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Journal articles on the topic 'Familial breast cancer'

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Author: Grafiati

Published: 4 June 2021

Last updated: 29 January 2023

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1

Sukumaran, Shobini, and Kunal Chawathey. "Familial breast cancer." InnovAiT: Education and inspiration for general practice 10, no. 2 (December 27, 2016): 82–88. http://dx.doi.org/10.1177/1755738016685893.

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Breast cancer is the most common malignancy in women; it affects about one in eight women. Familial breast cancer typically presents earlier than sporadic breast cancer, and is more often bilateral than in sporadic cases. Ovarian cancer is more common in familial breast cancer. A large number of studies have confirmed an increased breast cancer risk in patients with a significant family history of breast cancer. The breast cancer genotype has an autosomal dominant pattern of transmission. This article considers familial breast cancer and various aspects of breast cancer management in primary care, including the genetics of familial breast cancer, and guidelines on referral to secondary care.

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2

Hemminki, Kari, Jan Sundquist, and Andreas Brandt. "Familial Mortality and Familial Incidence in Cancer." Journal of Clinical Oncology 29, no. 6 (February 20, 2011): 712–18. http://dx.doi.org/10.1200/jco.2010.30.5664.

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Purpose An overwhelming majority of data on familial risk in cancer is based on incident cancer, whereas familiality in cancer mortality is largely unknown. If fatal form of cancer was a highly familial subtype, then familial risk for mortality may exceed that of incidence, which would be particularly relevant for clinical decision making and counseling. Patients and Methods The individuals in the nationwide Swedish Family-Cancer Database were classified according to family history of fatal and nonfatal cancer. Familial risks of incident and fatal concordant cancer were calculated for offspring based on their parental family history using a Cox model with hazard ratio (HR); offspring without family history were the reference. Results Most HRs for offspring incident cancers were somewhat higher for fatal compared with nonfatal parental family history. For breast (HR, 1.87 fatal v 1.66 nonfatal; P < .001) and prostate (HR, 2.30 fatal v 1.84 nonfatal; P < .001) cancers, 51.0% of patients with familial breast cancer and 56.6% of patients with prostate cancer had fatal family history. HRs for death in offspring according to a fatal compared with nonfatal family history were significantly increased for colorectal (HR, 1.76 v 1.47, respectively; P = .02), breast (HR, 1.97 v 1.51, respectively; P = .002), and prostate (HR, 2.03 v 1.59, respectively; P = .002) cancers. TNM classification did not seem to differ between the family histories. We showed also that an overwhelming proportion of offspring were diagnosed after the parental death. Conclusion Familial breast, prostate, and colorectal cancers might have a yet unidentified genetic component associated with poorer survival. It may be useful to record survival data in family history records.

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3

Fourquet, Alain, Dominique Stoppa-Lyonnet, Youlia M. Kirova, Brigitte Sigal-Zafrani, and Bernard Asselain. "Familial Breast Cancer." American Journal of Clinical Oncology 32, no. 2 (April 2009): 127–31. http://dx.doi.org/10.1097/coc.0b013e31817f9e1c.

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4

Weber, Barbara L. "Familial Breast Cancer." Clinical Chemistry 40, no. 4 (April 1, 1994): 639–40. http://dx.doi.org/10.1093/clinchem/40.4.639.

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5

Phipps, R. F., and P. M. Perry. "Familial breast cancer." Postgraduate Medical Journal 64, no. 757 (November 1, 1988): 847–49. http://dx.doi.org/10.1136/pgmj.64.757.847.

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6

Lalloo, F., and D. G. Evans. "Familial Breast Cancer." Clinical Genetics 82, no. 2 (April 13, 2012): 105–14. http://dx.doi.org/10.1111/j.1399-0004.2012.01859.x.

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7

Emery, J. "Familial breast cancer." Family Practice 14, no. 5 (October 1, 1997): 422. http://dx.doi.org/10.1093/fampra/14.5.422.

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8

Jones, Corinne, David J. Oliver, and Anthony J. Van Merwyk. "Familial male breast cancer." Medical Journal of Australia 164, no. 10 (May 1996): 640. http://dx.doi.org/10.5694/j.1326-5377.1996.tb122226.x.

