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1. Frizzell KM, Kraus WL: PARP inhibitors and the treatment of breast cancer: beyond BRCA1/2? Breast Cancer Res; 2009;11(6):111
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PARP inhibitors and the treatment of breast cancer: beyond BRCA1/2?
  • Poly(ADP-ribose) polymerase (PARP) inhibitors have been explored as therapeutic agents for the treatment of hereditary breast and ovarian cancers harboring mutations in BRCA1 or BRCA2.
  • In a new study, Inbar-Rozensal and colleagues show that phenanthridine-derived PARP inhibitors promote cell cycle arrest and cell death in breast cancer cells lacking BRCA1 and BRCA2 mutations and prevent the growth of tumors from xenografts of these cells in immunocompromised mice.
  • These results suggest a potential broader utility of PARP-1 inhibitors in the treatment of breast cancer, although further mechanistic studies are needed.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Enzyme Inhibitors / pharmacology. Genes, BRCA1. Genes, BRCA2. Phenanthridines / pharmacology. Poly(ADP-ribose) Polymerase Inhibitors

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  • [CommentOn] Breast Cancer Res. 2009;11(6):R78 [19891779.001]
  • (PMID = 20017885.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK069710
  • [Publication-type] Comment; Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Phenanthridines; 0 / Poly(ADP-ribose) Polymerase Inhibitors; EC 2.4.2.30 / PARP1 protein, human
  • [Other-IDs] NLM/ PMC2815546
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2. de Plater L, Laugé A, Guyader C, Poupon MF, Assayag F, de Cremoux P, Vincent-Salomon A, Stoppa-Lyonnet D, Sigal-Zafrani B, Fontaine JJ, Brough R, Lord CJ, Ashworth A, Cottu P, Decaudin D, Marangoni E: Establishment and characterisation of a new breast cancer xenograft obtained from a woman carrying a germline BRCA2 mutation. Br J Cancer; 2010 Oct 12;103(8):1192-200
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  • [Title] Establishment and characterisation of a new breast cancer xenograft obtained from a woman carrying a germline BRCA2 mutation.
  • BACKGROUND: The BRCA2 gene is responsible for a high number of hereditary breast and ovarian cancers, and studies of the BRCA2 biological functions are limited by the lack of models that resemble the patient's tumour features.
  • The aim of this study was to establish and characterise a new human breast carcinoma xenograft obtained from a woman carrying a germline BRCA2 mutation.
  • METHODS: A transplantable xenograft was obtained by grafting a breast cancer sample into nude mice.
  • The biological and genetic profiles of the xenograft were compared with that of the patient's tumour using histology, immunohistochemistry (IHC), BRCA2 sequencing, comparative genomic hybridisation (CGH), and qRT-PCR.
  • RESULTS: Histological profile identified the tumour as a basal-like triple-negative breast cancer.
  • Targeted BRCA2 DNA sequencing of the xenograft showed the presence of the mutation previously identified in the carrier.
  • The therapeutic assessment of the xenograft showed sensitivity to anthracyclin-based chemotherapy and resistance to docetaxel.
  • The xenograft was also highly sensitive to radiotherapy and cisplatin-based treatments.
  • CONCLUSIONS: This study describes a new human breast cancer xenograft obtained from a BRCA2-mutated patient.
  • This xenograft provides a new model for the pre-clinical drug development and for the exploration of the drug response biological basis.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Genes, BRCA2. Germ-Line Mutation
  • [MeSH-minor] Adult. Animals. Anthracyclines / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Culture Techniques. Cell Line, Tumor. Comparative Genomic Hybridization. DNA Mutational Analysis. Female. Heterozygote. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous. Xenograft Model Antitumor Assays / methods

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  • (PMID = 20877358.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines
  • [Other-IDs] NLM/ PMC2967069
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3. Lux MP, Fasching PA, Beckmann MW: Hereditary breast and ovarian cancer: review and future perspectives. J Mol Med (Berl); 2006 Jan;84(1):16-28
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  • [Title] Hereditary breast and ovarian cancer: review and future perspectives.
  • Breast cancer (BC) is the most frequent carcinoma in women.
  • The cumulative risk for the disease is 10% up to the age of 80 years.
  • A familial history of BC and ovarian cancer (OC) is a significant risk factor.
  • Some 5-10% of all cases of BC and 25-40% of cases in patients under the age of 35 years have a hereditary origin.
  • BRCA1/BRCA2 mutations are responsible for 3-8% of all cases of BC and 30-40% of familial cases.
  • About 80% of families with a history of OC have BRCA1 mutations, while 15% have BRCA2 mutations.
  • Women at risk can receive counseling from interdisciplinary cancer genetics clinics, while those at high risk can receive genetic testing.
  • Risk calculation programs can define the risks and assist in decision making for genetic testing and clinical options.
  • Clinical options require information on the risks of the disease and its mutation status.
  • It is not currently known whether intensified early cancer detection is individually beneficial, but this is currently the option that is the least invasive and least burdensome to the patient.
  • Although hereditary BC has different pathological characteristics and the BRCA mutation is an independent negative prognostic factor, there are currently no special treatment guidelines.
  • Without adjuvant hormone therapy or chemotherapy, the overall survival in BRCA mutation carriers is reduced.
  • Chemotherapy regimens involving platinum are particularly beneficial in the treatment of hereditary BC.
  • [MeSH-major] Breast Neoplasms / genetics. Genetic Predisposition to Disease. Ovarian Neoplasms / genetics
  • [MeSH-minor] BRCA1 Protein. BRCA2 Protein. Female. Genetic Counseling. Humans. Prognosis. Risk Factors. Syndrome


