Relevant bibliographies by topics / Breast – Cancer – Genetic aspects

Academic literature on the topic 'Breast – Cancer – Genetic aspects'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Breast – Cancer – Genetic aspects.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Breast – Cancer – Genetic aspects"

1

Steel, M., A. Thompson, and J. Clayton. "Genetic aspects of breast cancer." British Medical Bulletin 47, no. 2 (1991): 504–18. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072488.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Krasteva, M., Sv Angelova, and Zl Gospodinova. "Molecular-Genetic Aspects of Breast Cancer." Acta Medica Bulgarica 41, no. 2 (December 1, 2014): 67–79. http://dx.doi.org/10.1515/amb-2014-0024.

Full text
Abstract:
Summary Breast cancer is the most frequent malignancy among women. Advances in breast cancer knowledge have deciphered the involvement of a number of tumor suppressor genes and proto-oncogenes in disease pathogenesis. These genes are part of the complex biochemical pathways, which enable cell cycle control and maintenance of genome integrity. Their function may be disrupted as a result of alterations in gene sequence or misregulation of gene expression including alterations in DNA methylation pattern. The present review summarizes the main findings on major breast cancer related genes BRCA1/2, p53, ATM, CHEK2, HER2, PIK3CA and their tumorigenic inactivation/activation. The potential clinical importance of these genes with respect to patients’ prognosis and therapy are also discussed. The possible implication of other putative breast cancer related genes is also outlined. The first elaborate data on the genetic and epigenetic status of the above mentioned genes concerning Bulgarian patients with the sporadic form of the disease are presented. The studies indicate for a characteristic mutational spectrum in some of the genes for the Bulgarian patients and specific correlation between the status of different genes and clinicopathological characteristics.
APA, Harvard, Vancouver, ISO, and other styles
3

Berghe, H. Van Den. "Some Genetic Aspects of Breast Cancer." Acta Clinica Belgica 48, sup15 (January 1993): 17–18. http://dx.doi.org/10.1080/17843286.1993.11718347.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Surbone, Antonella. "The ethical challenge of genetic testing for breast cancer." Medicina e Morale 48, no. 3 (June 30, 1999): 469–84. http://dx.doi.org/10.4081/mem.1999.799.

Full text
Abstract:
The scientific importance of our recently acquired ability to test for heredity predisposition to breast and ovarian cancers is paralleled only by its social and ethical relevance. Dilemmas are common in all genetic testing, but they assume particular nuances in the setting of breast cancer. Due to its devastating nature and to its increasing incidence, breast cancer is a central issue in women’s health. Breast cancer patients and women in general are often deeply involved in understanding the disease process and the treatment options, as they are in discussing the psychological, social and moral ramifications. This paper is a reflection upon some qualitative aspects of the debate that surrounds genetic testing for breast and ovarian cancer, as they have emerged in my encounters with breast cancer patients prior to their decision to consider genetic testing. The five recurrent themes identified in those conversations may or may not be representative of other practice situations, but they illustrate some fundamental philosophical, ethical and moral questions which exist at the core of our human essence and of our moral agency, and which point to the unavoidable intertwinement of medicine, culture, normativity and philosophy, vis-à-vis the many questions raised by genetics. The Author has intentionally refrained from questionnaires, which could betray the complexity of our thinking process, and from the vignettes, as they could betray confidentiality. The paper concludes that the correct answers to the dilemmas posed by genetic testing for breast cancer predisposition can only arise from a blend of medical, social and philosophical analysis.
APA, Harvard, Vancouver, ISO, and other styles
5

Li, Shuai, Tuong L. Nguyen, Tu Nguyen-Dumont, James G. Dowty, Gillian S. Dite, Zhoufeng Ye, Ho N. Trinh, et al. "Genetic Aspects of Mammographic Density Measures Associated with Breast Cancer Risk." Cancers 14, no. 11 (June 2, 2022): 2767. http://dx.doi.org/10.3390/cancers14112767.

