER1 expression in breast cancer cells by switching on the GPER1 enhancer, which can be blocked by enhancer deletion through the CRISPR/Cas9 system. Collectively, our findings reveal novel mechanistic insights into TSG dysfunction in cancer development, and provide evidence that reactivation of TSG by enhancer switching may be a promising alternative strategy for clinical breast cancer treatment.
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Dissertations / Theses on the topic "Tumour suppressor genes; Breast cancer"

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Gornall, Robert J. "TP53 polymorphisms and haplotypes in breast, cervical and ovarian cancer." Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310562.

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Koreth, John. "Molecular pathology of breast carcinogenesis : the role of chromosome 11q mutations." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244718.

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Allinen, M. (Minna). "DNA damage response genes and chromosome 11q21-q24 candidate tumor suppressor genes in breast cancer." Doctoral thesis, University of Oulu, 2002. http://urn.fi/urn:isbn:9514267141.

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Abstract As the defects in DNA repair and cell cycle control are known to promote tumorigenesis, a proportion of inherited breast cancers might be attributable to mutations in the genes involved in these functions. In the present study, three such genes, TP53, CHK2 and ATM, which are also associated with known cancer syndromes, were screened for germline mutations in Finnish breast cancer patients. In combination with our previous results, three TP53 germline mutations, Tyr220Cys, Asn235Ser and Arg248Gln, were detected in 2.6% (3/108) of the breast cancer families. The only observed CHK2 alteration with a putative effect on cancer susceptibility, Ile157Thr, segregated ambiguously with the disease, and was also present in cancer-free controls. The available functional data, however, suggests that the altered CHK2 in some way promote tumorigenesis. Furthermore, compared to the other studied populations, Ile157Thr seems to be markedly enriched in Finland. Thus, the clinical significance of Ile157Thr requires further investigation among Finnish cancer patients. ATM germline mutations appear to contribute to a small proportion of the hereditary breast cancer risk, as two distinct ATM mutations, Ala2524Pro and 6903insA, were found among three families (1.9%, 3/162) displaying breast cancer. They all originated from the same geographical region as the AT families with the corresponding mutations, possibly referring to a founder effect concerning the distribution of these mutations in the Finnish population. The genes important for tumorigenesis in sporadic disease might also contribute to familial breast cancer. Therefore, four putative LOH targets genes in chromosome 11q21-q24 were screened for intragenic mutations, and five were analyzed for epigenetic inactivation in sporadic breast tumors. The lack of somatic intragenic mutations in MRE11A, PPP2R1B, CHK1 and TSLC1 led us next to investigate promoter region hypermethylation as a mechanism capable of silencing these genes, as well as the ATM gene. Only TSLC1 demonstrated involvement of CpG island methylation, which was especially prominent in three tumors. This suggests that together with LOH, methylation could result in biallelic inactivation of the TSLC1 gene in breast cancer.
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Sawan, Ali Sadek. "Tumour suppressor and anti-metastatic gene expression in human breast cancer : an immunohistochemical study." Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239797.

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Quinn, Jennifer E. "BRCA1 mediated G2/M cell cycle arrest in response to taxol." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326034.

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Ohta, Naomi. "Human umbilical cord matrix mesenchymal stem cells suppress the growth of breast cancer by expression of tumor suppressor genes." Thesis, Kansas State University, 2013. http://hdl.handle.net/2097/16730.

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Master of Science
Department of Anatomy and Physiology
Masaaki Tamura
Previous studies have shown that both human and rat umbilical cord matrix mesenchymal stem cells (UCMSC) possess the ability to control the growth of breast carcinoma cells. Comparative analysis of two types of UCMSC suggest that rat UCMSC-dependent growth regulation is significantly stronger than that of human UCMSC. Accordingly, the present study was designed to clarify their different tumoricidal abilities by analyzing gene expression profiles in two types of UCMSC. Gene expression profiles were studied by microarray analysis using Illumina HumanRef-8-V2 and RatRef-12 BeadChip for the respective UCMSC. The gene expression profiles were compared to untreated naïve UCMSC and those co-cultured with species-matched breast carcinoma cells; human UCMSC vs. MDA-231 human carcinoma cells and rat UCMSC vs. Mat B III rat carcinoma cells. The following selection criteria were used for the screening of candidate genes associated with UCMSC-dependent tumoricidal ability; 1) gene expression difference should be at least 1.5 fold between naive UCMSC and those co-cultured with breast carcinoma cells; 2) they must encode secretory proteins and 3) cell growth regulation-related proteins. These analyses screened 17 common genes from human and rat UCMSC. The comparison between the two sets of gene expression profiles identified that two tumor suppressor genes, adipose-differentiation related protein (ADRP) and follistatin (FST), were specifically up-regulated in rat UCMSC, but down-regulated in human UCMSC when they were co-cultured with the corresponding species’ breast carcinoma cells. The suppression of either protein by the addition of a specific neutralizing antibody in co-culture of rat UCMSC with Mat B III cells significantly abrogated UCMSC ability to attenuate the growth of carcinoma cells. Over-expression of both genes by adenovirus vector in human UCMSC enhanced their 4 ability to suppress the growth of MDA-231 cells. In the breast carcinoma lung metastasis model generated with MDA-231 cells, systemic treatment with FST-over-expressing human UCMSC significantly attenuated the tumor burden. These results suggest that both ADRP and FST may play important roles in exhibiting stronger tumoricidal ability in rat UCMSC than human UCMSC and imply that human UCMSC can be transformed into stronger tumoricidal cells by enhancing tumor suppressor gene expression.
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McGrath, Julie Elaine. "Genetic Screen Identifies Candidate Breast Cancer Tumor Dormancy Suppressor Genes Using Cellecta's Decipher Pooled shRNA Libraries." Thesis, State University of New York at Buffalo, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=1600789.