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4. Roukos DH, Briasoulis E: Individualized preventive and therapeutic management of hereditary breast ovarian cancer syndrome. Nat Clin Pract Oncol; 2007 Oct;4(10):578-90
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  • [Title] Individualized preventive and therapeutic management of hereditary breast ovarian cancer syndrome.
  • Life-saving, risk-reducing medical interventions are required for women with a BRCA1/2 mutation.
  • Genetic counseling should be offered at specialized familial breast-cancer clinics and gene-mutation analysis should be recommended on the basis of personal and family-history-based risk criteria.
  • Tamoxifen is an alternative approach only for BRCA2 mutation carriers.
  • The comprehensive, clinical decision-making Ioannina algorithm provided here can facilitate the complex preventive strategic approach.
  • Newly diagnosed BRCA1/2 carriers might benefit from extensive surgery and a specific pharmacological treatment, but data to support this strategy are limited.
  • Microarray gene-expression studies show that breast tumors from BRCA1 carriers are predominantly of basal subtype (i.e. triple negative) and BRCA2 carriers are of luminal subtype (i.e. estrogen-receptor-positive).
  • Although optimum management of women with familial susceptibility to breast and ovarian cancer has not yet been prospectively validated, data indicate substantial benefits when an individualized evidence-based prevention strategy is provided by an experienced team.
  • [MeSH-major] Breast Neoplasms / genetics. Genetic Predisposition to Disease. Neoplastic Syndromes, Hereditary / prevention & control. Ovarian Neoplasms / genetics
  • [MeSH-minor] Female. Genes, BRCA1. Genes, BRCA2. Genetic Counseling. Genetic Testing. Humans. Mastectomy. Ovariectomy. Tamoxifen / therapeutic use


5. Zhou C, Smith JL, Liu J: Role of BRCA1 in cellular resistance to paclitaxel and ionizing radiation in an ovarian cancer cell line carrying a defective BRCA1. Oncogene; 2003 Apr 24;22(16):2396-404
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  • [Title] Role of BRCA1 in cellular resistance to paclitaxel and ionizing radiation in an ovarian cancer cell line carrying a defective BRCA1.
  • BRCA1, the gene responsible for approximately half of all cases of hereditary breast cancer and almost all cases of combined hereditary breast and ovarian cancer, has been implicated in the maintenance of genomic stability through DNA repair.
  • This function is mediated, at least in part, through two tandem BRCA1 C-terminal (BRCT) repeats.
  • The role of BRCA1 in the development of ovarian cancer is poorly understood, partially owing to the lack of ovarian cancer cell lines with defective BRCA1.
  • The purpose of this study was to further characterize an endometrioid ovarian cancer cell line, SNU-251, which was previously reported to carry a nonsense mutation (from G to A) at amino acid 1815 of BRCA1.
  • In addition, we examined the role of BRCA1 in the cell cycle and in the responses to the chemotherapy drug paclitaxel and ionizing radiation.
  • Loss of the C-terminal 49 amino acids due to this point mutation did not affect the expression of the truncated BRCA1 protein, but caused a loss of transcriptional activation of the endogenous p21(WAF1/CIP1) gene, and could not sustain arrest in the G(2)/M phase of the cell cycle.
  • The BRCA1 mutation in SNU-251 cells inhibited BRCA1 subnuclear assembly for DNA-damage repair and increased cellular sensitivity to ionizing radiation and paclitaxel.
  • This sensitivity was reversed by reintroduction of ectopic wild-type BRCA1.
  • Our results suggest that the deletion of the C-terminal 49 amino acids of BRCA1 results in a loss of BRCA1 function in the SNU-251 cell line.
  • BRCA1 helps to mediate the resistance to both radiation and paclitaxel.
  • Therefore, SNU-251 may be a useful model for studying the molecular mechanism of BRCA1 in the resistance of ovarian cancer to ionizing radiation and chemotherapy treatment and in the development of hereditary human ovarian cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. BRCA1 Protein / metabolism. Ovarian Neoplasms / metabolism. Paclitaxel / pharmacology
  • [MeSH-minor] Cell Line. Drug Resistance, Neoplasm. Female. Humans. In Vitro Techniques. PTEN Phosphohydrolase. Phosphoric Monoester Hydrolases / genetics. Phosphoric Monoester Hydrolases / metabolism. Radiation, Ionizing. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism

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  • (PMID = 12717416.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / BRCA1 Protein; 0 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; P88XT4IS4D / Paclitaxel
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6. Indraccolo S, Tisato V, Agata S, Moserle L, Ferrari S, Callegaro M, Persano L, Palma MD, Scaini MC, Esposito G, Fassina A, Nicoletto O, Plebani M, Chieco-Bianchi L, Amadori A, D'Andrea E, Montagna M: Establishment and characterization of xenografts and cancer cell cultures derived from BRCA1 -/- epithelial ovarian cancers. Eur J Cancer; 2006 Jul;42(10):1475-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment and characterization of xenografts and cancer cell cultures derived from BRCA1 -/- epithelial ovarian cancers.
  • The BRCA1 gene is responsible for a high number of hereditary breast and ovarian cancers that cluster in families with a strong genetic predisposition.
  • Despite intense investigation, the accumulating findings on BRCA1 biological functions have not yet been translated into specific therapeutic approaches, also due to the lack of suitable experimental models.
  • The purpose of this study was to establish and characterize cell cultures and xenografts from patients with BRCA1 -/- ovarian cancers.
  • We derived two ovarian cancer cell lines, termed PD-OVCA1 and PD-OVCA2, both from patients previously treated with chemotherapy, that propagate in SCID mice as well as in vitro for a limited number of passages.
  • A detailed molecular characterization highlighted both constitutive and somatic genetic events that abrogate BRCA1 gene function.
  • Both cell lines were shown to lose the wild type BRCA1 allele; intriguingly, these deletions were apparently accompanied by gain of one or more copies of the mutant alleles.
  • The PD-OVCA1 and PD-OVCA2 ovarian cancer cell lines will provide a valuable tool for new experimental models for the study of BRCA1-associated tumour biology.
  • [MeSH-major] Genes, BRCA1. Ovarian Neoplasms / pathology. Tumor Cells, Cultured / pathology


7. Mullan PB, Gorski JJ, Harkin DP: BRCA1--a good predictive marker of drug sensitivity in breast cancer treatment? Biochim Biophys Acta; 2006 Dec;1766(2):205-16
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  • [Title] BRCA1--a good predictive marker of drug sensitivity in breast cancer treatment?
  • There are currently only two predictive markers of response to chemotherapy for breast cancer in routine clinical use, namely the Estrogen receptor-alpha and the HER2 receptor.
  • The breast and ovarian cancer susceptibility gene BRCA1 is an important genetic factor in hereditary breast and ovarian cancer and there is increasing evidence of an important role for BRCA1 in the sporadic forms of both cancer types.
  • Our group and numerous others have shown in both preclinical and clinical studies that BRCA1 is an important determinant of chemotherapy responses in breast cancer.
  • In this review we will outline the current understanding of the role of BRCA1 as a determinant of response to DNA damaging and microtubule damaging chemotherapy.
  • We will then discuss how the known functions of this multifaceted protein may provide mechanistic explanations for its role in chemotherapy responses.
  • [MeSH-major] BRCA1 Protein / genetics. BRCA1 Protein / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Breast Neoplasms / genetics. DNA Repair / genetics. Drug Resistance, Neoplasm / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Microtubules / drug effects


8. Verstappen CC, Heimans JJ, Hoekman K, Postma TJ: Neurotoxic complications of chemotherapy in patients with cancer: clinical signs and optimal management. Drugs; 2003;63(15):1549-63
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  • [Title] Neurotoxic complications of chemotherapy in patients with cancer: clinical signs and optimal management.
  • Neurotoxic side effects of chemotherapy occur frequently and are often a reason to limit the dose of chemotherapy.
  • Since bone marrow toxicity, as the major limiting factor in most chemotherapeutic regimens, can be overcome with growth factors or bone marrow transplantation, the use of higher doses of chemotherapy is possible, which increases the risk of neurotoxicity.
  • Chemotherapy may cause both peripheral neurotoxicity, consisting mainly of a peripheral neuropathy, and central neurotoxicity, ranging from minor cognitive deficits to encephalopathy with dementia or even coma.
  • The vinca-alkaloids, cisplatin and the taxanes are amongst the most important drugs inducing peripheral neurotoxicity.
  • These drugs are widely used for various malignancies such as ovarian and breast cancer, and haematological cancers.
  • Chemotherapy-induced neuropathy is clearly related to cumulative dose or dose-intensities.
  • Patients who already have neuropathic symptoms due to diabetes mellitus, hereditary neuropathies or earlier treatment with neurotoxic chemotherapy are thought to be more vulnerable for the development of chemotherapy-induced peripheral neuropathy.
  • Risk factors are high doses, frequent administration and radiotherapy preceding methotrexate chemotherapy, which appears to be more neurotoxic than methotrexate as single modality.
  • [MeSH-minor] Dose-Response Relationship, Drug. Drug Administration Schedule. Humans

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  • (PMID = 12887262.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 105
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9. Drew Y, Calvert H: The potential of PARP inhibitors in genetic breast and ovarian cancers. Ann N Y Acad Sci; 2008 Sep;1138:136-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The potential of PARP inhibitors in genetic breast and ovarian cancers.
  • The abundant nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1), represents an important novel target in cancer therapy.
  • Inhibitors of PARP-1 have been shown to enhance the cytotoxic effects of ionizing radiation and DNA damaging chemotherapy agents, such as the methylating agents and topoisomerase I inhibitors.
  • Recent in vitro and in vivo evidence suggests that PARP inhibitors could be used not only as chemo/radiotherapy sensitizers, but as single agents to selectively kill cancers defective in DNA repair, specifically cancers with mutations in the breast cancer associated (BRCA) 1 and 2 genes.
  • This theory of selectively exploiting cells defective in one DNA repair pathway by inhibiting another is a major breakthrough in the treatment of cancer.
  • BRCA1/2 mutations are responsible for the majority of genetic breast/ovarian cancers, known as the hereditary breast ovarian cancer syndrome.
  • This review summarizes the preclinical and clinical evidence for the potential of PARP inhibitors in genetic breast and ovarian cancers.
  • [MeSH-major] Breast Neoplasms / drug therapy. Enzyme Inhibitors / therapeutic use. Genetic Predisposition to Disease. Ovarian Neoplasms / drug therapy. Poly(ADP-ribose) Polymerase Inhibitors
  • [MeSH-minor] Female. Genes, BRCA1. Genes, BRCA2. Humans. Mutation


