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NCI CANCERLIT^® Search: BRCA1 Gene - September 2002

National Cancer Institute^®
Last Modified: September 1, 2002

Codon-substitution models for detecting molecular adaptation at individual sites along specific lineages.
Ovarian cancer in BRCA-positive women: vigilance is mandatory despite screening programs.
Breast and ovarian cancer screening practices in healthy women with a strong family history of breast or ovarian cancer.
Detection of large rearrangements of exons 13 and 22 in the BRCA1 gene in German families.
BRCA1 regulates the interferon gamma-mediated apoptotic response.
BRCA1 facilitates microhomology-mediated end joining of DNA double strand breaks.
Risk-reduction mastectomy: clinical issues and research needs.
BRCA1 transcriptionally regulates damaged DNA binding protein (DDB2) in the DNA repair response following UV-irradiation.
Participation of BRCA1 in the DNA repair response...via transcription.
Cancer: the chromatin connection.
Transitional cell ovarian carcinoma in a BRCA1 mutation carrier.
Phosphorylation of serine 1387 in Brca1 is specifically required for the Atm-mediated S-phase checkpoint after ionizing irradiation.
Roles of BRCA1 in centrosome duplication.
Singular value decomposition regression models for classification of tumors from microarray experiments.
Breast cancer after prophylactic bilateral mastectomy in women with a BRCA1 or BRCA2 mutation.
Risk-reducing salpingo-oophorectomy in women with a BRCA1 or BRCA2 mutation.
Prophylactic oophorectomy in carriers of BRCA1 or BRCA2 mutations.
Oophorectomy in carriers of BRCA mutations.
Oophorectomy in carriers of BRCA mutations.
Oophorectomy in carriers of BRCA mutations.
Oophorectomy in carriers of BRCA mutations.
BRCA1-related malignancies in a family presenting with von Recklinghausen's disease.

1
UI - 12032247
AU - Yang Z; Nielsen R
TI - Codon-substitution models for detecting molecular adaptation at individual sites along specific lineages.
SO - Mol Biol Evol 2002 Jun;19(6):908-17
AD - Galton Laboratory, Department of Biology, University College London. z.yang@ucl.ac.uk
The nonsynonymous (amino acid-altering) to synonymous (silent) substitution rate ratio (omega = d(N)/d(S)) provides a measure of natural selection at the protein level, with omega = 1, >1, and <1, indicating neutral evolution, purifying selection, and positive selection, respectively. Previous studies that used this measure to detect positive selection have often taken an approach of pairwise comparison, estimating substitution rates by averaging over all sites in the protein. As most amino acids in a functional protein are under structural and functional constraints and adaptive evolution probably affects only a few sites at a few time points, this approach of averaging rates over sites and over time has little power. Previously, we developed codon-based substitution models that allow the omega ratio to vary either among lineages or among sites. In this paper we extend previous models to allow the omega ratio to vary both among sites and among lineages and implement the new models in the likelihood framework. These models may be useful for identifying positive selection along prespecified lineages that affects only a few sites in the protein. We apply those branch-site models as well as previous branch- and site-specific models to three data sets: the lysozyme genes from primates, the tumor suppressor BRCA1 genes from primates, and the phytochrome (PHY) gene family in angiosperms. Positive selection is detected in the lysozyme and BRCA genes by both the new and the old models. However, only the new models detected positive selection acting on lineages after gene duplication in the PHY gene family. Additional tests on several data sets suggest that the new models may be useful in detecting positive selection after gene duplication in gene family evolution.

2
UI - 11858898
AU - Sloots K; Ausems MG; de Haan HH
TI - Ovarian cancer in BRCA-positive women: vigilance is mandatory despite screening programs.
SO - Eur J Obstet Gynecol Reprod Biol 2002 Mar 10;101(2):196-8
AD - Department of Obstetrics and Gynaecology, Isala Clinics, Location Sophia, Dr. Van Heesweg 2, 8025 AB, Zwolle, The Netherlands.
A young BRCA-1 positive woman turned out to have advanced stage ovarian cancer despite an ensuring check-up 4 months earlier. Much remains unknown regarding the efficacy of screening programs, when applied to individuals predisposed for an inherited malignancy. Therefore, vigilance is mandatory when dealing with women with a positive family history of mammarian and/or ovarian cancer.