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Breast cancer cell dormancy is a significant clinical problem which contributes to the development of distant metastasis and disease relapse. Currently, no therapies exist which can effectively detect or eradicate dormant cancer cells.

In this study, we utilized a 3D co-culture dormancy model, recapitulating the inhibitory hematopoietic stem cell niche, which interacts with MDA-MB-231 cells, causing them to enter a state of growth arrest. The knockdown of emerging dormancy regulator gene, p38/MAPK14, in MDA-MB-231 cells allows previously dormant cells to “break” dormancy and re-enter the cell cycle when grown in the inhibitory niche. Using the newly described in vitro dormancy model, we performed a genomic shRNA library screen, and identified several p38-regulated breast cancer dormancy suppressor gene candidates. Two p38-regulated gene candidates were investigated further. Knockdown of transcription factors and p38 substrates, HBP1 and BHLHB3, in MDA-MB-231 cells lead to re-activation (proliferation) of once indolent cells when cultured in the inhibitory niche.

The present study illustrates the role of p38 and p38-regulated genes in breast cancer dormancy within the microenvironment of the inhibitory (endosteal) hematopoietic stem cell niche. Additionally, we have identified a list of ~700 breast cancer dormancy suppressor candidate genes. Further analysis and validation experiments are needed to classify novel molecular players and signaling pathways involved in tumor cell dormancy from the list of candidate genes generated in this study.

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Lu, Chi-Sheng. "The role of BRCA1/BARD1 in breast cancer a dissertation /." San Antonio : UTHSC, 2008. http://proquest.umi.com.libproxy.uthscsa.edu/pqdweb?did=1605126591&sid=11&Fmt=2&clientId=70986&RQT=309&VName=PQD.

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Dang, Raymond K. B. "Molecular detection of minimal residual disease in breast cancer and leukaemias using p53 tumour suppressor gene mutations as markers." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/22132.

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The use of peripheral blood progenitor cell (PBPC) transplantation is an important advance in the treatment of breast cancer and acute leukaemias, and these conditions are among the commonest indications for this procedure. Inevitably, there is concern that malignant cells may contaminate progenitor cell harvests and be re-infused during transplantation and cause disease relapse. Various methods are available for the detection of such minimal residual disease (MRD), and the key aim of this project was to evaluate the feasibility of using a tumour-specific marker, namely mutations within the p53 gene, for this purpose. This provided a useful model to assess the feasibility of using subtle genetic changes to detect MRD within PBPC harvests from patients with malignant diseases. The first step involved the use of denaturing gradient gel electrophoresis (DGGE) to screen original tumour tissues for mutations to be used as disease markers, in 5 individually PCR-amplified DNA fragments (A to E) covering exons 5 to 8 of p53. The technique was first optimised using cell lines known to contain p53 mutations in each fragment. Optimisation was performed with respect to electrophoresis temperature, time, voltage and polyacrylamide cross-linker. The sensitivity of DGGE in detecting a mutation in a mixed cell population was determined by diluting tumour cells in wild type (WT) cells. Although the presence of a mutation could be demonstrated when tumour cells occurred as 5% of total, a representation of at least 40% was required for the mutant homoduplex to be isolated for sequencing. Clinical samples studied were from 51 breast cancer patients, 38 of whom had metastatic disease or at high risk of metastasis, and 13 had high risk stage II/III disease randomised in a clinical study investigating PBPC transplantation and adjuvant therapy, and from 29 patients with acute leukaemias. A positive result was obtained in 14 of 51 primary breast cancer patients (1 was positive in 2 different fragments) and 3 of 29 patients with acute leukaemias.
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Milner, Ben J. "The role of tumour suppressor genes in ovarian cancer." Thesis, University of Aberdeen, 1993. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU555006.