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9

Lakhani, Sunil R., Michael J. O'Hare, and Alan Ashworth. "Profiling familial breast cancer." Nature Medicine 7, no. 4 (April 2001): 408–10. http://dx.doi.org/10.1038/86464.

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10

Maxwell, Kara N., and Susan M. Domchek. "Familial Breast Cancer Risk." Current Breast Cancer Reports 5, no. 3 (July 3, 2013): 170–82. http://dx.doi.org/10.1007/s12609-013-0117-9.

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11

Hauser, Alan R., Irving J. Lerner, and Richard A. King. "Familial male breast cancer." American Journal of Medical Genetics 44, no. 6 (December 1, 1992): 839–40. http://dx.doi.org/10.1002/ajmg.1320440626.

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12

Pelttari, Liisa M., Sofia Khan, Mikko Vuorela, Johanna I. Kiiski, Sara Vilske, Viivi Nevanlinna, Salla Ranta, et al. "RAD51B in Familial Breast Cancer." PLOS ONE 11, no. 5 (May 5, 2016): e0153788. http://dx.doi.org/10.1371/journal.pone.0153788.

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13

BERCHUCK, ANDREW, MICHAEL CARNEY, JONATHAN M. LANCASTER, JEFFREY MARKS, and ANDREW P. FUTREAL. "Familial Breast-Ovarian Cancer Syndromes." Clinical Obstetrics and Gynecology 41, no. 1 (March 1998): 157–66. http://dx.doi.org/10.1097/00003081-199803000-00022.

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14

Powles, T. "Tamoxifen and familial breast Cancer." European Journal of Cancer 38, no. 11 (February 2002): S18. http://dx.doi.org/10.1016/s0959-8049(02)80015-6.

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15

Evans, D. G. R., I. S. Fentiman, K. McPherson, D. Asbury, B. A. J. Ponder, and A. Howell. "Fortnightly Review: Familial breast cancer." BMJ 308, no. 6922 (January 15, 1994): 183–87. http://dx.doi.org/10.1136/bmj.308.6922.183.

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16

Bingham, Hal G. "Familial breast cancer in males." Plastic and Reconstructive Surgery 80, no. 4 (October 1987): 653. http://dx.doi.org/10.1097/00006534-198710000-00069.

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17

Anderson, David E. "Familial versus sporadic breast cancer." Cancer 70, S4 (September 15, 1992): 1740–46. http://dx.doi.org/10.1002/1097-0142(19920915)70:4+<1740::aid-cncr2820701615>3.0.co;2-1.

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18

Anderson, David E., and Michael D. Badzioch. "Risk of familial breast cancer." Cancer 56, no. 2 (July 15, 1985): 383–87. http://dx.doi.org/10.1002/1097-0142(19850715)56:2<383::aid-cncr2820560230>3.0.co;2-0.

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19

Cao, Wenming, Yun Gao, Hongjian Yang, Shang-Nao Xie, Xuli Meng, Zhi-Wen Pan, zhan-Hong Chen, et al. "Variations of DICER1 sequence in Chinese women with BRCA1/BRCA2 negative familial breast cancer." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e12557-e12557. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e12557.