3
UI - 11881908
AU - Isaacs C; Peshkin BN; Schwartz M; Demarco TA; Main D; Lerman C
TI - Breast and ovarian cancer screening practices in healthy women with a strong family history of breast or ovarian cancer.
SO - Breast Cancer Res Treat 2002 Jan;71(2):103-12
AD - Department of Medical Oncology, Lombardi Cancer Center, Georgetown University, Washington, DC 20007-2197, USA. isaacsc@georgetown.edu
Studies in women with a family history of cancer demonstrate a wide variability in the uptake of cancer screening measures. Little data exist regarding the breast and ovarian cancer screening practices of women who are members of hereditary breast cancer families. In order to address this issue, we examined the screening behaviors and the determinants of screening in a clinic based group of 216 women with a strong family history of breast or ovarian cancer who were participating in a free genetic counseling and testing research program. At baseline, prior to obtaining genetic counseling or testing, 50% of women ages 30-39, 83% of those age 40-49, 69% of those 50-64, and 53% of those >65 reported having a mammogram in the prior year. Adherence to mammography recommendations was correlated with age, number of relatives with breast cancer, and income. Twenty percent of participants had at least one CA- 125 performed and 31 % had ever obtained a screening ultrasound. Having at least one relative with ovarian cancer was very strongly associated with ovarian cancer screening [OR = 12.3, 95% CI = 4.6-33 for CA-125; OR=4.9, 95% CI=2.4, 10.1 for ultrasound]. No association between cancer worries/distress and either breast or ovarian cancer screening was found. In conclusion, the breast and ovarian screening uptake in healthy women from hereditary breast cancer families is suboptimal, even for women over age 50, for whom annual mammography is clearly indicated. These findings indicate a need for better education about screening guidelines for high-risk women.

4
UI - 12114493
AU - Hofmann W; Wappenschmidt B; Berhane S; Schmutzler R; Scherneck S
TI - Detection of large rearrangements of exons 13 and 22 in the BRCA1 gene in German families.
SO - J Med Genet 2002 Jul;39(7):E36

5
UI - 12011077
AU - Andrews HN; Mullan PB; McWilliams S; Sebelova S; Quinn JE; Gilmore PM;
TI - McCabe N; Pace A; Koller B; Johnston PG; Haber DA; Harkin DP BRCA1 regulates the interferon gamma-mediated apoptotic response.
SO - J Biol Chem 2002 Jul 19;277(29):26225-32
AD - Department of Oncology, Cancer Research Centre, The Queen's University Belfast, Belfast BT9 7AB, Northern Ireland.
BRCA1 is a tumor suppressor gene implicated in transcriptional regulation. We have generated cell lines with inducible expression of BRCA1 as a tool to identify downstream targets that may be important mediators of BRCA1 function. Oligonucleotide array-based expression profiling identified 11 previously described interferon regulated genes that were up-regulated following inducible expression of BRCA1. Northern blot analysis revealed that a subset of the identified targets including IRF-7, MxA, and ISG-54 were synergistically up-regulated by BRCA1 in the presence of interferon gamma (IFN-gamma) but not interferons alpha or beta. Importantly, IFN-gamma-mediated induction of IRF-7 and MxA was attenuated in the BRCA1 mutant cell line HCC1937, an effect that was rescued following reconstitution of exogenous wild type BRCA1 in these cells. Furthermore, reconstituted BRCA1 sensitized HCC1937 cells to IFN-gamma-induced apoptotic cell death. This study identifies BRCA1 as a component of the IFN-gamma-regulated signaling pathway and suggests that BRCA1 may play a role in the regulation of IFN-gamma-mediated apoptosis.