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The role of tumour suppressor genes, in particular p53 and DCC, was investigated in human ovarian cancer. p53 codes for a DNA-binding nuclear phosphoprotein whose expression, in the wild-type form, is essential in the control of the cell cycle. Loss of function of this gene by mutation allows unrestrained cell proliferation to occur. The function of the DCC gene is not yet fully understood. A total of 29 malignant epithelial ovarian tumours, 15 of borderline malignancy, and 12 benign tumours were collected for study. Allele loss analysis confirmed that deletion of the p53 and DCC genes had occurred in 40&'37 and 41&'37 of the malignant tumours respectively. Two additional regions of loss were also identified at 17p13.3 (63&'37 ) and 17q23-qter (83&'37 ). Using SSCP analysis and direct DNA sequencing of exons 5 to 8, 52&'37 of the malignant tumours studied were found to have a p53 mutation. No mutations were found in any of the borderline or benign tumours. Immunocytochemical analysis of tissue sections from each of the tumours demonstrated that p53 over-expression had occurred in 55&'37 of the malignant tumours studied, and also in one of the borderline tumours. In total, 66&'37 of the malignant tumours were shown to have a p53 abnormality with either a mutation and/or protein over-expression. No correlation was found between any of the molecular abnormalities and either FIGO stage, the histopathological type of tumour, or the degree of tumour cell differentiation. However, a strong correlation was found between DCC allele loss and p53 mutation, and five out of six of the women whose tumours had both of these abnormalities died between 10 and 48 months after initial diagnosis. Finally, linkage analysis was carried out on a large breast/ovarian cancer family and it was confirmed that neither a mutation in the p53 gene nor a mutation in the DCC gene were responsible for the inherited predisposition to cancer.
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Books on the topic "Tumour suppressor genes; Breast cancer"

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Tumor suppressor genes in breast cancer. Hauppauge (NY), USA: Nova Publishers, 2008.

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Phillips, Stewart Mark Anthony. The loss of tumour suppressor genes in prostate cancer. Birmingham: University of Birmingham, 1995.

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Fabre, Aurélie. Immunostaining and DNA analysis of Wilms' tumour (WT1) suppressor gene in ductal carcinoma in situ (DCIS) of the breast: Thesis. 1998.

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Hodgkiss, Andrew. Introduction to cancer biology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0001.

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A brief introduction to cancer biology, aimed at psychiatrists, is offered. Selective DNA transcription, the cell cycle, receptor tyrosine kinases, and cell signalling pathways are introduced, using the EGFR/RAS/MAPK pathway as an exemplar. The molecular pathology of oncogenesis is summarized, including discussion of oncogenes, tumour suppressor genes, and examples of driver mutations. The exploitation of such mutations in stratified medicine, using molecularly targeted agents, is mentioned. Finally, Hanahan and Weinberg’s six hallmarks of cancer are listed, adding angiogenesis and metastasis to the picture of oncogenesis.
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Book chapters on the topic "Tumour suppressor genes; Breast cancer"

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Smith, Helene S. "Tumor-suppressor genes in breast cancer progression." In Cancer Treatment and Research, 79–96. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2592-9_5.

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Callahan, Robert. "The Role of Tumor Suppressor Genes in Breast Cancer Progression." In Endocrinology of Breast Cancer, 119–32. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-699-7_9.

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Uctepe, Eyyup, Muradiye Acar, Esra Gunduz, and Mehmet Gunduz. "Oncogenes and Tumor Suppressor Genes as a Biomarker in Breast Cancer." In Omics Approaches in Breast Cancer, 41–51. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-0843-3_3.

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Vigneri, Riccardo, and Ira D. Goldfine. "The biological and clinical roles of increased insulin receptors in human breast cancer." In Oncogenes and Tumor Suppressor Genes in Human Malignancies, 193–209. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3088-6_9.

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Zou, Zhiqiang, Anthony Anisowicz, Kristina Rafidi, and Ruth Sager. "Down Regulation of Candidate Tumor Suppressor Genes in Breast Cancer." In The Cell Cycle, 319–22. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_37.

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Steeg, Patricia S. "Suppressor genes in breast cancer: An overview." In Cancer Treatment and Research, 45–57. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3500-3_3.

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Jones, A. S. "Tumour Suppressor Genes and Head and Neck Cancer." In Advances in Oto-Rhino-Laryngology, 249–60. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000059071.

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Allred, D. Craig, Richard Elledge, Gary M. Clark, and Suzanne A. W. Fuqua. "The p53 tumor-suppressor gene in human breast cancer." In Cancer Treatment and Research, 63–77. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2592-9_4.

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Tripathy, Debasish, and Christopher C. Benz. "Activated oncogenes and putative tumor suppressor genes involved in human breast cancers." In Oncogenes and Tumor Suppressor Genes in Human Malignancies, 15–60. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3088-6_2.