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e12557 Background: Germline mutations in identified breast cancer susceptibility genes account for less than 20% of Chinese familial breast cancers. Dicer is an essential component of the microRNA producing machinery and germline mutations of DICER1 gene have been confirmed in familial pleuropulmonary blastoma, ovarian sex cord-stromal tumor and so on. Moreover, low expression of DICER1 is frequently detected in breast cancer. However, whether germline mutations of DICER1 occur in familial breast cancers remains unknown. Methods: 65 breast cancer probands from BRCA1/BRCA2 negative Chinese breast cancer families were used for screening of germline mutations in DICER1. In addition, 100 unrelated healthy females were enrolled as the controls. Polymerase chain reaction (PCR)-sequencing assay was employed to screen mutations in the entire coding regions and exon-intron boundaries of DICER1. Genotype and haplotype analyses were studied by widely available programs. Results: No deleterious mutations were identified in the 65 breast cancer probands. However, we found 12 germline variations and 4 of which were novel. In addition, the G allele frequency of rs2297730 (IVS12-91 A>G) was higher in familial breast cancer patients group than that in healthy controls group (OR = 1.873, 95% CI: 1.174-2.988, P = 0.008), and the A/G genotype were significantly associated with familial breast cancer (OR = 3.133; 95% CI: 1.562-6.287, P = 0.004). According to the minimum value of Akaike’s Information Criterion (AIC), the best genetic model was dominant. In addition, the haplotype GCGGAT was significantly associated with familial breast cancer (OR = 2.17, 95% CI: 1.20-3.91, P = 0.011). Conclusions: Although none of deleterious mutations were identified in the DICER1 gene, the current study provided a haplotype analysis of the DICER1 gene polymorphisms. We showed a significantly increased risk of BRCA1/BRCA2 negative familial breast cancer for DICER1 IVS12-91 A>G variant. It might be a potential risk marker for breast cancer in thus population.

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20

Shi, Chanjuan, Ralph H. Hruban, and Alison P. Klein. "Familial Pancreatic Cancer." Archives of Pathology & Laboratory Medicine 133, no. 3 (March 1, 2009): 365–74. http://dx.doi.org/10.5858/133.3.365.

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Abstract Context.—Approximately 5% to 10% of individuals with pancreatic cancer report a history of pancreatic cancer in a close family member. In addition, several known genetic syndromes, such as familial breast cancer (BRCA2), the Peutz-Jeghers syndrome, and the familial atypical multiple mole melanoma syndrome, have been shown to be associated with an increased risk of pancreatic cancer. The known genes associated with these conditions can explain only a portion of the clustering of pancreatic cancer in families, and research to identify additional susceptibility genes is ongoing. Objective.—To provide an understanding of familial pancreatic cancer and the pathology of familial exocrine pancreatic cancers. Data Sources.—Published literature on familial aggregation of pancreatic cancer and familial exocrine pancreatic tumors. Conclusions.—Even in the absence of predictive genetic testing, the collection of a careful, detailed family history is an important step in the management of all patients with pancreatic cancer. While most pancreatic cancers that arise in patients with a family history are ductal adenocarcinomas, certain subtypes of pancreatic cancer have been associated with familial syndromes. Therefore, the histologic appearance of the pancreatic cancer itself, and/or the presence and appearance of precancerous changes in the pancreas, may increase the clinical index of suspicion for a genetic syndrome.

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21

Gonda, Kenji, Shoichiro Horita, Yuko Maejima, Seiichi Takenoshita, and Kenju Shimomura. "Soluble interleukin-2 receptor as a predictive and prognostic marker for patients with familial breast cancer." Science Progress 104, no. 3 (July 2021): 003685042110395. http://dx.doi.org/10.1177/00368504211039590.

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The incidence of breast cancer increases annually, and it has become common within families of breast cancer patients. Interleukin-2 activates cytotoxic T lymphocytes, which are important for cancer immunity. To identify markers of increased familial breast cancer risk, soluble interleukin-2 receptor levels and immunologic factors were investigated in familial breast cancer and non-familial breast cancer patients. Of 106 untreated breast cancer patients in this study, 24 had familial breast cancer and 82 had non-familial breast cancer. The patients’ soluble interleukin-2 receptor, interleukin-10, vascular endothelial growth factor, interleukin-17, regulatory T cell, myeloid-derived suppressor cell, white blood cell, and C-reactive protein levels, and their neutrophil-to-lymphocyte ratios were measured, and their prognoses were compared according to the soluble interleukin-2 receptor levels. Additionally, postoperative tissues from the patients with high soluble interleukin-2 receptor levels were stained with programmed cell death ligand 1 and cluster of differentiation 8. The soluble interleukin-2 receptor level in the familial breast cancer patients was significantly higher, and it showed significantly stronger correlations with the neutrophil-to-lymphocyte ratio and the interleukin-10, vascular endothelial growth factor, interleukin-17, regulatory T cell, myeloid-derived suppressor cell, white blood cell, and C-reactive protein levels, than in the non-familial breast cancer patients. The regulatory T cell and myeloid-derived suppressor cell levels were significantly higher in the patients with high soluble interleukin-2 receptor levels, and the overall survival and disease-free-survival rates were significantly worse for the familial breast cancer patients than for the non-familial breast cancer patients. Triple-negative breast cancer tissues from the familial breast cancer patients with high soluble interleukin-2 receptor levels stained well for programmed cell death ligand 1 and cluster of differentiation 8. Soluble interleukin-2 receptor levels can be used to predict the prognosis of familial breast cancer patients. Prospectively identifying patients who are less likely to have non-familial breast cancer is vital for improving their overall survival.