10. Prat J, Ribé A, Gallardo A: Hereditary ovarian cancer. Hum Pathol; 2005 Aug;36(8):861-70
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  • [Title] Hereditary ovarian cancer.
  • Family history is the strongest risk factor for ovarian cancer.
  • Three clinical manifestations of hereditary ovarian cancer have been recognized:.
  • (1) "site-specific" ovarian cancer, (2) the breast and ovarian cancer syndrome, and (3) the hereditary nonpolyposis colorectal cancer (HNPCC; Lynch II) syndrome.
  • The first 2 groups are associated with germ line mutations in the BRCA1 and BRCA2 tumor suppressor genes, whereas HNPCC is associated with germ line mutations in the DNA mismatch repair (MMR) genes, primarily hMLH1 and hMSH2.
  • At least 10% of all epithelial ovarian cancers are hereditary, with mutations in the BRCA genes accounting for approximately 90% of cases and most of the remaining 10% attributable to HNPCC.
  • Hereditary ovarian cancers exhibit distinct clinicopathologic features compared with sporadic cancers.
  • The cumulative lifetime risk of ovarian cancer is 40% to 50% for BRCA1 mutation carriers and 20% to 30% for BRCA2 mutation carriers.
  • Mutations of BRCA1 and BRCA2 are mainly of the frameshift or nonsense variety.
  • Most ovarian cancers associated with germ line BRCA mutations are diagnosed at a younger age and are high-grade and advanced-stage serous carcinomas.
  • BRCA mutations do not seem to play a significant role in the development of mucinous or borderline ovarian tumors.
  • Hereditary ovarian cancers have a distinctly better clinical outcome with longer overall survival and recurrence-free interval after chemotherapy than sporadic cancers.
  • Women with a family history including 2 or more first- or second-degree relatives with either ovarian cancer alone or both breast and ovarian cancers should undertake prophylactic oophorectomy immediately after childbearing has been completed to reduce the risk of ovarian cancer.
  • The cumulative risk of ovarian cancer in HNPCC families is more than 12%.
  • Ovarian cancer in HNPCC syndrome is diagnosed at younger age than in the general population.
  • [MeSH-major] Genetic Predisposition to Disease / genetics. Ovarian Neoplasms / genetics
  • [MeSH-minor] Female. Genes, BRCA1. Genes, BRCA2. Humans. Mutation. Risk Factors


11. Chi D, Zivanovic O, Kolev V, Yu C, Levine DA, Sonoda Y, Abu-Rustum NR, Huh J, Barakat RR, Kattan MW: Nomogram for predicting 5-year survival after primary surgery for epithelial ovarian cancer. J Clin Oncol; 2009 May 20;27(15_suppl):5523

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nomogram for predicting 5-year survival after primary surgery for epithelial ovarian cancer.
  • Our objective was to develop a nomogram based on established prognostic factors to predict the probability of 5-year disease-specific survival (DSS) after primary surgery for patients with epithelial ovarian cancer (EOC) and to compare its predictive accuracy with the currently used FIGO staging system.
  • All patients received platinum-based systemic chemotherapy postop.
  • The most predictive nomogram was constructed using the following 7 predictor variables: age, ASA status, family history suggestive of hereditary breast/ovarian cancer syndrome, preoperative serum albumin level, FIGO stage, tumor histology, and residual disease status after primary surgery.
  • This nomogram was internally validated using bootstrapping and shown to have excellent calibration with a bootstrap-corrected CI of 0.721.
  • CONCLUSIONS: We developed a nomogram to predict 5-year DSS after primary surgery for EOC.

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  • (PMID = 27962481.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Oktay K, Kim J, Barad D, Gleicher N, Babayev S: Association of BRCA1 mutations with diminished ovarian reserve: A common genetic mechanism for breast/ovarian cancer, and infertility? J Clin Oncol; 2009 May 20;27(15_suppl):11039

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of BRCA1 mutations with diminished ovarian reserve: A common genetic mechanism for breast/ovarian cancer, and infertility?
  • : 11039 Background: 25% of all breast cancers (BC) occur prior to menopause and preservation of fertility is an important quality of life issue for these women.
  • We recently reported an ovarian stimulation (OS) protocol utilizing letrozole for women with BC who wish to preserve their fertility by embryo freezing.
  • METHODS: We analyzed the letrozole-OS data to assess the association between BRCA mutations and number of oocytes retrieved, which is the most direct non-invasive method of assessing ovarian reserve.
  • Of those, 14 (30%) were BRCA+; 9 BRCA1+, 4 BRCA2+, and 1 + for both.
  • Age-adjusted poor response (PR) rate (<4 oocytes retrieved) was significantly higher in BRCA+ (28.6%; 4/14) compared to BRCA- (3%;1/33, p=0.009) and untested (2.9%; 1/35, p=0.007).
  • All poor responders were BRCA1+ with one also having a mutation in BRCA2.
  • A BRCA mutation was associated with 17.7 times the relative risk (RR) of PR (95% CI 1.4-214; p=0.024).
  • The mean number of oocytes was significantly lower in BRCA1+ but not BRCA2+ compared to BRCA- and untested (p=0.05).
  • BRCA1 but not BRCA2 mutations were associated with PR with a RR of 24.0 (95% CI 1.9-298; p=0.013).
  • When only mutations of known clinical significance were included, the RR for PR further increased (RR=36, 95% CI 2.5-503; p=0.008) suggesting a common mechanism between BRCA-induced cancer and premature diminishment of oocyte reserve.
  • CONCLUSIONS: Because women with BRCA1 mutations may have DOR prematurely, they should be counseled for possible higher risk of ovarian failure and infertility after chemotherapy, and referred for fertility preservation.
  • Diminished ovarian reserve may be a new component of the Hereditary Breast Ovarian Cancer Syndrome.