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Spandidos, Demetrios A. "The Role of Oncogenes and Onco-Suppressor Genes in Human Breast Cancer." In Breast Cancer: Biological and Clinical Progress, 3–10. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3494-5_1.

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Conference papers on the topic "Tumour suppressor genes; Breast cancer"

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Jiang, Wenhao, and Qixuan Zhong. "Towards Quantifying Genetic Interactions Among Tumor Suppressor Genes in Breast Cancer." In ICBBE '19: 2019 6th International Conference on Biomedical and Bioinformatics Engineering. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3375923.3375935.

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Khan, Md Asaduzzaman, Meiling Zheng, and Junjiang Fu. "Abstract 3834: Epigenetic modification of oncogenes or tumor suppressor genes by thymoquinone in triple negative breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3834.

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Khan, Md Asaduzzaman, Meiling Zheng, and Junjiang Fu. "Abstract 3834: Epigenetic modification of oncogenes or tumor suppressor genes by thymoquinone in triple negative breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3834.

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Chimonidou, Maria, Areti Strati, Nikos Malamos, Vassilis Georgoulias, and Evi Lianidou. "Abstract 4813: DNA methylation of tumor suppressor and metastasis suppressor genes in primary tumors, circulating tumor cells and cell free DNA in the same breast cancer patients." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4813.

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Liu, Zhongfa, Liping Du, Shujun Liu, Zhiliang Xie, Xiaokui Mo, Jianhua Yu, Lai-chu Wu, et al. "Abstract 581: Complementary reactivation of tumor suppressor genes in breast cancer cells by curcumin and curcumin O-glucuronide." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-581.

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Thomas, Margaret, Krysta Coyle, Mohammad Sultan, Luzhe Pan, Dae-Gyun Ahn, Patrick Lee, Carman Giacomantonio, and Paola Marcato. "Abstract P1-06-02: Identifying hypermethylated tumor suppressor genes in breast cancer with an in vivo total genome knockdown screen." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p1-06-02.

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van Diest, P., C. Moelans, H. Monsuur, and R. de Weger. "Quantitative Copy Number Analysis of Onco- and Tumor Suppressor Genes in Invasive Breast Cancer by Dedicated Multiplex Ligation-Dependent Probe Amplification." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5168.

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NouriEmamzadeh, Fatemeh, Beverly Word, Ebony Cotton, Kai Littlejohn, Gustavo Miranda-Carboni, and Beverly Lyn-Cook. "Abstract 5196: Vorinostat exhibits anticancer effects through modulation of nuclear receptors and tumor suppressor genes in sub-types of triple negative breast cancer cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5196.

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NouriEmamzadeh, Fatemeh, Beverly Word, Ebony Cotton, Kai Littlejohn, Gustavo Miranda-Carboni, and Beverly Lyn-Cook. "Abstract 5196: Vorinostat exhibits anticancer effects through modulation of nuclear receptors and tumor suppressor genes in sub-types of triple negative breast cancer cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-5196.

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Alvarez, Carolina, Teresa Tapia, Valeria Cornejo, Andres Aravena, Wanda Fernandez, Manuel Alvarez, Mauricio Camus, Alejandro Maass, and Pilar Carvallo. "Abstract 5077: Array CGH genomic profile of hereditary breast cancer tumors: Identification of tumor suppressor genes in deleted regions, determination of promoter hypermethylation and their protein expression in tumor biopsies." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5077.

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Reports on the topic "Tumour suppressor genes; Breast cancer"

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Hamaguchi, Masaaki. Cloning of Tumor Suppressor Genes in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada415804.

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Hamaguchi, Masaaki. Cloning of Tumor Suppressor Genes in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada425534.

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Qi, Chao. Identification of Novel Tumor Suppressor Genes for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada453400.

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Goate, Alison M. Tumor Suppressor Genes in Early Breast Cancer and its Progression. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada383203.

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Magee, Kendra P. Methylation of Select Tumor Suppressor Genes in Sporadic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada374288.

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To, Minh D. Characterization of Putative Proto-Oncogenes and Tumor Suppressor Genes that are Transcriptionally Deregulated in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada383235.

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To, Minh. Characterization of Putative Proto-Oncogenes and Tumor Suppressor Genes That Are Transcriptionally Deregulated in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada392990.

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Johnstone, Cameron N. Identification of Novel Tumor Suppressor Genes in Human Breast Cancer Using Nonsense-Mediated mRNA Decay Inhibition (NMDI)-Microarray Analysis. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada486033.

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Clarke, Robert, and Yuelin Zhu. Suppressor Genes in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada384057.

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Clarke, Robert R. Suppressor Genes in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada405468.

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