The DOI matches its Crossref record; 39 of the 41 references it cites were found in a registry or an index.
Promoter Hypermethylation and BRCA1 Inactivation in Sporadic Breast and Ovarian Tumors
Abstract
BACKGROUND: Inherited mutations in the BRCA1 gene may be responsible for almost half of inherited breast carcinomas. However, somatic (acquired) mutations in BRCA1 have not been reported, despite frequent loss of heterozygosity (LOH or loss of one copy of the gene) at the BRCA1 locus and loss of BRCA1 protein in tumors. To address whether BRCA1 may be inactivated by pathways other than mutations in sporadic tumors, we analyzed the role of hypermethylation of the gene's promoter region. METHODS: Methylation patterns in the BRCA1 promoter were assessed in breast cancer cell lines, xenografts, and 215 primary breast and ovarian carcinomas by methylation-specific polymerase chain reaction (PCR). BRCA1 RNA expression was determined in cell lines and seven xenografts by reverse transcription-PCR. P values are two-sided. RESULTS: The BRCA1 promoter was found to be unmethylated in all normal tissues and cancer cell lines tested. However, BRCA1 promoter hypermethylation was present in two breast cancer xenografts, both of which had loss of the BRCA1 transcript. BRCA1 promoter hypermethylation was present in 11 (13%) of 84 unselected primary breast carcinomas. BRCA1 methylation was strikingly associated with the medullary (67% methylated; P =.0002 versus ductal) and mucinous (55% methylated; P =.0033 versus ductal) subtypes, which are overrepresented in BRCA1 families. In a second series of 66 ductal breast tumors informative for LOH, nine (20%) of 45 tumors with LOH had BRCA1 hypermethylation, while one (5%) of 21 without LOH was methylated (P =.15). In ovarian neoplasms, BRCA1 methylation was found only in tumors with LOH, four (31%) of 13 versus none of 18 without LOH (P =.02). The BRCA1 promoter was unmethylated in other tumor types. CONCLUSION: Silencing of the BRCA1 gene by promoter hypermethylation occurs in primary breast and ovarian carcinomas, especially in the presence of LOH and in specific histopathologic subgroups. These findings support a role for this tumor suppressor gene in sporadic breast and ovarian tumorigenesis.
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“Given that changes in BRCA1 promoter status contribute to sporadic tumors [64,65], mutations outside the reading frame or changes in promoter methylation status could alter FANCJ expression and contribute to tumorigenesis.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [65]
In the citing paper
“Given that changes in BRCA1 promoter status contribute to sporadic tumors [64,65], mutations outside the reading frame or changes in promoter methylation status could alter FANCJ expression and contribute to tumorigenesis.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [65]
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“BRCA1 overexpression in leukoplakia followed by subsequent underexpression in tongue squamous cell carcinoma was also already described [26].”
BackgroundInfluentialClinicopathological Correlates of γδ T Cell Infiltration in Triple-Negative Breast Cancer
Boissière‐Michot, F., Chabab, G., Mollévi, C., Guiu, S., Lopez‐Crapez, E., Ramos, J., Bonnefoy, N., Lafont, V., & Jacot, W. (2021) · Cancers · doi:10.3390/cancers13040765 · Cited by 28
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“BRCA1 mutation accounts for nearly half of familial breast cancers (OMIM 604370), but BRCA1 is also down-regulated in sporadic breast tumors without germline mutation [12].”
BackgroundLack of Germ-Line Promoter Methylation in BRCA1 -Negative Families with Familial Breast Cancer
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“An epigenetic dysfunction in the BRCA1 pathway has been hypothesized to facilitate sporadic BLBC, and BRCA1 gene promoter methylation has been implicated in over 60% of medullary and metaplastic breast cancers of basal-like phenotype [111].”
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“In the Krasteva et al (22) and Ignatov et al (21) studies, which found a better clinical prognosis in patients with BRCA1 promoter methylation, they used Baldwin's primer (30) while others used Esteller's primer (31).”
Site-Specific DNA Demethylation as a Potential Target for Cancer Epigenetic Therapy
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“In breast and ovarian cancers, BRCA1 is inactivated by hypermethylation within the promoter region of the gene [8].”