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  • (PMID = 27963991.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Zhong Y, Sheng XG, Ma ZF, Ma YB, Liu NF, Chen YT, Gao R, Wang YY, Sun L: [Clinicopathological characteristics of hereditary ovarian cancer syndrome]. Zhonghua Fu Chan Ke Za Zhi; 2009 Sep;44(9):676-80
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  • [Title] [Clinicopathological characteristics of hereditary ovarian cancer syndrome].
  • OBJECTIVE: To explore the clinicopathological characteristics of hereditary ovarian cancer syndrome (HOCS).
  • 2007, among 580 cases of primary ovarian cancer, 42 cases (hereditary group), who had a positive family history of ovarian cancer and met the diagnostic criteria of HOCS, were analyzed retrospectively.
  • One hundred cases without a family history of ovarian cancer were enrolled randomizely as control group (sporadic group).
  • There were 90% belong to serous adenocarcinoma in the hereditary group, while 84% in the sporadic group.
  • Fourteen cases (33%,14/42) were previously untreated in the hereditary group, while 40 cases (40%, 40/100) in the sporadic group.
  • There were 15 cases (36%, 15/42) underwent secondary surgery and 15 cases (36%, 15/42) underwent third surgery or more in hereditary group, while 50 cases (50%,50/100) and 27 cases (27%, 27/100) in the sporadic group.
  • The mean number of chemotherapy cycles received in two groups was 13.3 and 11.8 (P > 0.05).
  • The 3-year and 5-year survival rate in hereditary group were 73.6% and 54.9% respectively, compared with 47.4% and 21.2% (P < 0.05) in sporadic group.
  • CONCLUSION: Hereditary ovarian cancer mostly from maternal lineage are featuring in early age of onset, serous adenocarcinoma, advanced stage (stage III), and better prognosis after the comprehensive treated by cytoreductive surgery plus with chemotherapy.
  • [MeSH-major] Cystadenocarcinoma, Serous / genetics. Cystadenocarcinoma, Serous / pathology. Ovarian Neoplasms / genetics. Ovarian Neoplasms / pathology
  • [MeSH-minor] Adult. Age of Onset. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / genetics. Cisplatin / administration & dosage. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Female. Genetic Diseases, Inborn / pathology. Genetic Diseases, Inborn / therapy. Genetic Predisposition to Disease. Humans. Middle Aged. Neoplasm Staging. Pedigree. Prognosis. Retrospective Studies. Risk Factors


14. Levine DA, Federici MG, Reuter VE, Boyd J: Cell proliferation and apoptosis in BRCA-associated hereditary ovarian cancer. Gynecol Oncol; 2002 Jun;85(3):431-4
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  • [Title] Cell proliferation and apoptosis in BRCA-associated hereditary ovarian cancer.
  • OBJECTIVE: The goal was to test the hypothesis that cellular growth properties differ between hereditary and sporadic ovarian cancers.
  • METHODS: Cell proliferation and apoptosis were assessed in 67 tumors associated with deleterious germline BRCA mutations (hereditary) and 69 tumors without BRCA mutations (sporadic).
  • RESULTS: The mean number of Ki-67-immunopositive nuclei was significantly higher in ovarian cancers from the hereditary group compared with those from the sporadic group (P = 0.017).
  • Cell proliferation did not differ significantly between BRCA1- and BRCA2-associated hereditary tumors, and apoptosis did not differ significantly between the hereditary and sporadic tumors.
  • CONCLUSION: These data indicate that ovarian carcinomas associated with germline BRCA mutations have a significantly higher growth fraction than sporadic cancers.
  • This property may contribute to an improved response to cytotoxic chemotherapy, partially accounting for the longer recurrence-free interval and overall survival observed in the hereditary group.
  • [MeSH-major] Apoptosis / genetics. Genes, BRCA1. Genes, BRCA2. Ovarian Neoplasms / genetics. Ovarian Neoplasms / pathology
  • [MeSH-minor] Cell Division / genetics. Cell Nucleus / metabolism. Cohort Studies. Disease-Free Survival. Female. Germ-Line Mutation. Humans. Jews / genetics. Ki-67 Antigen / metabolism. Middle Aged. Neoplasm Staging. Retrospective Studies