Full text
Abstract:
Cumulus, Altocumulus, and Cirrocumulus are measures of mammographic density defined at increasing pixel brightness thresholds, which, when converted to mammogram risk scores (MRSs), predict breast cancer risk. Twin and family studies suggest substantial variance in the MRSs could be explained by genetic factors. For 2559 women aged 30 to 80 years (mean 54 years), we measured the MRSs from digitized film mammograms and estimated the associations of the MRSs with a 313-SNP breast cancer polygenic risk score (PRS) and 202 individual SNPs associated with breast cancer risk. The PRS was weakly positively correlated (correlation coefficients ranged 0.05–0.08; all p < 0.04) with all the MRSs except the Cumulus-white MRS based on the “white but not bright area” (correlation coefficient = 0.04; p = 0.06). After adjusting for its association with the Altocumulus MRS, the PRS was not associated with the Cumulus MRS. There were MRS associations (Bonferroni-adjusted p < 0.04) with one SNP in the ATXN1 gene and nominally with some ESR1 SNPs. Less than 1% of the variance of the MRSs is explained by the genetic markers currently known to be associated with breast cancer risk. Discovering the genetic determinants of the bright, not white, regions of the mammogram could reveal substantial new genetic causes of breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
6

Shatova, Yu S., E. A. Chebotareva, E. Yu Zlatnik, I. A. Novikova, D. I. Vodolazhskiy, and E. A. Dzhenkova. "Some clinical morphological and molecular genetic aspects in patients with clinical signs of hereditary breast cancer." Kazan medical journal 99, no. 2 (April 15, 2018): 224–29. http://dx.doi.org/10.17816/kmj2018-224.

Full text
Abstract:
Aim. To study the clinical morphological and molecular genetic characteristics of clinically hereditary breast cancer with and without verified mutation of BRCA1, BRCA2 compared to sporadic breast cancer. Methods. The study included 191 female patients with verified breast cancer stage I-IIA and clinical signs of hereditary breast cancer. In order to identify mutations in genes ВRCA1/2 molecular genetic analysis of deoxyribonucleic acid from peripheral blood leukocytes was performed. Results. The total frequency of mutations in the genes BRCA1 and ВRCA2 amounted 14.1% of the total number of examined patients. The most common mutation in clinically hereditary breast cancer among residents of the Rostov Region was 5382insC in BRCA1 gene, which corresponds to the nationwide data. Also common features of hereditary breast cancer compared to sporadic breast cancer were identified: young age at the time of disease manifestation, high prevalence of triple-negative cancer, history of infertility, increased level of p53 and androgen receptor expression, decreased level of aneuploid cell and proliferation index in the tumor. Conclusion. In a number of clinical morphological and molecular genetic parameters, clinically hereditary breast cancer differs from sporadic breast cancer. These indicators in the future can be used as criteria for selection of patients with clinically hereditary breast cancer without confirmed BRCA1/2 mutation by standard panels for in-depth genetic testing.
APA, Harvard, Vancouver, ISO, and other styles
7

Pöschl, Gudrun, Felix Stickel, Xiang D. Wang, and Helmut K. Seitz. "Alcohol and cancer: genetic and nutritional aspects." Proceedings of the Nutrition Society 63, no. 1 (February 2004): 65–71. http://dx.doi.org/10.1079/pns2003323.

Full text
Abstract:
Chronic alcohol consumption is a major risk factor for cancer of upper aero-digestive tract (oro-pharynx, hypopharynx, larynx and oesophagus), the liver, the colo-rectum and the breast. Evidence has accumulated that acetaldehyde is predominantly responsible for alcohol-associated carcinogenesis. Acetaldehyde is carcinogenic and mutagenic, binds to DNA and protein, destroys the folate molecule and results in secondary cellular hyper-regeneration. Acetaldehyde is produced by mucosal and cellular alcohol dehydrogenase, cytochrome P450 2E1 and through bacterial oxidation. Its generation and/or its metabolism is modulated as a result of polymorphisms or mutations of the genes responsible for these enzymes. Acetaldehyde can also be produced by oral bacteria. Smoking, which changes the oral bacterial flora, also increases salivary acetaldehyde. Cigarette smoke and some alcoholic beverages, such as Calvados, contain acetaldehyde. In addition, chronic alcohol consumption induces cytochrome P450 2E1 enxyme activity in mucosal cells, resulting in an increased generation of reactive oxygen species and in an increased activation of various dietary and environmental carcinogens. Deficiencies of riboflavin, Zn, folate and possibly retinoic acid may further enhance alcohol-associated carcinogenesis. Finally, methyl deficiency as a result of multiple alcohol-induced changes leads to DNA hypomethylation. A depletion of lipotropes, including methionine, choline, betaine and S-adenosylmethionine, as well as folate, results in the hypomethylation of oncogenes and may lead to DNA strand breaks, all of which are associated with increased carcinogenesis.
APA, Harvard, Vancouver, ISO, and other styles
8

Press, Nancy, Jennifer R. Fishman, and Barbara A. Koenig. "Collective Fear, Individualized Risk: the social and cultural context of genetic testing forbreast cancer." Nursing Ethics 7, no. 3 (May 2000): 237–49. http://dx.doi.org/10.1177/096973300000700306.