6
UI - 12039951
AU - Zhong Q; Chen CF; Chen PL; Lee WH
TI - BRCA1 facilitates microhomology-mediated end joining of DNA double strand breaks.
SO - J Biol Chem 2002 Aug 9;277(32):28641-7
AD - Department of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78245, USA.
BRCA1 is critical for the maintenance of genomic stability, in part through its interaction with the Rad50.Mre11.Nbs1 complex, which occupies a central role in DNA double strand break repair mediated by nonhomologous end joining (NHEJ) and homologous recombination. BRCA1 has been shown to be required for homology-directed recombination repair. However, the role of BRCA1 in NHEJ, a critical pathway for the repair of double strand breaks and genome stability in mammalian cells, remains elusive. Here, we established a pair of mouse embryonic fibroblasts (MEFs) derived from 9.5-day-old embryos with genotypes Brca1(+/+):p53(-/-) or Brca1(-/-):p53(-/-). The Brca1(-/-):p53(-/-) MEFs appear to be extremely sensitive to ionizing radiation. The contribution of BRCA1 in NHEJ was evaluated in these cells using three different assay systems. First, transfection of a linearized plasmid in which expression of the reporter gene required precise end joining indicated that Brca1(-/-) MEFs display a moderate deficiency when compared with Brca1(+/+) cells. Second, using a retrovirus infection assay dependent on NHEJ, a 5-10-fold reduction in retroviral integration efficiency was observed in Brca1(-/-) MEFs when compared with the Brca1(+/+) MEFs. Third, Brca1(-/-) MEFs exhibited a 50-100-fold deficiency in microhomology-mediated end-joining activity of a defined chromosomal DNA double strand break introduced by a rare cutting endonuclease I-SceI. These results provide evidence that Brca1 has an essential role in microhomology-mediated end joining and suggest a novel molecular basis for its caretaker role in the maintenance of genome integrity.

7
UI - 11535704
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. ms496r@nih.gov
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.

8
UI - 12170778
AU - Takimoto R; MacLachlan TK; Dicker DT; Niitsu Y; Mori T; el-Deiry WS
TI - BRCA1 transcriptionally regulates damaged DNA binding protein (DDB2) in the DNA repair response following UV-irradiation.
SO - Cancer Biol Ther 2002 Mar-Apr;1(2):177-86
AD - Laboratory of Molecular Oncology and Cell Cycle Regulation, Howard Hughes Medical Institute, Departments of Medicine, Genetics, and Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
The p53 and BRCA1 tumor suppressors are involved in repair processes and may cooperate to transactivate certain genes, including p21WAF/CIP1 and GADD45. We find that the Xeroderma Pigmentosum Complementation group E (XPE) mutated Damaged-DNA binding protein p48 (DDB2) is upregulated by BRCA1 in a p53-dependent manner following UVC, Adriamycin, or Cisplatin exposure. BRCA1 enhances p53 binding to the DDB2 promoter in vivo as well as p53-dependent transactivation of DDB2 promoter-reporter constructs through a classical p53 DNA responsive element. Antisense abrogation of BRCA1 expression abrogates upregulation of DDB2 after UVC or cisplatin exposure. Using a host cell reactivation assay, DNA repair activity is more significantly restored by introduction of BRCA1 into wt as compared to DDB2-deficient cells. Furthermore disappearance of the photoproducts cyclobutane pyrimidine dimer (CPD) and 6-4 photoproduct (6-4PP) was delayed by antisense abrogation of BRCA1 expression in UV-exposed human cells. Thus the DNA repair function of BRCA1 may be attributed in part to p53-dependent transcriptional induction of DDB2. Loss of BRCA1-dependent DDB2 repair function may contribute to cancer susceptibility and cellular sensitivity to DNA damage.

9
UI - 12212615
AU - Monteiro AN
TI - Participation of BRCA1 in the DNA repair response...via transcription.
SO - Cancer Biol Ther 2002 Mar-Apr;1(2):187-8
AD - Laboratory of Molecular Oncology, Strong Cancer Prevention Center and Department of Cell Biology, Weill Medical College of Cornell University, New York, New York 10021, USA.