BackgroundPoly (ADP-Ribose) Polymerase Inhibitor Hypersensitivity in Aggressive Myeloproliferative Neoplasms
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435 Candidate biomarkers of PARP inhibitor sensitivity in ovarian cancer beyond the BRCA genes
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“Whilst the former is more often seen in metaplastic and medullary cancers, the latter seems to be more prevalent in invasive ductal carcinomas of TNP [52,55,56] .”
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“For the detection of BRCA1 and MGMT methylation, we used the MSP primers from previous studies [49,50] after performing all of the optimization steps for real-time MSP; for the detection of CST6 and USP44 methylation, we used the real-time MSP assays that we previously developed and validated [46,48].”
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Epigenetic targeting in breast cancer: Therapeutic impact and future direction
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Validation and Implementation of BRCA1/2 Variant Screening in Ovarian Tumor Tissue
de Jonge, M. M., Ruano, D., van Eijk, R., van der Stoep, N., Nielsen, M., Wijnen, J., ter Haar, N. T., Baalbergen, A., Bos, M. E. M. M., Kagie, M. J., et al. (2018) · Journal of Molecular Diagnostics · doi:10.1016/j.jmoldx.2018.05.005 · Cited by 27
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HRness in Breast and Ovarian Cancers
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“Next, the combination of a PARPi (Veliparib) with carboplatin in addition to standard neoadjuvant chemotherapy with Docetaxel was evaluated in the BrighTNess trial, a phase III randomized study that included stage II–III TNBC.”
BackgroundInfluentialCommon Molecular Mechanisms of Mammary Gland Development and Breast Cancer
Mullan, P. B., & Millikan, R. C. (2007) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-007-7389-z · Cited by 24
Prognostic significance of the allelic loss of the BRCA1 gene in colorectal cancer
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“To estimate PCR sensitivity, titrated experiments were done using known amounts of methylated, genomic positive control DNA (1 Ag to 100 pg) spiked in unmethylated T47D genomic DNA for a total of 1 Ag (24).”
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Studying Therapy Response and Resistance in Mouse Models for BRCA1-Deficient Breast Cancer
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“BRCA1 inactivation by promoter hypermethylation is found in 13% of all primary breast cancers [20] and may in part explain why TNBC rarely harbor BRCA1 mutations, yet present with BRCA1 dysfunction [21].”
BackgroundThe Clinical and Pathological Profile of BRCA1 Gene Methylated Breast Cancer Women: A Meta-Analysis
Ruscito, I., Gasparri, M. L., Marco, M. P. D., Costanzi, F., Besharat, A. R., Papadia, A., Kuehn, T., Gentilini, O., Bellati, F., & Caserta, D. (2021) · Cancers · doi:10.3390/cancers13061391 · Cited by 26
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“An interesting example comes from ovarian cancer, where BRCA mutation was found to be related to platinum response, in contrast to tumors with hypermethylation of the BRCA promoter [113].”
Background“Targeting” Triple-Negative Breast Cancer: The Lessons Learned From BRCA1-Associated Breast Cancers
Nanda, R. (2011) · Seminars in Oncology · doi:10.1053/j.seminoncol.2011.01.007 · Cited by 24
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Myricetin Apoptotic Effects on T47D Breast Cancer Cells is a P53-Independent Approach
Soleimani, M., & Sajedi, N. (2020) · Asian Pacific Journal of Cancer Prevention · doi:10.31557/apjcp.2020.21.12.3697 · Cited by 23
“BRCA1 is a tumor suppressor gene that its expression is usually reduced or absent in approximately 30% of sporadic cases (Esteller et al., 2000; Yang et al., 2001).”
BackgroundCD81, a cell cycle regulator, is a novel target for histone deacetylase inhibition in glioma cells
Gensert, J. M., Baranova, O. V., Weinstein, D. E., & Ratan, R. R. (2007) · Neurobiology of Disease · doi:10.1016/j.nbd.2007.03.008 · Cited by 23
Xie, T., Dickson, K.-A., Yee, C., Ma, Y., Ford, C. E., Bowden, N. A., & Marsh, D. J. (2022) · Cancers · doi:10.3390/cancers14194621 · Cited by 26
“Methylation of the BRCA1 promoter that silences BRCA1 gene expression has been reported in ovarian cancer tissue [8,20,125].”