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22

Huang, Kai-Ling, Yu-Ling Liu, Ya-Ying Hsu, and Wen-Ling Kuo. "Retrospective Analysis of Clinicopathological Features and Familial Cancer History of Synchronous Bilateral Breast Cancer." Healthcare 9, no. 9 (September 13, 2021): 1203. http://dx.doi.org/10.3390/healthcare9091203.

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Bilateral breast cancer is a strong predictor of BRCA 1/2 mutation and hence one criterion indicated for hereditary genetic testing. The purpose of this study is to assess the characteristics of synchronous bilateral breast cancer (SBBC) and its association with personal and familial cancer traits. Patients diagnosed with SBBC in our institute between 1992 and 2018 were retrospectively reviewed, and the information of clinicopathological features, personal and family cancer history were analyzed. Of the 307 SBBCs enrolled, the growing case number generally aligned with the regional breast cancer incidence after the era of population-based mammography screening. SBBC patients had similar cancer stages but worse survival outcomes than those in the standard scenario. A total of 42.0% had mixed pathological diagnoses, and 22.8% had discordant immunohistochemistry (IHC) subtypes from both sides, which contributed to treatment challenges. The correlation of SBBC with hereditary breast and ovarian cancer (HBOC) syndrome was strongly implied, as 20.7% of our SBBC patients with known familial cancer histories had HOBC-related familial cancers (breast, ovarian, or prostate cancers). These findings highlight the need for genetic counseling and germline mutation testing in patients with SBBC. Early PARP inhibitor treatment should also be considered in high-risk cases for outcome improvement.

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23

Demeter, Joseph G., Norton G. Waterman, and Gerald D. Verdi. "Familial male breast carcinoma." Cancer 65, no. 10 (May 15, 1990): 2342–43. http://dx.doi.org/10.1002/1097-0142(19900515)65:10<2342::aid-cncr2820651029>3.0.co;2-y.

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24

Rogoża-Janiszewska, Emilia, Karolina Malińska, Cezary Cybulski, Anna Jakubowska, Jacek Gronwald, Tomasz Huzarski, Marcin Lener, et al. "Prevalence of Recurrent Mutations Predisposing to Breast Cancer in Early-Onset Breast Cancer Patients from Poland." Cancers 12, no. 8 (August 17, 2020): 2321. http://dx.doi.org/10.3390/cancers12082321.

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There are twenty recurrent mutations in six breast-cancer-predisposing genes in Poland (BRCA1, BRCA2, CHEK2, PALB2, NBN, and RECQL). The frequencies of the twenty alleles have not been measured in a large series of early-onset breast cancer patients from Poland unselected for family history. We genotyped 2464 women with breast cancer diagnosed below age 41 years for twenty recurrent germline mutations in six genes, including BRCA1, BRCA2 CHEK2, PALB2, NBN, and RECQL. A mutation in one of the six genes was identified in 419 of the 2464 early-onset breast cancer cases (17%), including 22.4% of those cases diagnosed below age 31. The mutation frequency was 18.8% for familial breast cancer cases and 6% for non-familial cases. Among women with breast cancer below age 31, the mutation frequency was 23.6% for familial cases and 17.4% in non-familial cases. The majority of mutations (76.2%) were seen in BRCA1 and BRCA2. In Poland, a panel of twenty recurrent mutations in six genes can identify a genetic basis for a high percentage of early-onset cases and testing is recommended for all women with breast cancer at age 40 or below.