Full text
Abstract:
The purpose of this article is to provide a critical examination of two aspects of culture and biomedicine that have helped to shape the meaning and practice of genetic testing for breast cancer. These are: (1) the cultural construction of fear of breast cancer, which has been fuelled in part by (2) the predominance of a ‘risk’ paradigm in contemporary biomedicine. The increasing elaboration and delineation of risk factors and risk numbers are in part intended to help women to contend with their fear of breast cancer. However, because there is no known cure or foolproof prevention for breast cancer, risk designations bring with them recommendations for vigilant surveillance strategies and screening guidelines. We argue that these in effect exacerbate women’s fears of breast cancer itself. The volatile combination of discourses of fear, risk and surveillance have significant ethical and social consequences for women’s lives and well-being. Genetic testing decisions are made within this context; if nurses understand this context they can play an important role in helping women to cope with the anxiety and fear of breast cancer risk.
APA, Harvard, Vancouver, ISO, and other styles
9

Miricescu, Daniela, Alexandra Totan, Iulia-Ioana Stanescu-Spinu, Silviu Constantin Badoiu, Constantin Stefani, and Maria Greabu. "PI3K/AKT/mTOR Signaling Pathway in Breast Cancer: From Molecular Landscape to Clinical Aspects." International Journal of Molecular Sciences 22, no. 1 (December 26, 2020): 173. http://dx.doi.org/10.3390/ijms22010173.

Full text
Abstract:
Breast cancer is a serious health problem worldwide, representing the second cause of death through malignancies among women in developed countries. Population, endogenous and exogenous hormones, and physiological, genetic and breast-related factors are involved in breast cancer pathogenesis. The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) is a signaling pathway involved in cell proliferation, survival, invasion, migration, apoptosis, glucose metabolism and DNA repair. In breast tumors, PIK3CA somatic mutations have been reported, located in exon 9 and exon 20. Up to 40% of PIK3CA mutations are estrogen receptor (ER) positive and human epidermal growth factor receptor 2 (HER2) -negative in primary and metastatic breast cancer. HER2 is overexpressed in 20–30% of breast cancers. HER1, HER2, HER3 and HER4 are membrane receptor tyrosine kinases involved in HER signaling to which various ligands can be attached, leading to PI3K/AKT activation. Currently, clinical studies evaluate inhibitors of the PI3K/AKT/mTOR axis. The main purpose of this review is to present general aspects of breast cancer, the components of the AKT signaling pathway, the factors that activate this protein kinase B, PI3K/AKT-breast cancer mutations, PI3K/AKT/mTOR-inhibitors, and the relationship between everolimus, temsirolimus and endocrine therapy.
APA, Harvard, Vancouver, ISO, and other styles
10

GOELEN, G., A. RIGO, B. NEYNS, W. BETZ, and J. DE GRÈVE. "Ethical Aspects of Genetic Counseling in Familial Breast and Ovarian Cancer." Annals of the New York Academy of Sciences 833, no. 1 Cancer (December 1997): 170–72. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48604.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Breast – Cancer – Genetic aspects"

1

Chiu, Yuk-tim, and 趙玉甜. "Sirtuin 6 expression in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48541254.