BackgroundEpigenetic mechanisms involved in melanoma pathogenesis and chemoresistance.
Martínez‐Cardús, A., Vizoso, M., Morán, S., & Manzano, J. L. (2015) · Europe PMC (PubMed Central) · doi:10.3978/j.issn.2305-5839.2015.06.20 · Cited by 24
“Epigenetic inactivation of particular tumor suppressor genes has been extensively implicated in tumor initiation, promotion and progression (2-6).”
BackgroundUK BRCA mutation testing in patients with ovarian cancer
George, A. J. (2015) · British Journal of Cancer · doi:10.1038/bjc.2015.396 · Cited by 22
“…been reported in DNA repair genes in approximately 9% of ovarian cancer, while BRCA1 promoter hypermethylation is reported in approximately 10% of high-grade serous and high-grade endometrioid ovarian cancer (Esteller et al, 2000; Cancer Genome Atlas Research Network, 2011; Pennington et al, 2014).”
BackgroundLalchungnunga, H., Hao, W., Maris, J. M., Asgharzadeh, S., Henrich, K., Westermann, F., Tweddle, D. A., Schwalbe, E. C., & Strathdee, G. R. (2022) · British Journal of Cancer · doi:10.1038/s41416-022-01988-z · Cited by 22
“A number of studies have identified potentially important tumour suppressor genes that are frequently inactivated due to promoter hypermethylation [9, 10].”
BackgroundEZH2-mediated epigenetic repression of DNA repair in promoting breast tumor initiating cells
Stefánsson, Ó. A., & Esteller, M. (2011) · Breast Cancer Research · doi:10.1186/bcr2871 · Cited by 22
“In breast cancer, epigenetic inactivation of the BRCA1 gene occurs through CpG island hypermethylation [ 14 ,15].”
Self-citationRzepecka, I. K., Szafron, L. M., Styś, A., Bujko, M., Plisiecka-Hałasa, J., Mądry, R., Osuch, B., Markowska, J., Bidziński, M., & Kupryjańczyk, J. (2012) · Cancer Genetics · doi:10.1016/j.cancergen.2011.12.005 · Cited by 22
Turnover of BRCA1 Involves in Radiation-Induced Apoptosis
Liu, W., Zong, W., Wu, G. Y., Fujita, T., Li, W., Wu, J. Q., & Wan, Y. (2010) · PLoS ONE · doi:10.1371/journal.pone.0014484 · Cited by 24
“Quantitative assessments of cDNA amplification for BRCA1 [35] and the internal reference gene 18S were performed by a fluorescence-based real-time detection method (Biorad, Munchen, Germany) and the SYBR Green SuperMIX (Biorad).”
MethodFounder mutation in the BRCA1 gene in Malay breast cancer patients from Singapore
Lee, A. S. G., Ho, G., Oh, P. C., Balram, C., Ooi, L. L., Lim, D. T. H., Wong, C. Y., & Hong, G. S. (2003) · Human Mutation · doi:10.1002/humu.9162 · Cited by 22
“%) cases, which is low compared to the frequencies of 11% to 16% detected in other studies from the United States (Rice et al., 1998; Esteller et al., 2000; Rice et al., 2000), United Kingdom (Catteau et al., 1999) and Australia (Bianco et al., 2000).”
MethodResultEnvironmental Factors, Genes, and the Development of Human Cancers
Roy, D., & Dorak, M. T. (2010) · Springer eBooks · doi:10.1007/978-1-4419-6752-7 · Cited by 22
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“…methylation of the BRCA1 promoter was detected in 11%–60% of sporadic breast tumors, correlating closely with low BRCA1 mRNA levels (Magdinier et al. 1998; Rice et al. 1998; Catteau et al. 1999; Esteller et al. 2000; Matros et al. 2005; Wei et al. 2005; Turner et al. 2007; Hsu et al. 2013).”