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25

Joó, József Gábor, Mónika Csanád, Katalin Tóth, Szabolcs Máté, and Zsolt Nagy. "Risk assessment in familial breast cancer." Orvosi Hetilap 152, no. 19 (May 2011): 758–62. http://dx.doi.org/10.1556/oh.2011.29110.

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Women with a history of breast cancer are common at centers for cancer genetic risk all over Europe. Given limited health care resources, managing this demand, while achieving good value for money coming from health services, is generally a major challenge. This paper recapitulates and summarizes the available methods of the risk assessment of familial breast cancer. After a systematic review of the literature Gail-model, Claus-model and BOADICEA-model were selected, as well as softwares (LINKAGE software; MENDEL v3.3 software) available in the application of these algorhythms are also summarized. Comparisons were made between the models concerning their advantages and disadvantages. The really reliable methods of risk estimation of familial breast cancer are always based on the analysis of the pedigree structure and allow the estimation of the patient’s probability of carrying a susceptibility gene under a particular genetic model, given her family history. For this method the knowledge of BRCA mutation status is absolutely indispensable. The methods of BRCA mutation analysis as well as the main characteristics of the occurrence of BRCA mutation carrier condition are discussed in details. Orv. Hetil., 2011, 152, 758–762.

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26

Bingham, Hal G. "Bilaterality in familial breast cancer patients." Plastic and Reconstructive Surgery 78, no. 1 (July 1986): 133. http://dx.doi.org/10.1097/00006534-198607000-00057.

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27

Bennett, I. C., M. Gattas, and B. T. Teh. "The management of familial breast cancer." Breast 9, no. 5 (October 2000): 247–63. http://dx.doi.org/10.1054/brst.2000.0208.

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28

Fisher, Carla L., Erin Maloney, Emily Glogowski, Karen Hurley, Shawna Edgerson, Wendy G. Lichtenthal, David Kissane, and Carma Bylund. "Talking About Familial Breast Cancer Risk." Qualitative Health Research 24, no. 4 (March 14, 2014): 517–35. http://dx.doi.org/10.1177/1049732314524638.

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29

Goodwin, Pamela J. "Management of familial breast cancer risk." Breast Cancer Research and Treatment 62, no. 1 (July 2000): 19–33. http://dx.doi.org/10.1023/a:1006470206271.

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30

Cornelisse, C. J., R. S. Cornelis, and P. Devilee. "Genes Responsible for Familial Breast Cancer." Pathology - Research and Practice 192, no. 7 (January 1996): 684–93. http://dx.doi.org/10.1016/s0344-0338(96)80090-2.

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31

Eerola, H., C. Blomqvist, E. Pukkala, S. Pyrhönen, and H. Nevanlinna. "Familial breast cancer in southern Finland." European Journal of Cancer 36, no. 9 (June 2000): 1143–48. http://dx.doi.org/10.1016/s0959-8049(00)00093-9.

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32

Ashworth, Alan. "Familial breast cancer: the first linkage." Lancet Oncology 10, no. 12 (December 2009): 1212. http://dx.doi.org/10.1016/s1470-2045(09)70235-9.

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33

Møller, P., E. M. Sager, P. Helgerud, C. Tropé, and S. Kvinnsland. "Early diagnosis of familial breast cancer." Breast 2, no. 3 (September 1993): 189. http://dx.doi.org/10.1016/0960-9776(93)90084-s.

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34

Hemminki, Kari, Jianguang Ji, Asta Försti, Jan Sundquist, and Per Lenner. "Survival in breast cancer is familial." Breast Cancer Research and Treatment 110, no. 1 (August 3, 2007): 177–82. http://dx.doi.org/10.1007/s10549-007-9692-7.

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35

Hatada, Takuya, Ikuji Aoki, Yoshifumi Saeki, Toru Nakai, and Joji Utsunomiya. "Four Cases of Familial Breast Cancer." Breast Cancer 2, no. 2 (October 1995): 155–57. http://dx.doi.org/10.1007/bf02966954.