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  • (PMID = 12051869.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA71840
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen
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15. Rabban JT, Barnes M, Chen LM, Powell CB, Crawford B, Zaloudek CJ: Ovarian pathology in risk-reducing salpingo-oophorectomies from women with BRCA mutations, emphasizing the differential diagnosis of occult primary and metastatic carcinoma. Am J Surg Pathol; 2009 Aug;33(8):1125-36
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  • [Title] Ovarian pathology in risk-reducing salpingo-oophorectomies from women with BRCA mutations, emphasizing the differential diagnosis of occult primary and metastatic carcinoma.
  • Risk-reducing salpingo-oophorectomy (RRSO) is an effective prophylactic procedure for women with mutations in BRCA1 or BRCA2 genes, both of which confer an increased lifetime risk for ovarian, tubal, peritoneal, and breast cancer.
  • In addition to lowering this risk, RRSO also offers the opportunity to detect occult early-stage fallopian tube or ovarian carcinoma.
  • The differential diagnosis of occult tubal/ovarian cancer includes a spectrum of benign tubal and ovarian alterations and also occult metastatic breast cancer, although only rare cases of the latter have been reported in RRSO.
  • Neoadjuvant breast cancer chemotherapy may contribute to diagnostic difficulty due to treatment-induced cytologic alterations.
  • With the aim of elucidating features which may help with differential diagnosis, this study reports the incidence and pathologic features of benign ovarian alterations, benign ovarian tumors, and occult primary and metastatic malignancies in prophylactic oophorectomies from 108 women with a BRCA mutation and from 35 women with other strong risk factors for hereditary breast/ovarian carcinoma.
  • We direct particular emphasis on morphologic features of primary ovarian lesions that may mimic occult metastatic breast cancer.
  • We also evaluate histologic alterations due to neoadjuvant breast cancer chemotherapy in the ovary and fallopian tube of patients who received such treatment immediately preceding RRSO.
  • Comparison is made to ovarian metastases of breast cancer in our hospital-based population of breast cancer patients, none of whom underwent RRSO.
  • Overall, 69% of RRSO patients had a personal history of breast cancer.
  • Neoadjuvant breast cancer chemotherapy was administered in 15%.
  • Occult primary carcinoma occurred in 7 (6.5%) BRCA patients (5 in fallopian tube, 1 in fallopian tube and ovary, 1 in ovary).
  • Ovarian metastasis of breast cancer occurred in 1 (1%) BRCA patient undergoing RRSO and in up to a similar proportion (0.8%) of the hospital-based population of breast cancer patients.
  • Abundant foamy, vacuolated cytoplasm due to neoadjuvant chemotherapy exposure was notable.
  • In contrast, ovarian metastases in the non-RRSO population were all clinically detected, bilateral, large, and exhibited well-developed malignant cytologic features.
  • None of the normal cell types in the ovary or tube demonstrated any cytologic alterations in RRSO patients who received neoadjuvant chemotherapy.
  • The main morphologic mimics of metastasis with superimposed chemotherapy-induced alterations in RRSO were stromal hyperthecosis (n=8), nodular hyperthecosis (n=2), adrenal rests (n=3), hilus cell nodules (n=43), and hilus cell hyperplasia (n=4).
  • Occult primary ovarian carcinoma was reliably distinguished from ovarian metastases of breast cancer by WT-1+, p53+, mammaglobin-, GCDPF-immunoprofile.
  • These results demonstrate that evaluation of RRSO specimens requires awareness of a spectrum of ovarian lesions which may mimic occult primary or metastatic carcinoma; awareness of the masquerading effects of neoadjuvant chemotherapy; and awareness of the potential morphologic differences between occult metastatic breast cancer in RRSO and non-RRSO specimens.
  • [MeSH-major] Genes, BRCA1. Genes, BRCA2. Ovarian Neoplasms / genetics. Ovarian Neoplasms / pathology. Ovarian Neoplasms / prevention & control
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Diagnosis, Differential. Fallopian Tubes / surgery. Female. Genetic Predisposition to Disease. Humans. Mutation. Neoplasms, Multiple Primary / genetics. Neoplasms, Multiple Primary / pathology. Neoplasms, Multiple Primary / prevention & control. Ovariectomy. Ovary / drug effects. Ovary / pathology. Risk Factors

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  • (PMID = 19440148.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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16. Rhiem K, Wappenschmidt B, Bosse K, Köppler H, Tutt AN, Schmutzler RK: Platinum sensitivity in a BRCA1 mutation carrier with advanced breast cancer. Clin Oncol (R Coll Radiol); 2009 Aug;21(6):448-50
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  • [Title] Platinum sensitivity in a BRCA1 mutation carrier with advanced breast cancer.
  • Although BRCA1-associated breast carcinomas are frequently detected in nodal-negative stage, they typically present with an aggressive histopathological phenotype that is reflected by a poor prognosis and an increased risk for distant metastatic spread.
  • Recent in vitro data suggest a high sensitivity of BRCA1-associated carcinomas to platinum-based chemotherapy and a lower sensitivity to anthracyclines and taxanes.
  • This is explained by the key role of BRCA1 in DNA double-strand repair via homologous recombination, thereby leading to a higher sensitivity to DNA intercalating agents, such as platinum.
  • Here we present the case of a woman suffering from BRCA1-associated metastatic breast carcinoma that was resistant to docetaxel, but responded strongly to cisplatin-containing chemotherapy.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Genes, BRCA1. Germ-Line Mutation. Organoplatinum Compounds / therapeutic use

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  • (PMID = 19249193.001).
  • [ISSN] 1433-2981
  • [Journal-full-title] Clinical oncology (Royal College of Radiologists (Great Britain))
  • [ISO-abbreviation] Clin Oncol (R Coll Radiol)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Organoplatinum Compounds
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17. Ganz PA: Breast cancer, menopause, and long-term survivorship: critical issues for the 21st century. Am J Med; 2005 Dec 19;118 Suppl 12B:136-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Breast cancer, menopause, and long-term survivorship: critical issues for the 21st century.
  • Breast cancer accounts for 33% of all incident cancers in women in North America, and there are an estimated >2 million breast cancer survivors in the United States today.
  • Ovarian hormones are intimately involved in the initiation and promotion of breast cancer development, with targeted endocrine therapies being the most widely used as anticancer treatment.
  • It is not surprising that these treatments frequently cause persistent menopausal symptoms in breast cancer survivors.
  • In addition, adjuvant chemotherapy often induces premature menopause in younger patients with breast cancer.
  • Some women at high risk for the development of breast cancer (e.g., precancerous breast disease, carriers of deleterious hereditary predisposition genes) experience vasomotor symptoms as a result of tamoxifen therapy or preventive oophorectomy.
  • Clinical management of menopausal symptoms in these settings is complicated by the relative prohibition of hormonal therapies and the fact that breast cancer-directed therapies often exacerbate these menopausal symptoms.
  • [MeSH-major] Breast Neoplasms. Menopause / physiology. Survivors
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Female. Humans. Menopause, Premature. Primary Ovarian Insufficiency / chemically induced. Primary Ovarian Insufficiency / drug therapy. Risk

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  • (PMID = 16414339.001).
  • [ISSN] 1555-7162
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Publication-type] Consensus Development Conference, NIH; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 60
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18. Goldman M, O'Hair K: Women's health, breast health: a review of the gynecologic effects of breast cancer. Obstet Gynecol Surv; 2009 Jul;64(7):469-80; quiz 499
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Women's health, breast health: a review of the gynecologic effects of breast cancer.
  • Breast cancer is very common and seen in both premenopausal and postmenopausal women.
  • Research into prevention, better screening, and more effective treatments is occurring continually, and changes are translated into clinical practice relatively quickly.
  • It is important for women's health care providers to have an understanding of breast cancer treatments and the gynecologic side effects.
  • For premenopausal women interested in fertility, options should be discussed prior to chemotherapy.
  • Issues pertaining to pregnancy after breast cancer should be discussed in a multidisciplinary fashion, involving the obstetrician/gynecologist, breast surgeon, and oncologist.
  • Ovarian suppression is often used as part of breast cancer treatment in premenopausal women with hormone positive disease, and menopausal symptoms may be severe.
  • Hormonal therapies including tamoxifen and the aromatase inhibitors are used in the treatment of hormone positive breast cancers.
  • Each of these drugs has a variety of gynecologic implications.
  • Understanding the options for treatment for menopausal complaints in breast cancer patients is important for women's health providers.
  • Although most breast cancers are sporadic, a small percentage will be due to mutations in the BRCA genes.
  • It is important for women's health providers to take an appropriate family history and refer to genetic counselors for possible testing when hereditary cancer is suspected.
  • This review focuses on the various women's health issues pertaining to breast cancer and treatment.
  • [MeSH-major] Breast Neoplasms / complications. Genital Diseases, Female / etiology. Pregnancy Complications, Neoplastic / etiology

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  • (PMID = 19545455.001).
  • [ISSN] 1533-9866
  • [Journal-full-title] Obstetrical & gynecological survey
  • [ISO-abbreviation] Obstet Gynecol Surv
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 125
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19. Murray MM, Mullan PB, Harkin DP: Role played by BRCA1 in transcriptional regulation in response to therapy. Biochem Soc Trans; 2007 Nov;35(Pt 5):1342-6
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  • [Title] Role played by BRCA1 in transcriptional regulation in response to therapy.
  • BRCA1 (breast-cancer susceptibility gene 1) is a tumour suppressor, implicated in the hereditary predisposition to breast and ovarian cancer.
  • BRCA1 has been implicated in a number of cellular processes including DNA repair and recombination, cell cycle checkpoint control, chromatin remodelling and ubiquitination.
  • In addition, substantial data now exist to suggest a role for BRCA1 in transcriptional regulation; BRCA1 has been shown to interact with the Pol II holoenzyme complex and to interact with multiple transcription factors, such as p53 and c-Myc.
  • We have previously identified a range of BRCA1 transcriptional targets and have linked these to specific cellular pathways, including cell cycle checkpoint activation and apoptosis.
  • Current research is focused on the transcriptional mechanisms that underpin the association of BRCA1 deficiency with increased sensitivity to DNA damage-based chemotherapy and resistance to spindle poisons.
  • [MeSH-major] Breast Neoplasms / therapy. Genes, BRCA1. Transcription, Genetic / genetics
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. DNA Damage. DNA Repair. Genes, cdc. Humans. Spindle Apparatus / drug effects