10
UI - 12142002
AU - Goldman MA
TI - Cancer: the chromatin connection.
SO - Trends Genet 2002 Aug;18(8):390-1
AD - Dept of Biology, San Francisco State University, San Francisco, CA 94132-1722, USA. Goldman@sfu.edu
The American Association for Cancer Research's 93rd Annual Meeting was

11
UI - 11975969
AU - Rao GG; Ashfaq R; Schorge JO
TI - Transitional cell ovarian carcinoma in a BRCA1 mutation carrier.
SO - Obstet Gynecol 2002 May;99(5 Pt 2):944-6
AD - Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
BACKGROUND: BRCA1 mutation carriers are at high risk of developing epithelial ovarian cancer, but the transitional cell variant has not been previously reported in these patients. CASE:A nulligravid, perimenopausal woman underwent exploratory laparotomy for a pelvic mass, ascites, and omental caking. Intraoperatively, frozen section of a tumor implant revealed high-grade epithelial ovarian carcinoma. Optimal surgical cytoreduction was performed. The final surgical pathology confirmed International Federation of Gynecology and Obstetrics stage IIIC transitional cell ovarian carcinoma. Her family history was significant for a sister with premenopausal breast cancer and a paternal aunt with ovarian cancer. The patient was counseled and elected to undergo genetic testing. Comprehensive gene sequence analysis detected the germline BRCA1 5382insC mutation. CONCLUSION: Transitional cell ovarian carcinoma is a rare histologic variant of epithelial ovarian cancer that may occur in BRCA1 mutation carriers.

12
UI - 12183412
AU - Xu B; O'Donnell AH; Kim ST; Kastan MB
TI - Phosphorylation of serine 1387 in Brca1 is specifically required for the Atm-mediated S-phase checkpoint after ionizing irradiation.
SO - Cancer Res 2002 Aug 15;62(16):4588-91
AD - Department of Hematology-Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Although it is well established that inheritance of mutations in the Brca1 gene significantly increases the chances of developing breast or ovarian cancers, the mechanisms underlying this specific tumor susceptibility remain to be clarified. It is clear that one of the roles of the Brca1 protein is to facilitate cellular responses to DNA damage. We recently reported that Brca1 function is required for appropriate cell cycle arrests after ionizing irradiation in both the S-phase and the G2 phase of the cell cycle. We also found that mutation of serine 1423 in Brca1, a target of Atm phosphorylation, abrogates the G2-M checkpoint but not the ionizing irradiation-induced S-phase checkpoint. Here we demonstrate that mutation of serine 1387 in Brca1, another target of Atm phosphorylation, conversely abrogates the radiation-induced S-phase arrest but does not affect the G2-M checkpoint. Thus, these two posttranslational modifications of Brca1 have two distinct functional roles in the protein. In addition, although mutation of this site abrogates the ionizing irradiation-induced S-phase arrest, it does not adversely affect cell survival after irradiation. This demonstrates that loss of this checkpoint function by itself does not affect cell survival and suggests that some other function of Brca1 alters cell survival after DNA damage.

13
UI - 12214252
AU - Deng CX
TI - Roles of BRCA1 in centrosome duplication.
SO - Oncogene 2002 Sep 9;21(40):6222-7
AD - Genetics of Development and Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 10/9N105, 10 Center Drive, Bethesda, Maryland, MD 20892, USA. chuxiad@bdg10.niddk.nih.gov
Centrosome duplication is under precise control and occurs only once in a normal mammalian cell cycle. Disruption of this process causes centrosome amplification, unequal segregation of chromosomes and, ultimately, tumorigenesis. Recent studies indicate that breast cancer suppressor gene 1 (BRCA1) plays an important role in regulating centrosome duplication. BRCA1 is located in the centrosome and binds to gamma-tubulin. It interacts with a variety of proteins that regulate centrosome duplication, including BRCA2, CDK2-Cyclin A, CDK2-Cyclin E, Gadd45, p21, p53 and Rb. Furthermore, targeted disruption of murine BRCA1 results in centrosome amplification, suggesting that BRCA1 serves as a negative regulator for centrosome duplication. This review will examine these data and discuss possible relationships between BRCA1 and its interacting proteins in centrosome duplication.

