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National Cancer Institute®
Ultima Vez Modificado: 21 de noviembre del 2001
UI - 21468599
AU - Esteller M
TI - Epigenetic lesions causing genetic lesions in human cancer: promoter hypermethylation of DNA repair genes.
SO - Eur J Cancer 2000 Dec;36(18):2294-300
AD - Division of Cancer Biology, The Johns Hopkins Oncology Center, Baltimore, MD 21231, USA. firstname.lastname@example.org
The existence of genetic alterations affecting genes involved in cellular proliferation and death, such as TP53 and K-ras, is one of the most common features of tumour cells. Recently, gene inactivation by promoter hypermethylation has been demonstrated. Methylation is the main epigenetic modification in mammals and abnormal methylation of the CpG islands located in the promoter region of the genes leads to transcriptional silencing. Examples include the p16INK4a, p15INK4B, p14ARF, Von Hippel-Lindau (VHL), the oestrogen and progesterone receptors, E-cadherin, death associated protein (DAP) kinase and the first tumour suppressor gene described, retinoblastoma (Rb) gene. In most cases, methylation involves loss of expression, absence of a coding mutation and restoration of transcription by the use of demethylating agents. However, is there a linkage between genetic and epigenetic alterations? Our results show one side of this puzzle demonstrating that epigenetic lesions drive genetic lesions in cancer. Four specific epigenetic lesions, promoter hypermethylation of the DNA mismatch repair gene hMLH1, the DNA alkyl-repair gene O(6)-methylguanine-DNA methyltransferase (MGMT), the detoxifier glutathione S-transferase P1 (GSTP1) and the familial breast cancer gene BRCA1 may lead to four specific genetic lesions, microsatellite instability, G to A transitions, steroid-related adducts and double-strand breaks in DNA. This is probably only the beginning of an extensive list of epigenetic events that change and make the genetic environment of the transformed cell unstable.
UI - 21427140
AU - Stefanek M; Hartmann L; Nelson W
TI - Risk-reduction mastectomy: clinical issues and research needs.
SO - J Natl Cancer Inst 2001 Sep 5;93(17):1297-306
AD - Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD, USA. email@example.com
Risk-reduction mastectomy (RRM), also known as bilateral prophylactic mastectomy, is a controversial clinical option for women who are at increased risk of breast cancer. High-risk women, including women with a strong family history of breast cancer and BRCA1/2 mutation carriers, have several clinical options: risk-reduction surgery (bilateral mastectomy and bilateral oophorectomy), surveillance (mammography, clinical breast examination, and breast self-examination), and chemoprevention (tamoxifen). We review research in a number of areas central to our understanding of RRM, including recent data on 1) the effectiveness of RRM in reducing breast cancer risk, 2) the perception of RRM among women at increased risk and health-care providers, 3) the decision-making process for follow-up care of women at high risk, and 4) satisfaction and psychological status after surgery. We suggest areas of future research to better guide high-risk women and their health-care providers in the decision-making process.
UI - 21453507
AU - Evans D; Lalloo F; Shenton A; Boggis C; Howell A
TI - Uptake of screening and prevention in women at very high risk of breast cancer.
SO - Lancet 2001 Sep 15;358(9285):889-90
Management of women at high lifetime risk of familial breast cancer is hampered because of limited data concerning the appropriateness of treatment options. Over the past 8 years women at very high (>40%) lifetime risk of breast cancer have had the option of entering two chemoprevention treatment trials, a magnetic resonance imaging (MRI) breast screening study, or a risk-reducing mastectomy (RRM) study. Only 10% of eligible women have entered one of the chemotherapy trials with a similar proportion opting for RRM (>50% in mutation carriers) compared with 60% opting for MRI screening. Future chemotherapy trials will have to be designed to address this poor recruitment.
UI - 21445115
AU - Vogel VG
TI - Reducing the risk of breast cancer with tamoxifen in women at increased risk.