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36

Hemminki, Kari, Asta Försti, and Bowang Chen. "Breast and prostate cancer: familial associations." Nature Reviews Cancer 10, no. 7 (July 2010): 523. http://dx.doi.org/10.1038/nrc2795-c1.

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37

Eerola, Hannaleena, Carl Blomqvist, Seppo Pyrhönen, and Heli Nevanlinna. "Familial Breast Cancer in Southern Finland." Disease Markers 15, no. 1-3 (1999): 105. http://dx.doi.org/10.1155/1999/451750.

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38

WATTS, R. A., and P. MERRY. "FAMILIAL EOSINOPHlLIC FASCIITIS AND BREAST CANCER." Rheumatology 33, no. 1 (1994): 93–94. http://dx.doi.org/10.1093/rheumatology/33.1.93.

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39

Mogelvang, Christian. "Emotion, Illogic, and Familial Breast Cancer." Plastic and Reconstructive Surgery 95, no. 4 (April 1995): 740–41. http://dx.doi.org/10.1097/00006534-199504000-00018.

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40

Anderson, David E., and Michael D. Badzioch. "Survival in familial breast cancer patients." Cancer 58, no. 2 (July 15, 1986): 360–65. http://dx.doi.org/10.1002/1097-0142(19860715)58:2<360::aid-cncr2820580227>3.0.co;2-f.

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41

Siraganian, Patricia A., Paul H. Levine, Patricia Madigan, and John J. Mulvihill. "Familial breast cancer in black Americans." Cancer 60, no. 7 (October 1, 1987): 1657–60. http://dx.doi.org/10.1002/1097-0142(19871001)60:7<1657::aid-cncr2820600739>3.0.co;2-z.

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42

Brody, Larry, Lucio Castilla, Jeffrey Struewing, Mike Erdos, and Francis S. Collins. "Mechanisms of familial breast cancer causation." Cancer Genetics and Cytogenetics 84, no. 2 (October 1995): 129. http://dx.doi.org/10.1016/0165-4608(96)85212-5.

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43

Anderson, David E., and Michael D. Badzioch. "Bilaterality in familial breast cancer patients." Cancer 56, no. 8 (October 15, 1985): 2092–98. http://dx.doi.org/10.1002/1097-0142(19851015)56:8<2092::aid-cncr2820560835>3.0.co;2-7.

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44

Bergqvist, J., A. Latif, S. A. Roberts, K. D. Hadfield, F. Lalloo, A. Howell, D. G. Evans, and W. G. Newman. "RASSF1A polymorphism in familial breast cancer." Familial Cancer 9, no. 3 (April 2, 2010): 263–65. http://dx.doi.org/10.1007/s10689-010-9335-8.

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45

Güth, Uwe, Dieter Müller, Dorothy Jane Huang, Ellen Obermann, and Hansjakob Müller. "Strictly defined familial male breast cancer." Familial Cancer 10, no. 1 (November 9, 2010): 73–77. http://dx.doi.org/10.1007/s10689-010-9400-3.

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46

Pelucchi, Claudio, Eva Negri, Alessandra Tavani, Silvia Franceschi, and Carlo La Vecchia. "Attributable risk for familial breast cancer." International Journal of Cancer 102, no. 5 (November 13, 2002): 548–49. http://dx.doi.org/10.1002/ijc.10760.

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47

Rayoo, M., M. Yan, E. A. Takano, G. J. Bates, P. J. Brown, A. H. Banham, and S. B. Fox. "Expression of the forkhead box transcription factor FOXP1 is associated with oestrogen receptor alpha, oestrogen receptor beta and improved survival in familial breast cancers." Journal of Clinical Pathology 62, no. 10 (July 20, 2009): 896–902. http://dx.doi.org/10.1136/jcp.2009.065169.