14
UI - 11928474
AU - Ghosh D
TI - Singular value decomposition regression models for classification of tumors from microarray experiments.
SO - Pac Symp Biocomput 2002;():18-29
AD - Department of Biostatistics, University of Michigan, 1420 Washington Heights, Ann Arbor, MI 48109-2029, USA. ghoshd@umich.edu
An important problem in the analysis of microarray data is correlating the high-dimensional measurements with clinical phenotypes. In this paper, we develop predictive models for associating gene expression data from microarray experiments with such outcomes. They are based on the singular value decomposition. We propose new algorithms for performing gene selection and gene clustering based on these predictive models. The estimation procedure using the regression models occurs in two stages. First, the gene expression measurements are transformed using the singular value decomposition. The regression parameters in the model linking the principal components with the clinical responses are then estimated using maximum likelihood. We demonstrate the application of the methodology to data from a breast cancer study.

15
UI - 11463009
AU - Meijers-Heijboer H; van Geel B; van Putten WL; Henzen-Logmans SC;
TI - Seynaeve C; Menke-Pluymers MB; Bartels CC; Verhoog LC; van den Ouweland AM; Niermeijer MF; Brekelmans CT; Klijn JG Breast cancer after prophylactic bilateral mastectomy in women with a BRCA1 or BRCA2 mutation.
SO - N Engl J Med 2001 Jul 19;345(3):159-64
AD - Department of Medical Oncology, Erasmus University Medical Center, Rotterdam, The Netherlands.
BACKGROUND: Women with a BRCA1 or BRCA2 mutation have a high risk of breast cancer and may choose to undergo prophylactic bilateral total mastectomy. We investigated the efficacy of this procedure in such women. METHODS: We conducted a prospective study of 139 women with a pathogenic BRCA1 or BRCA2 mutation who were enrolled in a breast-cancer surveillance program at the Rotterdam Family Cancer Clinic. At the time of enrollment, none of the women had a history of breast cancer. Seventy-six of these women eventually underwent prophylactic mastectomy, and the other 63 remained under regular surveillance. The effect of mastectomy on the incidence of breast cancer was analyzed by the Cox proportional-hazards method in which mastectomy was modeled as a time-dependent covariate. RESULTS: No cases of breast cancer were observed after prophylactic mastectomy after a mean (+/-SE) follow-up of 2.9+/-1.4 years, whereas eight breast cancers developed in women under regular surveillance after a mean follow-up of 3.0+/-1.5 years (P=0.003; hazard ratio, 0; 95 percent confidence interval, 0 to 0.36). The actuarial mean five-year incidence of breast cancer among all women in the surveillance group was 17+/-7 percent. On the basis of an exponential model, the yearly incidence of breast cancer in this group was 2.5 percent. The observed number of breast cancers in the surveillance group was consistent with the expected number (ratio of observed to expected cases, 1.2; 95 percent confidence interval, 0.4 to 3.7; P=0.80). CONCLUSIONS: In women with a BRCA1 or BRCA2 mutation, prophylactic bilateral total mastectomy reduces the incidence of breast cancer at three years of follow-up.