Full text
Abstract:
Sirtuins (Silent Information Regulator Two (SIR2) protein) are NAD-dependent protein deacetylases, originally discovered in yeast. Sirtuins play a critical role in the regulation of different cellular processes involving aging, chromatin silencing and cellular differentiation. SIRT6 is a member of Sirtuins and plays a role in regulation of DNA repair and suppression of genomic instability. Many studies have shown SIRT6 to be associated with diseases of aging, including cancer. The finding by our collaborator that SIRT6 expression was found in chemotherapy-resistant breast cancer cell lines stimulated this study which aims to explore the role of SIRT6 expression as a prognostic marker in breast cancer. One hundred and eighteen breast cancer samples in tissue microarray blocks were examined for SIRT6 expression by immunohistochemistry. As SIRT6 expression is predominantly located in the nucleus but with a small fraction in cytoplasm, the calculation of nuclear or cytoplasmic localization scores were divided by total localization scores to increase accuracy. The nuclear localization scores represent the SIRT6 expression in breast cancer. Statistical analysis was performed using SPSS software. SIRT6 overexpression in the nucleus was significantly associated with poorer overall survivals (p=0.018) while low cytoplasmic expression of SIRT6 was also associated with poorer overall survivals (p=0.014). There was no relationship between SIRT6 expression and disease-specific survivals. By multivariate analysis, SIRT6 expression was an independent predicator of poorer overall survivals. These results suggest that SIRT6 overexpression induces apoptosis in cancer cells through deacetylation of transcription factor p65. SIRT6 interacts with and deacetylates p65 to activate nuclear factor kappa B gene linked to cancer. Also high levels of SIRT6 were associated with resistance to paclitaxel and epirubicin inMCF-7 breast cancer cell lines. This provides evidence that Sirt6 is an important prognostic marker and therapeutic target for breast cancer.
published_or_final_version
Pathology
Master
Master of Medical Sciences
APA, Harvard, Vancouver, ISO, and other styles
2

Lau, Tsz-kwan, and 劉子筠. "The expression of RIP140 in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193544.

Full text
Abstract:
Breast cancer is the most common cancer in females worldwide. RIP140 was one of the first proteins recognized as nuclear receptor transcriptional cofactor which interacts with several nuclear receptors. RIP140 plays a central role in metabolic tissues with multifunctional co-regulation. It is an essential protein required for energy homeostasis and mammary gland development. RIP140 has been found to be involved in development of breast cancer in response to estrogen. RIP140 is recruited by estrogen receptors in the presence of estrogen. Increasing levels of estrogen and RIP140 stimulate their transcription and regulate proliferation and differentiation of mammary glands. We hypothesize that RIP140 may be over expressed in breast cancer and may be correlated with clinicopathological features and may thus serve as a possible new prognostic marker in breast cancer. In our study, the correlation between the RIP140 expression and survival was investigated by immunohistochemistry (IHC), and analyzed by Pearson’s chi-square and Kaplan Meier analysis. Cox regression analysis was performed to examine the relationship between clinic-pathological parameters and the survival. Total of one hundred and eighteen breast cancer samples were examined for the RIP140 staining localization in breast cancer cells. Our results showed that the IHC staining of RIP140 was observed in both cytoplasm and nucleus of breast cancer cells. The ER positive staining was significantly correlated with high nuclear expression of RIP140, but not RIP140 cytoplasmic expression. Thus nuclear RIP140 expression was examined for correlation with other clinic-pathological features and patient survival. The correlation between nuclear RIP140 expression and clinic-pathological features by Pearson’s chi-square test showed that high RIP140 nuclear staining score is associated with ER positive status (p-value=0.041) and tumor stage (p-value=0.008). Kaplan Meier test shown that nuclear RIP140 expression is not significant associated with either overall survival or disease-specific survival. However, a trend of high nuclear RIP140 score was observed with poorer overall and disease-specific survival though not statistically significant. To conclude, our results suggest RIP140 is not a useful prognostic marker for breast cancer. Further investigation with larger sample size is necessary to improve the statistical significance of the test.
published_or_final_version
Pathology
Master
Master of Medical Sciences
APA, Harvard, Vancouver, ISO, and other styles
3

Wong, Yim-han, and 黃艷嫺. "Expression of sirtuin 1 in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193549.