BackgroundLi, A., & Meyre, D. (2014) · Current Psychiatry Reviews · doi:10.2174/1573400510666140630170549 · Cited by 23
“For examples, methylation of tumor suppressor gene BRCA1 is associated with breast cancer, and inactivated DNA repair gene MGMT is associated with glioblastomas [127, 128].”
BackgroundAberrant epigenetic and transcriptional events associated with breast cancer risk
Marino, N., German, R., Podicheti, R., Rusch, D. B., Rockey, P., Huang, J., Sandusky, G. E., Temm, C. J., Althouse, S. K., Nephew, K. P., et al. (2022) · Clinical Epigenetics · doi:10.1186/s13148-022-01239-1 · Cited by 21
“Hypermethylation in specific gene promoters is indeed linked to 31 carcinogenesis through transcriptional silencing of tumor suppressor genes or regulatory regions within the 32 genome leading to dysregulation of cell growth, cancer initiation and progression (55-57).”
BackgroundSuper-enhancer-associated gene CAPG promotes AML progression
Ma, Q., Zhao, M., Long, B., & Li, H. (2023) · Communications Biology · doi:10.1038/s42003-023-04973-1 · Cited by 21
BRCA1-related gene signature in breast cancer the role of ER status and molecular type
Lisowska, K. M. (2010) · Frontiers in Bioscience-Elite · doi:10.2741/e227 · Cited by 21
Chromatin Remodeling Agents for Cancer Therapy
Dario, L., Rosa, M., Mariela, E., Roberto, G., & Cinti, C. (2008) · Reviews on Recent Clinical Trials · doi:10.2174/157488708785700320 · Cited by 22
“, colon and stomach) [24], whereas GSTP1 is characteristic of steroid-related neoplasm such as breast, liver, and prostate [25, 26].”
BackgroundTrials With Impact on Clinical Management
Bookman, M. A. (2009) · International Journal of Gynecological Cancer · doi:10.1111/igc.0b013e3181c36ea0 · Cited by 21
Candidate Gene DNA Methylation Associations with Breast Cancer Characteristics and Tumor Progression
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Resistance to cis- and carboplatin initiated by epigenetic changes in ovarian cancer patients
Schwarzenbach, H., & Gahan, P. B. (2019) · Cancer Drug Resistance · doi:10.20517/cdr.2019.010 · Cited by 20
“In many cancers, including ovarian cancer, a decrease in the global methylation of the heterochromatic chromosome regions results in the activation of a number of oncogenes, whilst the locus-specific hypermethylation of specific CpG island regions associated with promoters of tumor suppressor genes results in their in…”
BackgroundScumaci, D., Tammè, L., Fiumara, C. V., Pappaianni, G., Concolino, A., Leone, E., Faniello, M. C., Quaresima, B., Ricevuto, E., Costanzo, F. S., et al. (2015) · PLoS ONE · doi:10.1371/journal.pone.0129762 · Cited by 21
“Moreover, the occurrence of a BRCA1-like gene expression profile in sporadic BC due to methylation-mediated silencing, highlights the need for the use of subjects with analogous gene expression profiling [39].”
BackgroundModel of transcriptional regulation of the BRCA1–NBR2 bi-directional transcriptional unit
Suen, T.-C., Tang, M., & Goss, P. E. (2005) · Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression · doi:10.1016/j.bbaexp.2005.01.014 · Cited by 23
Multipoint methylation and expression analysis of tumor suppressor genes in human renal cancer cells
Kawakami, T., Okamoto, K., Ogawa, O., & Okada, Y. (2003) · Urology · doi:10.1016/s0090-4295(02)02110-6 · Cited by 21
Circulating nucleic acids as a tumor marker.
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Targeting Homologous Recombination Repair in Cancer
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Quesada, S., Fabbro, M., & Solassol, J. (2022) · Cancers · doi:10.3390/cancers14051132 · Cited by 21
“Indeed, BRCA1 promoter methylation (-CpG+) has been characterized for decades [36].”