16
UI - 12023992
AU - Kauff ND; Satagopan JM; Robson ME; Scheuer L; Hensley M; Hudis CA; Ellis
TI - NA; Boyd J; Borgen PI; Barakat RR; Norton L; Castiel M; Nafa K; Offit K Risk-reducing salpingo-oophorectomy in women with a BRCA1 or BRCA2 mutation.
SO - N Engl J Med 2002 May 23;346(21):1609-15
AD - Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York 10021, USA.
BACKGROUND: Risk-reducing salpingo-oophorectomy is often considered by carriers of BRCA mutations who have completed childbearing. However, there are limited data supporting the efficacy of this approach. We prospectively compared the effect of risk-reducing salpingo-oophorectomy with that of surveillance for ovarian cancer on the incidence of subsequent breast cancer and BRCA-related gynecologic cancers in women with BRCA mutations. METHODS: All women with BRCA1 or BRCA2 mutations identified during a six-year period were offered enrollment in a prospective follow-up study. A total of 170 women 35 years of age or older who had not undergone bilateral oophorectomy chose to undergo either surveillance for ovarian cancer or risk-reducing salpingo-oophorectomy. Follow-up involved an annual questionnaire, telephone contact, and reviews of medical records. The time to cancer in the two groups was compared by Kaplan-Meier analysis and a Cox proportional-hazards model. RESULTS: During a mean follow-up of 24.2 months, breast cancer was diagnosed in 3 of the 98 women who chose risk-reducing salpingo-oophorectomy and peritoneal cancer was diagnosed in 1 woman in this group. Among the 72 women who chose surveillance, breast cancer was diagnosed in 8, ovarian cancer in 4, and peritoneal cancer in 1. The time to breast cancer or BRCA-related gynecologic cancer was longer in the salpingo-oophorectomy group, with a hazard ratio for subsequent breast cancer or BRCA-related gynecologic cancer of 0.25 (95 percent confidence interval, 0.08 to 0.74). CONCLUSIONS: Salpingo-oophorectomy in carriers of BRCA mutations can decrease the risk of breast cancer and BRCA-related gynecologic cancer.

18
UI - 12324566
AU - Zhuang SH; Leonard GD; Swain SM
TI - Oophorectomy in carriers of BRCA mutations.
SO - N Engl J Med 2002 Sep 26;347(13):1037-40; discussion 1037-40

19
UI - 12353511
AU - Peshkin BN; DeMarco TA; Schwartz MD
TI - Oophorectomy in carriers of BRCA mutations.
SO - N Engl J Med 2002 Sep 26;347(13):1037-40; discussion 1037-40

20
UI - 12353512
AU - Anderson WF; Brawley OW; Chang S
TI - Oophorectomy in carriers of BRCA mutations.
SO - N Engl J Med 2002 Sep 26;347(13):1037-40; discussion 1037-40

21
UI - 12353513
AU - Whitfield GA
TI - Oophorectomy in carriers of BRCA mutations.
SO - N Engl J Med 2002 Sep 26;347(13):1037-40; discussion 1037-40

22
UI - 12217765
AU - Ceccaroni M; Genuardi M; Legge F; Lucci-Cordisco E; Carrara S; D'Amico
TI - F; Greggi S; Scambia G BRCA1-related malignancies in a family presenting with von Recklinghausen's disease.
SO - Gynecol Oncol 2002 Sep;86(3):375-8
AD - Department of Obstetrics and Gynecology, Catholic University of the Sacred Heart, Largo E. Gemelli 8, 00168 Rome, Italy.
BACKGROUND: The association between neurofibromatosis and gynecologic malignancies is rarely reported in the literature. Both BRCA1 and NF1 genes are located on the long arm of chromosome 17. CASE: We have observed a pedigree showing several individuals affected by both type 1 neurofibromatosis (NF1) and breast or coelomatic cancers. The number of individuals affected, their degree of relationship, and the early age at onset were suggestive of an hereditary breast/ovarian cancer syndrome. Linkage analysis was performed in order to establish whether markers in the chromosome 17 region containing the BRCA1 and NF1 loci were shared by affected individuals. Screening for BRCA1 mutations was performed by PTT and SSCP. Analysis of chromosome 17 DNA markers in the five family members tested show that three individuals affected by both NF1 and carcinomas share a common haplotype including the NF1 and BRCA1 loci on chromosome 17. Mutation analysis showed the presence of a nonsense mutation within BRCA1 exon 12 in two individuals, mother and daughter, affected by breast and peritoneal cancer, respectively, as well as in the son, who had rectal cancer at the early age of 27 years. All three subjects also had NF1. CONCLUSION: The concurrence of NF1 and hereditary breast/ovarian cancer in this family is likely due to the presence of two linked mutations at the NF1 and BRCA1 loci.

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NCI CANCERLIT^® Search: BRCA1 Gene - September 2002

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NCI CANCERLIT® Search: BRCA1 Gene - September 2002

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NCI CANCERLIT^® Search: BRCA1 Gene - September 2002