Full text
Abstract:
Breast cancer is the most frequent malignancy in women. Recent studies have proposed that sirtuin 1 (SIRT1) may play a certain role in the tumorgenesis and disease progression of cancer. Therefore, in this study, we demonstrate the localization of SIRT1 in the breast cancer cells by immunohistochemistry method and try to correlate the expression level of SIRT1 with various clinical-pathological parameters as well as the survival time of breast cancer patients. One hundred and eighteen breast cancer cases, arrayed as dual‐cores, were studied in the tissue microarray blocks for their SIRT1 nuclear and cytoplasmic stain. The expression of SIRT1 is found in over 95% of the tumor samples. Although the active functioning site of SIRT1 is known to be mainly the nucleus, both nuclear and cytoplasmic localization score are assessed separately for SIRT1 expression for more accurate statistically analysis. By bi‐variate Pearson correlation analysis, high nuclear localization of SIRT1 is significantly correlated with low tumor grade (p=0.006) and ER (p=0.001) and PR positive status (p=0.044). Moreover, the cytoplasmic localization score of SIRT1 shows positive correlation with tumor grade (p=0.010). The relationship of SIRT1 expression and survival time of breast cancer patient was studied by Kaplan‐Meier analysis. Despite a marginal fail in obtaining a statistically significant result, the trend in survival curve clearly indicated that nuclear localization of SIRT1 is associated with a poorer overall survival (p=0.052). Although the pathway of how SIRT1 affects the survival of breast cancer patient is still unknown, many studies suggested that it is largely due to the deacetylated inactivation of p53 tumor suppressor protein by SIRT1. In conclusion, we propose that nuclear localization of SIRT1 can be a potential prognostic factor of breast cancer patients.
published_or_final_version
Pathology
Master
Master of Medical Sciences
APA, Harvard, Vancouver, ISO, and other styles
4

Flach, Susanne. "Structural variation of the genome in breast cancer." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648565.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Cheng, Wan-biu, and 鄭雲標. "Genetic analysis on the EPHB2 gene in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45009946.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Wu, Lai-han, and 胡麗嫻. "Expression of FOXO3a in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011515.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Webster, Lucy R. "Diagnostic molecular profiling of ductal carcinoma in situ of the breast." Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28109.

Full text
Abstract:
The introduction of population-based mammographic screening has led to a dramatic increase in the diagnosis of ductal carcinoma in situ (DCIS) of the breast; with DCIS now accounting for approximately 25-35% of all screen-detected breast cancers. Epidemiological, histopathological and molecular studies have provided compelling evidence to support the notion that DCIS is a direct precursor of invasive cancer; although such data also indicate that DCIS represents a highly heterogeneous group of lesions. Some women with DCIS will develop life-threatening invasive cancer, whereas others may not. Currently, determination of the malignant potential of an individual DCIS lesion is very difficult, making selection of optimal treatment from the range of options available challenging. Histopathology has long been used to classify invasive breast tumours into biologically relevant sub-classes; although for DCIS there is still no universally accepted histological grading system. In recent years, gene expression profiling of invasive breast cancer has demonstrated that superior classification, prognostication and prediction can be achieved. Therefore, the principal aim of this study was to use classic histopathology and contemporary molecular biological methods to better classify DCIS lesions according to their inherent malignant potential. A significant difficulty in studying in situ breast cancer is a lack of rational endpoints against which potential markers can be judged; consequently initial studies were directed at identifying a rational surrogate end-point for use in subsequent molecular studies. Through the examination of a large cohort of screen-detected breast cancers, we demonstrated that the grade of concomitant invasive breast cancer was the best surrogate end-point to examine the malignant potential of in situ disease due to its direct relationship with breast cancer biology and established correlation with breast cancer survival. Another significant limitation to molecular studies of DCIS is the heterogeneity of breast tissue and the small size and limited extent of in situ lesions. Therefore, in this thesis laser capture microdissection and nucleic acid amplification techniques were successfully optimised and applied to a well-characterised cohort of DCIS lesions and adjacent areas of pre-malignant and benign epithelium. Gene expression profiling analysis of this cohort of laser capture microdissected samples was successfully performed on 36K oligonucleotide microarrays. Supervised analysis was used to identify genes differentially expressed between DCIS lesions associated with grade 1 and grade 3 invasive cancer. The “DCIS discriminative gene list” comprised 173 oligonucleotide probes and according to the relative expression of the top 100 genes samples were clustered into two biologically relevant groups. In addition, a gene expression grade index (GGI) was calculated and using a defined cut-point the DCIS lesions were classified into the same “low” and “high” molecular grade groups that had highly significant correlations with histopathologic and biological factors including DCIS nuclear grade, cell polarisation, necrosis, ER, PR, HERZ, p53 and Ki67. Further support for the clinical relevance of the gene expression derived DCIS classification was provided by the strong correlation between the molecular grade groups and both disease-free and overall survival in two independent invasive breast cancer cohorts. lmportantly, work described in this thesis also demonstrated that the gene-expression derived classification can be closely approximated using a combination of routinely available features including DCIS nuclear grade and accurate Ki67 scoring of the in situ component; thus offering a novel, biologically significant and clinically useful DCIS classification system. Results from array-based comparative genomic hybridisation (aCGH) analyses further supported the biological relevance of the gene-expression derived classification and identified potential candidate chromosomal regions underlying the variable malignant potential of in situ breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
8