BackgroundOubaddou, Y., Oukabli, M., Fenniche, S., Elktaibi, A., Elochi, M. R., Bouzidi, A. A., Qmichou, Z., Dakka, N., Diorio, C., Richter, A. M., et al. (2023) · Genes · doi:10.3390/genes14091680 · Cited by 20
“[24], the sense of primers U binds to the 1536 bp position of the GenBank sequence “U37574,” while the sense of primers M binds to the 1543 bp position of the same sequence [24] (Figure 1a).”
BackgroundMethodInfluentialRadosa, M. P., Häfner, N., Camara, O., Diebolder, H., Mothes, A. R., Winzer, H., Jansen, L., Dürst, M., & Runnebaum, I. B. (2011) · International Journal of Gynecological Cancer · doi:10.1097/igc.0b013e318227c990 · Cited by 20
GPER Promoter Methylation Controls GPER Expression in Breast Cancer Patients
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“One example is the methylation of the tumor suppressor gene BRCA1 (18) in breast and ovarian cancers.”
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Unraveling Breast Cancer Heterogeneity Through Transcriptomic and Epigenomic Analysis
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“Both BRCA1 and ESR1 gene methylation are also associated with medullary breast cancer, a histologic special type prevalent in BRCA1 carriers.(69,72) Expression microarray and CGH have determined that medullary breast cancer is a distinct genomic subgroup of BLBC.”
BackgroundZhai, L., Li, S., Li, H., Zheng, Y., Lang, R., Fan, Y., Gu, F., Guo, X., Zhang, X., & Fu, L. (2015) · Europe PMC (PubMed Central) · Cited by 20
Integrated genomic analyses of ovarian carcinoma
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“Raphael(28), Fabio Vandin(28), Peter W.”
Molecular Targeted Therapy in Ovarian Cancer
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ZNF350 promoter methylation accelerates colon cancer cell migration
Tanaka, H., Kuwano, Y., Nishikawa, T., Rokutan, K., & Nishida, K. (2018) · Oncotarget · doi:10.18632/oncotarget.26353 · Cited by 20
“This mechanism is highly prevalent and well-illustrated by the hyper-methylation of the promoters of RB1 in retinoblastoma [7], of the MLH1 promoter in colon cancer [8, 9], and of the BRCA1 promoter in breast cancer [10].”
BackgroundHarada, H., Miyamoto, K., Yamashita, Y., Nakano, K., Taniyama, K., Miyata, Y., Ohdan, H., & Okada, M. (2013) · Cancer · doi:10.1002/cncr.27754 · Cited by 19
“Germline mutations in the breast cancer susceptibility gene 1 (BRCA1) elevate the risk of breast and ovarian cancer development;(12) hypermethylation of the BRCA1 promoter has been demonstrated in sporadic breast and ovarian cancers.(13,14) It is now known that BRCA1 is a tumor suppressor gene that encodes a multifunc…”
BackgroundThike, A. A., Tan, P. H., Ikeda, M., & Iqbal, J. (2015) · Histopathology · doi:10.1111/his.12801 · Cited by 19
Cancer gene discovery in mouse and man
Mattison, J., van der Weyden, L., Hubbard, T., & Adams, D. J. (2009) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2009.03.001 · Cited by 21
Nair, R., Kumar, J., Jose, J., Somasundaram, V., Hemalatha, S., Sengodan, S., Nadhan, R., Anilkumar, T., & Srinivas, P. (2016) · Scientific Reports · doi:10.1038/srep26631 · Cited by 18
Scott, C. M., Joo, J.-H. E., O’Callaghan, N., Buchanan, D. D., Clendenning, M., Giles, G. G., Hopper, J. L., Wong, E. M., & Southey, M. C. (2016) · PLoS ONE · doi:10.1371/journal.pone.0165436 · Cited by 19
Aberrant DNA methylation defines isoform usage in cancer, with functional implications
Chen, Y.-C., & Elnitski, L. L. (2019) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1007095 · Cited by 19
Genta, S., Martorana, F., Stathis, A., & Colombo, I. (2021) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2021.103539 · Cited by 20
Gonzalo, V., Castellvı́-Bel, S., Balaguer, F., Pellisé, M., Ocaña, T., & Castells, A. (2008) · Gastroenterología y Hepatología · doi:10.1157/13114573 · Cited by 19
Simon-Kayser, B., Scoul, C., Renaudin, K., Jézéquel, P., Bouchot, O., Rigaud, J., & Bezieau, S. (2005) · Genes Chromosomes and Cancer · doi:10.1002/gcc.20170 · Cited by 19
“This is particularly true for ‘‘caretaker’’ tumor-suppressor genes such as the BRCA1 gene, which does not show point mutations in sporadic breast cancer (Esteller et al., 2000).”