SO - J Clin Oncol 2001 Sep 15;19(18 Suppl):87S-92S
AD - Magee-Women's Hospital, University of Pittsburgh Cancer Institute Breast Program, University of Pittsburgh, Pittsburgh, PA 15213, USA. firstname.lastname@example.org
Validated quantitative models are available that permit the accurate estimation of a woman's risk of developing invasive breast cancer during a specified period of time. Data from the National Surgical Adjuvant Breast and Bowel Project Breast Cancer Prevention Trial indicate that tamoxifen can reduce the risk of developing breast cancer by at least 49% in women who are at increased risk. All premenopausal women whose 5-year risk of developing breast cancer is 1.67% or greater derive a net benefit from taking tamoxifen for risk reduction. Women who have either lobular carcinoma-in-situ or atypical ductal or lobular hyperplasia derive an even greater net benefit. Women who carry mutations in either the BRCA1 or BRCA2 gene will also experience reduced incidence of breast cancer with tamoxifen. Although postmenopausal women derive a net benefit from tamoxifen through the reduction of both breast cancer and bone fracture event rates, the risks of both invasive endometrial cancer and thromboembolic events must be balanced in older women. Physicians should identify appropriate candidates with whom to discuss the possible benefits of tamoxifen for reducing the risk of breast cancer.
UI - 21243555
AU - Tsuchida S; Ikemoto S; Tagawa M
TI - Microsatellite polymorphism in intron 14 of the canine BRCA1 gene.
SO - J Vet Med Sci 2001 Apr;63(4):479-81
AD - Division of Veterinary Surgery, Nippon Veterinary and Animal Science University, Musashino-shi, Tokyo, Japan.
Microsatellite polymorphism due to differences in CT dinucleotide repeats was demonstrated in intron 14 of the canine BRCA1 gene. Genotype analysis of 103 unrelated dogs from 30 different breeds detected the presence of five alleles, including 10 of the expected 15 genotypes. Gene frequencies were biased and all alleles with the exception of one were below 0.1. This polymorphism, which occurs at the intron of canine BRCA1 should prove to be a useful marker for detecting the loss of heterozygosity (LOH). One of the more notable findings of the present study was the detection of homozygotes of rare alleles. This finding identified an accumulation of rare alleles in specific canine breeds and demonstrated the usefulness of this characteristic for the biological study of dog evolution.
UI - 21385555
AU - Boetes C; Stoutjesdijk M
TI - MR imaging in screening women at increased risk for breast cancer.
SO - Magn Reson Imaging Clin N Am 2001 May;9(2):357-72, vii
AD - Department of Radiology, University Medical Center St. Radboud, Nijmegen, The Netherlands. email@example.com
Hereditary breast cancer accounts for 5% to 10% of the total breast cancer burden. Screening of this group of women has been done by palpation and conventional mammography until recently, but because of the age group, mammography has a limited value. MR mammography has been demonstrated to be a reliable imaging modality in this group of patients.
UI - 21469896
AU - Chu CS; Morgan MA; Randall TC; Bandera CA; Rubin SC
TI - Survival of BRCA1 negative ovarian cancer patients based on family history.
SO - Gynecol Oncol 2001 Oct;83(1):109-14
AD - Division of Gynecologic Oncology, University of Pennsylvania Health System, Philadelphia, Pennsylvania 19104, USA. firstname.lastname@example.org
OBJECTIVE: To compare survival of ovarian cancer patients with and without a family history of breast or ovarian cancer who are known to be without mutations in BRCA1. METHODS: Patients with ovarian cancer were tested for germline mutations in BRCA1 by polymerase chain reaction amplification of DNA for single-strand conformation polymorphism and direct sequencing analysis to examine the 22 coding exons of BRCA1 in fresh and archived tumor specimens. Demographic and survival data were collected for statistical analysis. Survival data were calculated by the method of Kaplan and Meier and compared by the log-rank test. RESULTS: Of the 110 patients tested at our institution, 100 were noted to be negative for BRCA1 mutations. After exclusion of nonepithelial histologies, benign tumors, primary peritoneal carcinoma, and incomplete staging, 87 patients remained for analysis, of which 37 demonstrated a family history of breast or ovarian cancer. The two groups showed similar age at diagnosis, stage, grade, residual disease, and type of chemotherapy. Median actuarial survival was 75 months for those patients with a family history versus 70 months for those without (P = 0.73). Evaluation of patients with two or more relatives with breast or ovarian cancer also revealed no differences in survival. CONCLUSIONS: Family history of breast or ovarian cancer does not affect survival of patients with ovarian cancer in the absence of mutations in BRCA1. Previously described differences in survival among patients with BRCA1 mutations may be more related to genetic factors than to biases introduced by the presence of family history. Copyright 2001 Academic Press.