Khoo, Ui-soon, and 邱瑋璇. "Genetic susceptibility to gynaecological cancers in the Chinese population." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B25257365.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

陳遠光 and Yuen-kwong Chan. "Study on the role of genetic and epigenetic factors in relation to theBRCA genes in epithelial ovarian cancers." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B42576726.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

馮敬業 and King-yip Fung. "Screening of recurrent BRCA gene mutations in Chinese breast and ovarian cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31969720.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Breast – Cancer – Genetic aspects"

1

P, Yao Andrew, ed. New breast cancer research. New York: Nova Science Pub., 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Noorani, Hussein Zafer. Predictive genetic testing for breast and prostate cancer. Ottawa, Ont: Canadian Coordinating Office for Health Technology Assessment, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

1963-, Morrison Patrick J., Hodgson S. V, and Haites Neva E. 1947-, eds. Familial breast and ovarian cancer: Genetics, screening, and management. Cambridge: Cambridge University Press, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Davies, Kevin. Breakthrough: The race to find the breast cancer gene. New York: J. Wiley, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Breast cancer genes and the gendering of knowledge: Science and citizenship in the cultural context of the "new" genetics. Basingstoke [England]: Palgrave Macmillan, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

1959-, White Michael, ed. Breakthrough: The quest to isolate the gene for hereditary breast cancer. London: Macmillan, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Tumor suppressor genes in breast cancer. Hauppauge (NY), USA: Nova Publishers, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Shockney, Lillie. Top concerns about HER2 positive breast cancer. Sudbury, Mass: Jones & Bartlett Learning, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Hartikainen, Jaana. Genetic predispossition to breast and ovarian cancer in Eastern Finnish population. Kuopio: University of Kuopio, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Nieden, Andrea Zur. Zum Subjekt der Gene werden: Subjektivierungsweisen im Zeichen der Genetisierung von Brustkrebs. Bielefeld: Transcript, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Breast – Cancer – Genetic aspects"

1

MacKay, J., and M. Steel. "Genetic Aspects of Human Breast Cancer." In High-Risk Breast Cancer, 45–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73718-3_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Parshad, Ram, and Katherine K. Sanford. "Chromosomal Radiosensitivity as an Indicator of Genetic Predisposition to Breast Cancer." In Some Aspects of Chromosome Structure and Functions, 167–76. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-010-0334-6_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Derakhshan, Mohammad Kamran, and Mohammad Hamid Karbassian. "Psychiatric and Psychosocial Aspects of Breast Cancer Diagnoses and Treatments." In Cancer Genetics and Psychotherapy, 45–77. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64550-6_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Veronesi, Umberto. "Psychological Aspects." In Breast Cancer, 63–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-76054-9_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Mills, Gordon B., and Paula Trahan Rieger. "Genetic Predisposition to Breast Cancer." In Breast Cancer, 55–92. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-0-387-21842-7_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Kumar, Krishan, and S. K. Mattoo. "Psychosocial Aspects of Breast Cancer." In Breast Cancer, 567–75. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-4546-4_27.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Goldgar, David E., Michael R. Stratton, and Rosalind A. Eeles. "Familial breast cancer." In Genetic Predisposition to Cancer, 227–38. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-4501-3_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Pruneri, Giancarlo, and Francesca Boggio. "Prognostic and Predictive Role of Genetic Signatures." In Breast Cancer, 121–31. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48848-6_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Oestergaard, Mikkel Z., and Paul Pharoah. "Common Genetic Susceptibility Loci." In Breast Cancer Epidemiology, 301–20. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0685-4_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Mazumdar, Alok, Sumeet Jain, Satish Jain, and Shashanka Mohan Bose. "Management of Early Breast Cancer – Surgical Aspects." In Breast Cancer, 243–97. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-4546-4_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Breast – Cancer – Genetic aspects"

1

Mishatkina, T. V., S. B. Melnov, and E. V. Snytkov. "GENETIC AND SOCIO-BIOETHICAL ASPECTS OF BREAST CANCER PREDISPOSITION AMONG WOMEN OF SLAVIC AND CENTRAL ASIAN ETHNIC GROUPS." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute, 2021. http://dx.doi.org/10.46646/sakh-2021-1-64-68.