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  • (PMID = 17956347.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0200103
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 39
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20. Trainer AH, Lewis CR, Tucker K, Meiser B, Friedlander M, Ward RL: The role of BRCA mutation testing in determining breast cancer therapy. Nat Rev Clin Oncol; 2010 Dec;7(12):708-17
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  • [Title] The role of BRCA mutation testing in determining breast cancer therapy.
  • Landmark discoveries in the field of breast cancer research include the identification of germline BRCA mutations as a cause of hereditary disease, and the use of gene-expression profiling to identify distinct subtypes of breast cancer.
  • These findings, coupled with the availability of rapid germline testing, make it possible to identify a BRCA mutation carrier contemporaneous with a diagnosis of breast cancer.
  • For the first time, testing for a germline mutation that predisposes to cancer has the potential to influence the immediate surgical, radiotherapeutic, and drug treatment choices of an individual with a new diagnosis of breast cancer.
  • In this Review, we examine the implications of moving germline BRCA mutation testing from highly specialized family cancer clinics to mainstream settings.
  • [MeSH-major] Breast Neoplasms / genetics. Genes, BRCA1. Genes, BRCA2. Genetic Testing. Germ-Line Mutation. Neoplastic Syndromes, Hereditary / genetics
  • [MeSH-minor] Adult. Age of Onset. Case Management. Ethnic Groups / genetics. Female. Gene Expression Profiling. Genes, Dominant. Genetic Counseling. Genetic Predisposition to Disease. Humans. Mastectomy / psychology. Neoplasm Proteins / analysis. Neoplasm Proteins / genetics. Neoplasms, Second Primary / epidemiology. Neoplasms, Second Primary / prevention & control. Ovarian Neoplasms / epidemiology. Ovarian Neoplasms / genetics. Precision Medicine. Prognosis. Risk

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  • (PMID = 21060331.001).
  • [ISSN] 1759-4782
  • [Journal-full-title] Nature reviews. Clinical oncology
  • [ISO-abbreviation] Nat Rev Clin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins
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21. Foulkes WD: BRCA1 and BRCA2: chemosensitivity, treatment outcomes and prognosis. Fam Cancer; 2006;5(2):135-42
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  • [Title] BRCA1 and BRCA2: chemosensitivity, treatment outcomes and prognosis.
  • BRCA1 and BRCA2 are important breast and ovarian cancer susceptibility genes, and mutations in these two genes confer lifetime risks of breast cancer of up to 80% and ovarian cancer risks of up to 40%.
  • Clinico-pathological studies have identified features that are specific to BRCA1-related breast cancer, but this has been more difficult for BRCA2-related breast cancer.
  • Ovarian cancers due to BRCA1 or BRCA2 mutations cannot usually be distinguished from their non-hereditary counterparts on morphological grounds, but micro-array data suggest that differences do exist.
  • Prognostic studies have shown that breast cancer in a BRCA1 mutation carrier is likely to have a similar, or worse, outcome than that occurring in a BRCA2- or non-carrier of the same age.
  • By contrast, most studies indicate that women developing a BRCA1/2-related ovarian cancer have an improved survival compared with non-carriers, particularly if they receive platinum-based therapy.
  • In support of this, in vitro chemo-sensitivity studies have found that human cells lacking BRCA1 may be particularly sensitive to cisplatinum and to other drugs that cause double-strand breaks in DNA.
  • Nevertheless, in breast cancer, little is known regarding clinically important differences in response to chemotherapy between BRCA1/2 mutation carriers and non-carriers, and between different chemotherapeutic regimens within existing series of BRCA1/2 mutation carriers.
  • [MeSH-major] Breast Neoplasms / genetics. Genes, BRCA1. Genes, BRCA2. Ovarian Neoplasms / genetics
  • [MeSH-minor] DNA Methylation. Female. Humans. Mutation. Prognosis. Treatment Outcome

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  • (PMID = 16736282.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 85
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22. Beiner ME, Finch A, Rosen B, Lubinski J, Moller P, Ghadirian P, Lynch HT, Friedman E, Sun P, Narod SA, Hereditary Ovarian Cancer Clinical Study Group: The risk of endometrial cancer in women with BRCA1 and BRCA2 mutations. A prospective study. Gynecol Oncol; 2007 Jan;104(1):7-10
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  • [Title] The risk of endometrial cancer in women with BRCA1 and BRCA2 mutations. A prospective study.
  • OBJECTIVE: To evaluate the risk of endometrial cancer in women who carry a deleterious mutation in the BRCA1 or BRCA2 genes.
  • PATIENTS AND METHODS: Women known to carry a BRCA1 or BRCA2 mutation, aged 45 to 70, were identified from an international registry and were followed prospectively.
  • Study subjects were followed until diagnosis of endometrial cancer, ovarian cancer, death or the date of completion of the last questionnaire.
  • RESULTS: After an average follow-up period of 3.3 years, six women were diagnosed with endometrial cancer, compared to 1.13 cancers expected (SIR=5.3, p=0.0011).
  • The risk among women who were never exposed to tamoxifen treatment was not significantly elevated (SIR=2.7, p=0.17), but among the 226 participants who had used tamoxifen (220 as treatment and six for the primary prevention of breast cancer) the relative risk for endometrial cancer was 11.6 (p=0.0004).
  • CONCLUSION: The main contributor to the increased risk of endometrial cancer among BRCA carriers is tamoxifen treatment for a previous breast cancer.
  • The risk and benefits of prophylactic hysterectomy should be discussed with women with a BRCA mutation considering tamoxifen therapy.
  • [MeSH-major] Endometrial Neoplasms / genetics. Genes, BRCA1. Genes, BRCA2. Germ-Line Mutation
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Hormonal / adverse effects. Breast Neoplasms / drug therapy. Female. Follow-Up Studies. Humans. Middle Aged. Prospective Studies. Tamoxifen / adverse effects

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  • (PMID = 16962648.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 094ZI81Y45 / Tamoxifen
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