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Background:The role of FOXP1 in sporadic breast cancers has been widely studied but its role in familial breast cancers is yet unexplored.Aims:To investigate FOXP1 expression in different molecular subtypes of familial breast cancers and to correlate its expression with clinicopathological parameters, oestrogen receptors (ER) and survival.Methods:Immunohistochemical staining for FOXP1 was performed in 126 familial breast carcinomas comprising 35 BRCA1, 34 BRCA2 and 57 BRCAX.Results:Nuclear FOXP1 expression ranged from focal weak to widespread strong expression. Expression of FOXP1 was higher in familial breast cancers (54%) compared with sporadic cancers (46%) (p<0.001). There was a significant correlation between FOXP1 with ERα (p = 0.038) and ERβ (p = 0.007) in familial breast cancers. FOXP1 was more highly expressed in familial breast cancers compared with sporadic cancers for luminal (p = 0.021) and basal (p<0.001), but not HER2 and null phenotypes (both p>0.05). The absence of FOXP1 expression was associated with a shorter relapse-free (p = 0.025) and overall survival (p = 0.009) in familial breast cancer. Negativity for FOXP1 was associated with a significantly worse overall survival in BRCA2 cancers (p = 0.021) and there was a non-significant separation of the survival curves for BRCA1 cancers (p = 0.183). No differences in survival were seen for BRCAX cancers (p = 0.762).Conclusion:Results suggest that FOXP1 demonstrates different expression patterns in familial breast cancers than sporadic tumours, even in tumours showing similar phenotypes. They also suggest a different role of FOXP1 as a tumour suppressor in familial tumours, which is unrelated to ER expression and may impact on therapeutic options.

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48

Hemminki, Kari, and Pauli Vaittinen. "Familial breast cancer in the family-cancer database." International Journal of Cancer 77, no. 3 (July 29, 1998): 386–91. http://dx.doi.org/10.1002/(sici)1097-0215(19980729)77:3<386::aid-ijc13>3.0.co;2-6.

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49

Lindblom, Annika. "Familial breast cancer and genes involved in breast carcinogenesis." Breast Cancer Research and Treatment 34, no. 2 (May 1995): 171–83. http://dx.doi.org/10.1007/bf00665789.

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Kuhl, Christiane K., Simone Schrading, Claudia C. Leutner, Nuschin Morakkabati-Spitz, Eva Wardelmann, Rolf Fimmers, Walther Kuhn, and Hans H. Schild. "Mammography, Breast Ultrasound, and Magnetic Resonance Imaging for Surveillance of Women at High Familial Risk for Breast Cancer." Journal of Clinical Oncology 23, no. 33 (November 20, 2005): 8469–76. http://dx.doi.org/10.1200/jco.2004.00.4960.

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Abstract:

Purpose To compare the effectiveness of mammography, breast ultrasound, and magnetic resonance imaging (MRI) for surveillance of women at increased familial risk for breast cancer (lifetime risk of 20% or more). Patients and Methods We conducted a surveillance cohort study of 529 asymptomatic women who, based on their family history and/or mutational analysis, were suspected or proven to carry a breast cancer susceptibility gene (BRCA). A total of 1,542 annual surveillance rounds were completed with a mean follow-up of 5.3 years. Diagnostic accuracies of the three imaging modalities used alone or in different combinations were compared. Results Forty-three breast cancers were identified in the total cohort (34 invasive, nine ductal carcinoma-in-situ). Overall sensitivity of diagnostic imaging was 93% (40 of 43 breast cancers); overall node-positive rate was 16%, and one interval cancer occurred (one of 43 cancers, or 2%). In the analysis by modality, sensitivity was low for mammography (33%) and ultrasound (40%) or the combination of both (49%). MRI offered a significantly higher sensitivity (91%). The sensitivity of mammography in the higher risk groups was 25%, compared with 100% for MRI. Specificity of MRI (97.2%) was equivalent to that of mammography (96.8%). Conclusion Mammography alone, and also mammography combined with breast ultrasound, seems insufficient for early diagnosis of breast cancer in women who are at increased familial risk with or without documented BRCA mutation. If MRI is used for surveillance, diagnosis of intraductal and invasive familial or hereditary cancer is achieved with a significantly higher sensitivity and at a more favorable stage.

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