Full text
Abstract:
The publication was prepared based on the materials of the implementation of the joint Belarusian-Uzbek two-year scientific project “Genetic and socio-bioethical aspects of predisposition to breast cancer for women of Slavic and Central Asian ethnic groups.” The results of studies carried out from October 01, 2020 to March 15, 2021 are presented.
APA, Harvard, Vancouver, ISO, and other styles
2

Ferreira, Nancy, Darley Ferreira, and Thais Ferreira. "GENETIC EVALUATION OF MICROCALCIFICATIONS AS A PROGNOSTIC FACTOR." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2101.

Full text
Abstract:
Introduction: Breast cancer is the most recurring type of cancer among women, with reduced mortality at an initial stage of lesion. From a radiological perspective, perceived microcalcifications may be associated with histological findings such as proliferative injuries with or without atypical features and ductal carcinoma in situ. Currently, percutaneous and vacuum biopsies allow for the correlation between anatomoradiological and identification of previous lesions and those that offer the risk of cancer. No biomarker has been established to predict the risk of cancer in women diagnosed with benign mammary disease. Doing so could strengthen the possibility of stratifying the individual risk of benign injuries for cancer. The platelet-derived growth factor receptor A (PDGFRA) plays its part in tumor oncogenesis, angiogenesis, and metastasis, and its activation is found in some kinds of cancer. In contrast, DNA methylation standards are initial changes to the development of cancer and may be helpful in its early identification, being regulated by a family of enzymes called DNMTs (DNA methyltransferase). Methods: The aim of this study was to evaluate the profile of BI-RADS® 4 and 5 mammary microcalcification women carriers and determine the level of the gene expression of possible molecular markers in 37 patients with mammary microcalcification (paraffin blocks) and 26 patients with breast cancer (fresh in RNA later tissue) cared for at the Hospital Barão de Lucena’s Mastology Ambulatory. Anatomoradiological aspects along with clinical findings have been evaluated , and percentage rates have been calculated. The PDGFRA and DNMTs (DMNT3a) gene expressions have been established using quantitative polymerase chain reaction (qPCR), with the use of β-actin as reference gene. Discussion: In the patients with mammary microcalcification, the average age was 55.9; predominantly whiteskinned subjects (p<0.014). Most of them were mothers (p<0.001), and the average menarche age was 13. The subgroups that presented greater significance were patients classified BI-RADS® in category IV (67.6%) and histological findings of nonproliferative lesion (p<0.001). Lesions of the ductal carcinoma in situ type (100%) presented positive estrogen and progesterone receptors, and 94.6% have undergone sectorectomy surgery by prior needling (p<0.001). The most damaged breast was the left one (62.2%), and the most affected quadrant was the top lateral one (59.5%) (p<0.001). There was no family history in 83.8% of the cases. In the tested microcalcification samples, it was not possible to observe the expression of PDGFRA. Nevertheless, 15 out of 37 patients with microcalcification showed an increase in the gene expression of DMNT3a, most of them greater than Luminal and triple-negative cancer types. Conclusion: The data presented here highlight the improvement on the description of BI-RADS® 4 subclassification in order to better conduct the clinical decision and also demonstrated the potential of DNMTs evaluation in microcalcification samples as a strategy to access the understanding about the role of these molecules in the breast cancer development.
APA, Harvard, Vancouver, ISO, and other styles
3

Assis, Amilcar Alves, Mauro Passos, Rodrigo Kouzak, Karoline Evangelista, and Natasha Caldas. "BREAST CANCER IN YOUNG PATIENTS: PROGNOSTIC AND PROFILE EPIDEMIOLOGICAL ANALYSIS IN A TERTIARY HOSPITAL." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2093.