UI - 97322580
AU - Lynch HT; Lemon SJ; Durham C; Tinley ST; Connolly C; Lynch JF; Surdam J;
TI - Orinion E; Slominski-Caster S; Watson P; Lerman C; Tonin P; Lenoir G; Serova O; Narod S A descriptive study of BRCA1 testing and reactions to disclosure of test results.
SO - Cancer 1997 Jun 1;79(11):2219-28
AD - Creighton University, Department of Preventive Medicine, Omaha, Nebraska 68178, USA.
BACKGROUND: The identification of the BRCA1 gene is a powerful tool for predicting a patient's lifetime risk for carcinoma of the breast and ovary when she has hereditary breast/ovarian carcinoma (HBOC) syndrome. The process of BRCA1 testing and genetic counseling and participants' reactions to test results, are described. METHODS: Education about the natural history of HBOC syndrome and the pros and cons of genetic testing was provided to 14 HBOC families comprised of 2549 bloodline relatives. Of these, 388 underwent DNA testing. After informed consent was given by participants, formal linkage analysis and gene mutation studies were performed on the families. Qualitative data on intentions and emotional reactions were collected by physicians/counselors during the genetic counseling sessions. RESULTS: Of those tested, 181 received their results after further genetic counseling. Seventy-eight of them were positive and 100 were negative for BRCA1 gene mutation. Three had ambiguous findings. The most common reasons given for seeking DNA testing were concern about risk to children and concern about surveillance and prevention. Prophylactic mastectomy was considered by 35% of women who tested positive, whereas prophylactic oophorectomy was considered an important option by 76%. Twenty-five percent of both BRCA1 positive and negative individuals were concerned about discrimination by insurance companies. Eighty percent of those who tested negative reported emotional relief, whereas over one-third of those who tested positive reported sadness, anger, or guilt. CONCLUSIONS: DNA testing of patients with HBOC syndrome must be performed in the context of genetic counseling. The authors' results demonstrate the many complex clinical and nonclinical issues that are important in this process.
UI - 99317170
AU - Goldworth A
TI - Informed consent in the genetic age.
SO - Camb Q Healthc Ethics 1999 Summer;8(3):393-400
AD - Lucille Packard Children's Hospital, Stanford University, Palo Alto, CA, USA.
UI - 97299454
AU - Cunningham GC
TI - A public health perspective on the control of predictive screening for breast cancer.
SO - Health Matrix Clevel 1997 Winter;7(1):31-48
AD - Pacific Southwest Regional Genetics Network, USA.
UI - 97299456
AU - Dorff EN
TI - Jewish theological and moral reflections on genetic screening: the case of BRCA1.
SO - Health Matrix Clevel 1997 Winter;7(1):65-96
AD - University of Judaism, Los Angeles, CA, USA.
UI - 21230513
AU - Campbell M; Aprelikova ON; van der Meer R; Woltjer RL; Yee CJ; Liu ET;
TI - Jensen RA Construction and characterization of recombinant adenoviruses expressing human BRCA1 or murine Brca1 genes.
SO - Cancer Gene Ther 2001 Mar;8(3):231-9
AD - Department of Pathology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA. email@example.com
Recombinant adenoviruses expressing human BRCA1 (AdBRCA1), murine Brca1 (AdBrca1), three clinically relevant human mutant BRCA1 proteins (t340, C61G, and 1853Stop), or a murine Brca1 C-terminal deletion mutant were constructed and evaluated in vitro. These recombinants were capable of transducing high-level transgene expression to a wide variety of cell lines in vitro. Three independent methods were utilized to monitor cell growth following transduction with these recombinants. High-level expression of either the human or mouse wild-type BRCA1 protein was incompatible with maximal levels of cell growth. AdBRCA1 transduction inhibited the outgrowth of several human breast and ovarian cell lines in colony formation assays. Flow cytometric analysis revealed an accumulation of the transduced cells in the G0/G1 phase of the cell cycle. This BRCA1-mediated accumulation of cells in G0/G1 was accompanied by an increase in the cellular level of hypophosphorylated pRB. Ad mutant BRCA1 t340, C61G, and 1853Stop viruses were impaired, to varying degrees, in their ability to transduce a growth-arrested state to the target cells. Using these same three criteria, overexpression of murine Brca1 by AdBrca1 was also capable of transducing a growth-arrested state to human cells. Deletion of the C-terminus of Brca1 diminished this activity. This panel of adenoviruses may be useful reagents as part of an approach to understand the function of BRCA1/Brca1 in normal breast and ovary and help to define the tumor suppressor defect (s) conferred by clinical BRCA1 mutations in breast and ovarian cell tumorigenesis.
UI - 21236239
AU - Plon SE; Peterson LE; Friedman LC; Richards CS
TI - Mammography behavior after receiving a negative BRCA1 mutation test result in the Ashkenazim: a community-based study.
SO - Genet Med 2000 Nov-Dec;2(6):307-11
AD - Department of Pediatrics, Baylor College of Medicine, Houston, Texas, USA.
PURPOSE: To define the impact of a negative BRCA1 test result on subsequent breast cancer screening behavior in women. METHODS: Longitudinal study of a community-based sample of Ashkenazi Jews offered testing for the 185delAG BRCA1 mutation in 1996. Of 309 participants, 118 women were mutation negative, of average risk (based on family history of cancer), unaffected with breast cancer, and provided complete data at baseline, and Year 1 and Year 2 follow-up questionnaires. RESULTS: Women age 50 and older had 91.7% compliance with mammography for the year prior to entry (baseline), 88.3% during Year 1, 91.7% during Year 2 (no significant change; P = 0.775). Women under age 50 demonstrated an increase in mammography (49.2% at baseline, 62.7% Year 1, and 67.1% Year 2; P = 0.035). Both groups demonstrated significant decreases in breast cancer worry and perceived risk. Logistic regression analysis on having a mammogram at Year 2 showed that age, physician recommendation, worry, and perceived risk were all significant. CONCLUSION: Receipt of negative BRCA1 test results in a cohort of Ashkenazi Jewish women did not have a negative impact on mammography behavior 2 years after genetic testing.
UI - 21234529
AU - Arver B; Borg A; Lindblom A
TI - First BRCA1 and BRCA2 gene testing implemented in the health care system of Stockholm.
SO - Genet Test 2001 Spring;5(1):1-8
AD - Department of Molecular Medicin, Karolinska Institutet, Stockholm, Sweden. firstname.lastname@example.org
The aim of the study was to optimize the criteria for the BRCA1 and BRCA2 gene testing and to improve oncogenetic counseling in the Stockholm region. Screening for inherited breast cancer genes is laborious and a majority of tested samples turn out to be negative. The frequencies of mutations in the BRCA1 and BRCA2 genes differ across populations. Between 1997 and 2000, 160 families with breast and/or ovarian cancer were counseled and screened for mutations in the two genes. Twenty-five BRCA1 and two BRCA2 disease-causing mutations were found. Various factors associated with the probability of finding a BRCA1 mutation in the families were estimated. Age of onset in different generations and other malignancies were also studied. Families from our region in which both breast and ovarian cancer occur were likely to carry a BRCA1 mutation (34%). In breast-only cancer families, mutations were found only in those with very early onset. All breast- only cancer families with a mutation had at least one case of onset before 36 years of age and a young median age of onset (<43 years). Other malignancies than breast and ovarian cancers did not segregate in the BRCA1 families and surveillance for other malignancies is not needed, in general. Decreasing age of onset with successive generations was common and must be taken into account when surveillance options are considered.
UI - 21330096
AU - Ito Y; Noguchi S; Takeda T; Matsuura N
TI - Fas ligand expression in BRCA1-associated hereditary breast carcinoma clearly differs from that in sporadic breast carcinoma.
SO - Breast Cancer Res Treat 2001 Mar;66(2):95-100
AD - Department of Surgery, Osaka Seamen's Insurance Hospital, Japan.
BRCA1-associated hereditary breast carcinomas (HBCs) are diagnosed at a younger age and are known to show biological aggressiveness such as a high histological grade, frequent aneuploidy, compared to sporadic breast carcinomas. However, results of studies on their prognosis have been controversial. We hypothesized that some factors such as a high incidence of cell death could offset the aggressiveness of BRCA1-associated HBCs, and therefore investigated Fas and Fas ligand (Fas L) expression in 19 BRCA1-associated HBCs and 56 age-adjusted control cases. Glandepithelial and myoepithelial cells in the mammary glands expressed Fas in high incidence, but all were negative for Fas L. Fas was expressed in 89.5% of BRCA1-associated HBCs and 94.4% of the controls and no significant differences could be established between the two groups. However, in 73.7% of BRCA1-associated HBCs, Fas L was clearly expressed in the infiltrating mononuclear cells, whereas this was observed in only 14.3% of the control cases and statistical significance was established between the two groups (p < 0.0001). These results strongly suggest that carcinoma cells in BRCA1-associated HBCs are more likely to be attacked by mononuclear cells via Fas L, and this may explain, at least in part, the discrepancy with respect to the prognosis. On the other hand, carcinoma cells also expressed Fas L significantly more often (p < 0.0001) in BRCA1-associated HBCs (52.6%) than in sporadic cases (3.6%). This can be considered a kind of counterattack against the mononuclear cells or, alternatively, may enhance the Fas-Fas L pathway in an autocrine/paracrine fashion. The clinical significance of Fas L expressing carcinoma cells remains to be elucidated.
UI - 21363506
AU - Budhram-Mahadeo V; Moore A; Morris PJ; Ward T; Weber B; Sassone-Corsi P;
TI - Latchman DS The closely related POU family transcription factors Brn-3a and Brn-3b are expressed in distinct cell types in the testis.
SO - Int J Biochem Cell Biol 2001 Oct;33(10):1027-39
AD - Medical Molecular Biology Unit, Institute of Child Health, University College London, 30 Guilford Street, WC1N 1EH, London, UK.
Although the Brn-3a and Brn-3b POU family transcription factors were originally identified in neuronal cells, their expression in some non neuronal cell types has previously been reported. Here we report that Brn-3a and Brn-3b are also expressed in the testis with expression of each factor being observed at distinct stages of germ cell development. Thus, Brn-3a is expressed in spermatogonia whereas Brn-3b expression is observed in post-meiotic spermatids. In agreement with this, Brn-3a expression is detectable much earlier than that of Brn-3b in testes derived from sexually immature postnatal animals. Similarly, Brn-3b expression is absent in knock out mice lacking a functional CREM transcription factor in which the later stages of germ cell development do not occur, whereas Brn-3a expression is observed at similar levels in the testes of these knock out mice. Interestingly, the cellular pattern of Brn-3a expression during germ cell development coincides with that of the BRCA-1 anti-oncogene. Consistent with the possibility that Brn-3a may regulate expression of BRCA-1 in the testis, we have shown that Brn-3a can strongly activate the BRCA-1 promoter in co-transfection experiments whereas Brn-3b does not have this effect. Hence, as observed in neuronal cells, Brn-3a and Brn-3b may play distinct and important functional roles in the regulation of gene expression during germ cell development.
UI - 21485295
AU - Zanker KS; Anand M; Majumdar A; Daftary GV
TI - The Mumbai Conference on Molecular Targets in Cancer Cells: new paradigms in research and treatment.
SO - J Cancer Res Clin Oncol 2001 Oct;127(10):636-41
AD - Institute of Immunology, University of Witten/Herdecke, Germany. email@example.com
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