BackgroundLympho-vascular invasion in BRCA related breast cancer compared to sporadic controls
van Voss, M. R. H., van der Groep, P., Bart, J., van der Wall, E., & van Diest, P. J. (2010) · BMC Cancer · doi:10.1186/1471-2407-10-145 · Cited by 20
“922% of sporadic breast cancers have been described to show promoter hypermethylation of BRCA1 or loss of heterozygosity at the BRCA1 locus and these tumors are largely ER and PR negative, of ductal and medullary type, and high grade [48-52].”
Mammary gland biology and breast cancer
McGee, S. F., Lanigan, F. T., Gilligan, E., & Groner, B. (2006) · EMBO Reports · doi:10.1038/sj.embor.7400839 · Cited by 19
Nhukeaw, T., Hongthong, K., Dyson, P. J., & Ratanaphan, A. (2019) · APOPTOSIS · doi:10.1007/s10495-019-01544-w · Cited by 19
Methods for Analysis of DNA Methylation
Dobrovic, A. (2006) · Humana Press eBooks · doi:10.1385/1-59259-928-1:149 · Cited by 19
Methylation Profile of BRCA1, RASSF1A and ER in Vietnamese Women with Ovarian Cancer
Lan, V. T. T., Thuan, T. B., Thu, D. M., Uyển, N. Q., Ha, N. T., & To, T. V. (2013) · Asian Pacific Journal of Cancer Prevention · doi:10.7314/apjcp.2013.14.12.7713 · Cited by 18
Effect of DNA Methylation on the Development of Cancer
Holčáková, J. (2018) · Klinicka onkologie · doi:10.14735/amko20182s41 · Cited by 20
Metadata
- Authors
- Esteller, M.
- Affiliations
- Roswell Park Comprehensive Cancer Center (US)
- Corresponding author
- Esteller, M.
- ORCID
- Esteller, M.
- Venue
- Journal of the National Cancer Institute
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-04-05
- Volume
- 92
- Issue
- 7
- Pages
- 564-569
- ISSN
- 0027-8874 (ISSN-L)
- 1460-2105
- OpenAlex
- W2160234594
- Cited by
- 1,233
- References
- 41
- Citations by year
- 2026: 20 · 2025: 33 · 2024: 37 · 2023: 46 · 2022: 49 · 2021: 40 · 2020: 53 · 2019: 43 · 2018: 60 · 2017: 48 · 2016: 52 · 2015: 69 · 2014: 56 · 2013: 57 · 2012: 69
- FWCI
- 22.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- JNCI Journal of the National Cancer Institute (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Funders
- National Cancer Institute (R01CA043318, CA 43318)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Health Sciences › Medicine › Pathology and Forensic Medicine › Breast Lesions and Carcinomas
- Keywords
- BRCA1 promoter hypermethylation, sporadic breast cancer, ovarian cancer, loss of heterozygosity, gene silencing, tumor suppressor, medullary breast carcinoma, mucinous breast carcinoma, histological subtypes, epigenetic silencing, breast cancer xenografts
- MeSH terms
- Breast Neoplasms, Female, Humans, Methylation, Ovarian Neoplasms, Promoter Regions, Genetic, RNA, RNA, Neoplasm, Transplantation, Heterologous, Tumor Cells, Cultured, Gene Expression Regulation, Neoplastic, Carcinoma, Ductal, Breast, Genes, BRCA1, Loss of Heterozygosity, Reverse Transcriptase Polymerase Chain Reaction
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