Full text
Abstract:
Breast cancer is the second most prevalent and first in mortality in Brazilian women. Its incidence has increased in recent years in all age groups. According to the Instituto Nacional do Câncer in 2019, 59,700 new cases of breast cancer are expected, with an estimated risk of 56.33 cases per 100 women. The diagnosis of breast cancer is more frequent in women after 50 years of age; it is estimated that only 25% of all cases occur in women below the age of 50 years; however, there was a literature consensus that tumors in this young age group have a worse prognosis, both because they are biologically more aggressive and because of affect women outside the screening age group in Brazil; thus, the rate of locally advanced disease at diagnosis in this age group is considerably higher. It is suggested that early onset breast cancer is related to different etiological factors, histopathological aspects, and clinical outcomes, as compared to postmenopausal breast cancer. Thus, age becomes an important prognostic factor. Since breast cancer is a curable pathology, the type of therapeutic approach also varies, with proposed treatment tends to be more aggressive. With the advent and increasing availability of genetic tests, predisposition of breast cancer has increased the number of indications for prophylactic mastectomies, especially in younger age groups or notably in patients with known pathological mutations in BRCA1 and BRCA2 genes. However, the literature is still controversial regarding its impact on overall survival. Breast cancer diagnosed before the age of 50 years is a behavioral disease, with prognosis and approach very different from that diagnosed in postmenopausal women. Therefore, it is important to know the profile of these patients to provide optimal treatment and achieve the best outcomes.
APA, Harvard, Vancouver, ISO, and other styles
4

Kumar, N., A. Mishra, and S. Deo. "169 A prospective interventional study evaluating awareness and knowledge about genetic aspects of breast cancer and the effect of educational intervention: a real-life experience." In IGCS 2020 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2020. http://dx.doi.org/10.1136/ijgc-2020-igcs.147.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Rotaru, Ludmila, and Tudor Rotaru. "Ovarian cancer – genetic aspects." In XIth International Congress of Geneticists and Breeders from the Republic of Moldova. Scientific Association of Geneticists and Breeders of the Republic of Moldova, Institute of Genetics, Physiology and Plant Protection, Moldova State University, 2021. http://dx.doi.org/10.53040/cga11.2021.041.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Mansour, Nashat, Rouba Zantout, and Mirvat El-Sibai. "Mining breast cancer genetic data." In 2013 9th International Conference on Natural Computation (ICNC). IEEE, 2013. http://dx.doi.org/10.1109/icnc.2013.6818131.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lee, SGA. "Current genetic research in breast cancer." In Asian Breast Diseases Association (ABDA) 3rd Teaching Course: Advances in the Management of Breast Diseases. Kuantan, Malaysia: Asian Breast Diseases Association, 2005. http://dx.doi.org/10.2349/biij.1.1.e6-31.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

"BREAST CANCER DETECTION USING GENETIC PROGRAMMING." In International Conference on Bio-inspired Systems and Signal Processing. SciTePress - Science and and Technology Publications, 2008. http://dx.doi.org/10.5220/0001059203340341.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Chauhan, Ruchi, PK Vinod, and CV Jawahar. "Exploring Genetic-histologic Relationships in Breast Cancer." In 2021 IEEE 18th International Symposium on Biomedical Imaging (ISBI). IEEE, 2021. http://dx.doi.org/10.1109/isbi48211.2021.9434130.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Lukavenko, Ivan, Iryna Symonenko, and Diana Steblovs'ka. "BREAST TISSUE: BIOLOGICAL MECHANISMS OF DYSPLASIA AND GENETIC CRITERIA FOR DIAGNOSIS." In THEORETICAL AND PRACTICAL ASPECTS OF MODERN SCIENTIFIC RESEARCH. European Scientific Platform, 2021. http://dx.doi.org/10.36074/logos-30.04.2021.v2.39.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Breast – Cancer – Genetic aspects"

1

Merajver, Sofia. Genetic Determinants of Inflammatory Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada397618.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Merajver, Sofia D. Genetic Determinants of Inflammatory Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada429666.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Hunter, Kent W. Genetic Determinants of Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada368338.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Merajver, Sofia D. Genetic Determinants of Inflammatory Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada411488.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Merajver, Sofia D. Genetic Determinants of Inflammatory Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada425765.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Hunter, Kent W. Genetic Determinants of Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, June 1998. http://dx.doi.org/10.21236/ada352403.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kruger, Warren. Genetic Determinants of Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada392184.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Hait, William. Genetic Susceptibility to Cancer Chemotherapy in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada396563.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Hait, William N. Genetic Susceptibility to Cancer Chemotherapy in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada398401.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Halt, William N. Genetic Susceptibility to Cancer Chemotherapy in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada382957.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Breast – Cancer – Genetic aspects' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography