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Adherence to the World Cancer Research Fund/American Institute for Cancer Research recommendations and breast cancer risk.

https://arctichealth.org/en/permalink/ahliterature274979
Source
Int J Cancer. 2016 Jun 1;138(11):2657-64
Publication Type
Article
Date
Jun-1-2016
Author
Holly R Harris
Leif Bergkvist
Alicja Wolk
Source
Int J Cancer. 2016 Jun 1;138(11):2657-64
Date
Jun-1-2016
Language
English
Publication Type
Article
Keywords
Aged
Breast Neoplasms - epidemiology - genetics - pathology
Diet
Estrogen Receptor alpha - genetics
Female
Food Habits
Humans
Middle Aged
Prospective Studies
Risk factors
Surveys and Questionnaires
Sweden
United States
Abstract
The World Cancer Research Fund/American Association for Cancer Research (WCRF/AICR) has published eight nutrition-related recommendations for the prevention of cancer. However, few prospective studies have examined these recommendations by breast cancer hormone receptor subtype and only one case-control study has included the dietary supplements recommendation in their evaluation. We investigated whether adherence to the WCRF/AICR cancer prevention recommendations was associated with breast cancer incidence, overall and by hormone receptor subtype, in the Swedish Mammography Cohort. Among 31,514 primarily postmenopausal women diet and lifestyle factors were assessed with a self-administered food frequency questionnaire. A score was constructed based on adherence to the recommendations for body fatness, physical activity, energy density, plant foods, animal foods, alcoholic drinks and dietary supplements (score range 0-7). Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs). During 15 years of follow-up 1,388 cases of breast cancer were identified. Women who met six to seven recommendations had a 51% decreased risk of breast cancer compared to women meeting only zero to two recommendations (95% CI = 0.35-0.70). The association between each additional recommendation met and breast cancer risk was strongest for the ER-positive/PR-positive subtype (HR = 0.86; 95% CI = 0.79-0.94), while for the ER-negative/PR-negative subtype the individual recommendations regarding plant and animal foods were most strongly associated with reduced risk. Our findings support that adherence to the WCRF/AICR recommendations reduces breast cancer risk in a population of primarily postmenopausal women. Promoting these recommendations to the public could help reduce breast cancer incidence.
PubMed ID
26804371 View in PubMed
Less detail

Age of onset in familial breast cancer as background data for medical surveillance.

https://arctichealth.org/en/permalink/ahliterature98757
Source
Br J Cancer. 2010 Jan 5;102(1):42-7
Publication Type
Article
Date
Jan-5-2010
Author
A. Brandt
J Lorenzo Bermejo
J. Sundquist
K. Hemminki
Author Affiliation
Division of Molecular Genetic Epidemiology, German Cancer Research Centre (DKFZ), D-69120 Heidelberg, Germany. andreas.brandt@dkfz.de
Source
Br J Cancer. 2010 Jan 5;102(1):42-7
Date
Jan-5-2010
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Aged
Aged, 80 and over
Breast Neoplasms - epidemiology - genetics
Databases, Factual
Female
Humans
Longevity
Mass Screening - standards
Middle Aged
Mothers
Patient Selection
Population Surveillance
Proportional Hazards Models
Siblings
Sweden - epidemiology
Abstract
BACKGROUND: Familial breast cancers are known to be of early onset. This article provides differences in the age of onset of breast cancer and death by breast cancer between women with and without a family history. METHODS: The Swedish Family-Cancer Database was used to estimate the cumulative risk of breast cancer and death by breast cancer according to family history with a stratified Cox model. Family history was defined separately for affected mother or sister considering their diagnostic ages. RESULTS: The age to reach the same cumulative incidence as women without family history decreased with decreasing diagnostic age of the affected relative. Women with a maternal history reached the risk of women lacking a family history at the age of 50 years between 12.3 (mother affected 82 years) earlier. The trend for breast cancer mortality was essentially similar. CONCLUSIONS: Women with mother or sister affected by breast cancer are diagnosed and die at earlier ages than do women without family history. The differences depend on the diagnostic age of the affected relative. The present data may provide a rationale to derive recommendations for the starting age of screening in women with affected family members.
PubMed ID
19904271 View in PubMed
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Age-specific incidence rates for breast cancer in carriers of BRCA1 mutations from Norway.

https://arctichealth.org/en/permalink/ahliterature127153
Source
Clin Genet. 2013 Jan;83(1):88-91
Publication Type
Article
Date
Jan-2013
Author
P. Møller
L. Maehle
A. Vabø
N. Clark
P. Sun
S A Narod
Author Affiliation
Unit for Inherited Cancer, Section for Clinical Genetics, Department of Medical Genetics, Oslo University Hospital, Norway. moller.pal@gmail.com
Source
Clin Genet. 2013 Jan;83(1):88-91
Date
Jan-2013
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Aged
BRCA1 Protein - genetics
Breast Neoplasms - epidemiology - genetics
Female
Genetic Predisposition to Disease
Heterozygote
Humans
Middle Aged
Mutation
Norway
Penetrance
Risk factors
Abstract
Incidence rates of breast cancer among women with a BRCA1 mutation vary according to their reproductive histories and country of residence. To measure cancer incidence, it is best to follow-up cohort of healthy women prospectively. We followed up a cohort of 675 women with a BRCA1 mutation who did not have breast or ovarian cancer before inclusion and who had a normal clinical examination and mammography at first visit. After a mean of 7.1 years, 98 incident cases of breast cancer were recorded in the cohort. Annual cancer incidence rates were calculated, and based on these, a penetrance curve was constructed. The average annual cancer risk for the Norwegian women from age 25 to 70 was 2.0%. Founder mutations had lower incidence rate (1.7%) than less frequent mutations (2.5%) (p = 0.03). The peak incidence (3.1% annual risk) was observed in women from age 50 to 59. The age-specific annual incidence rates and penetrance estimate were compared with published figures for women from North America and from Poland. The risk of breast cancer to age 70 was estimated to be 61% for women from Norway, compared with 55% for women from Poland and 69% for women from North America.
PubMed ID
22320316 View in PubMed
Less detail

Alcohol consumption, body mass index and breast cancer risk by hormone receptor status: Women' Lifestyle and Health Study.

https://arctichealth.org/en/permalink/ahliterature273881
Source
BMC Cancer. 2015;15:881
Publication Type
Article
Date
2015
Author
Aesun Shin
Sven Sandin
Marie Lof
Karen L Margolis
Kyeezu Kim
Elisabeth Couto
Hans Olov Adami
Elisabete Weiderpass
Source
BMC Cancer. 2015;15:881
Date
2015
Language
English
Publication Type
Article
Keywords
Adult
Alcohol Drinking - adverse effects - pathology
Body mass index
Breast Neoplasms - epidemiology - genetics - pathology
Female
Humans
Life Style
Middle Aged
Postmenopause
Receptors, Estrogen - blood - genetics
Receptors, Progesterone - genetics
Risk factors
Sweden
Abstract
We aimed to estimate the effect of alcohol consumption on breast cancer risk and to test whether overweight and obesity modifies this association.
We included in the analysis 45,233 women enrolled in the Swedish Women's Lifestyle and Health study between 1991 and 1992. Participants were followed for occurrence of breast cancer and death until December 2009. Poisson regression models were used, and analyses were done for overall breast cancer and for estrogen receptor positive or negative (ER+, ER-) and progesterone receptor positive and negative (PR+, PR-) tumors separately.
A total of 1,385 breast cancer cases were ascertained during the follow-up period. Overall, we found no statistically significant association between alcohol intake and breast cancer risk after adjustment for confounding, with an estimated relative risk (RR) of 1.01 (95 % CI: 0.98-1.04) for an increment in alcohol consumption of 5 g/day. A statistically significant elevated breast cancer risk associated with higher alcohol consumption was found only among women with BMI =25 (RR 1.03, 95 % CI 1.0-1.05 per 5 g/day increase).
An increase in breast cancer risk with higher alcohol consumption was found for breast cancers in women with a BMI =25 kg/m(2).
Notes
Cites: Cancer Epidemiol Biomarkers Prev. 2012 Jul;21(7):1203-1222564867
Cites: Alcohol Alcohol. 2000 Sep-Oct;35(5):417-2311022013
Cites: Cancer Causes Control. 2001 Jan;12(1):47-5911227925
Cites: Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1375-8112433714
Cites: Br J Cancer. 2002 Nov 18;87(11):1234-4512439712
Cites: Cancer Epidemiol Biomarkers Prev. 2004 Mar;13(3):405-1115006916
Cites: Alcohol Clin Exp Res. 2004 May;28(5):780-515166654
Cites: N Engl J Med. 1987 May 7;316(19):1169-733574367
Cites: J Pharmacol Exp Ther. 1988 May;245(2):407-123367299
Cites: Prev Med. 1988 Nov;17(6):676-823072560
Cites: J Natl Cancer Inst. 1993 May 5;85(9):722-78478958
Cites: Proc Natl Acad Sci U S A. 1995 Apr 25;92(9):3650-77731959
Cites: JAMA. 1996 Dec 4;276(21):1747-518940324
Cites: JAMA. 1998 Feb 18;279(7):535-409480365
Cites: Alcohol Clin Exp Res. 1998 Aug;22(5):994-79726268
Cites: Alcohol Clin Exp Res. 1999 Jun;23(6):976-8210397281
Cites: Ann Epidemiol. 2006 Mar;16(3):230-4016230024
Cites: Cancer Causes Control. 2006 Aug;17(6):759-7016783604
Cites: Cancer Causes Control. 2007 May;18(4):361-7317364225
Cites: Int J Cancer. 2008 Apr 15;122(8):1832-4118067133
Cites: Ann Oncol. 2009 Mar;20(3):550-518765462
Cites: Lancet Oncol. 2009 Nov;10(11):1033-419891056
Cites: Anticancer Res. 2010 Jan;30(1):1-820150611
Cites: J Clin Oncol. 2010 Sep 10;28(26):4052-720644083
Cites: Eur J Epidemiol. 2011 Feb;26(2):81-9021267637
Cites: BMJ. 2011;342:d158421474525
Cites: Br J Cancer. 2011 Aug 23;105(5):709-2221772329
Cites: Br J Cancer. 2011 Dec 6;105 Suppl 2:S14-822158312
PubMed ID
26552431 View in PubMed
Less detail

Analysis of polymorphisms in the circadian-related genes and breast cancer risk in Norwegian nurses working night shifts.

https://arctichealth.org/en/permalink/ahliterature259189
Source
Breast Cancer Res. 2013;15(4):R53
Publication Type
Article
Date
2013
Author
Shanbeh Zienolddiny
Aage Haugen
Jenny-Anne Sigstad Lie
Helge Kjuus
Kristine Haugen Anmarkrud
Kristina Kjærheim
Source
Breast Cancer Res. 2013;15(4):R53
Date
2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Breast Neoplasms - epidemiology - genetics
Case-Control Studies
Circadian Rhythm - genetics
Female
Genetic Predisposition to Disease
Humans
Middle Aged
Norway - epidemiology
Nurses
Occupational Medicine
Odds Ratio
Polymorphism, Genetic
Polymorphism, Single Nucleotide
Risk
Abstract
Some studies have suggested that night work may be associated with an increased risk of breast cancer in nurses. We aimed to explore the role of circadian gene polymorphisms in the susceptibility to night work-related breast cancer risk.
We conducted a nested case-control study of Norwegian nurses comprising 563 breast cancer cases and 619 controls within a cohort of 49,402 Norwegian nurses ages 35 to 74 years. We studied 60 single-nucleotide polymorphisms (SNPs) in 17 genes involved in the regulation of the circadian rhythm in cases and controls. The data were analyzed in relation to the two exposure variables "maximum number of consecutive night shifts ever worked" and "maximum number of consecutive night shifts worked for at least 5 years." The odds of breast cancer associated with each SNP was calculated in the main effects analysis and in relation to night shift work. The statistically significant odds ratios were tested for noteworthiness using two Bayesian tests: false positive report probability (FPRP) and Bayesian false discovery probability (BFDP).
In the main effects analysis, CC carriers of rs4238989 and GG carriers of rs3760138 in the AANAT gene had increased risk of breast cancer, whereas TT carriers of BMAL1 rs2278749 and TT carriers of CLOCK rs3749474 had reduced risk. The associations were found to be noteworthy using both the FPRP and BFDP tests. With regard to the effect of polymorphisms and night work, several significant associations were observed. After applying FPRP and BFDP in women with at least four night shifts, an increased risk of breast cancer was associated with variant alleles of SNPs in the genes AANAT (rs3760138, rs4238989), BMAL1 (rs2290035, rs2278749, rs969485) and ROR-b (rs3750420). In women with three consecutive night shifts, a reduced risk of breast cancer was associated with carriage of variant alleles of SNPs in CLOCK (rs3749474), BMAL1 (rs2278749), BMAL2 (rs2306074), CSNK1E (rs5757037), NPAS2 (rs17024926), ROR-b (rs3903529, rs3750420), MTNR1A (rs131113549) and PER3 (rs1012477).
Significant and noteworthy associations between several polymorphisms in circadian genes, night work and breast cancer risk were found among nurses who had worked at least three consecutive night shifts.
Notes
Cites: Nurse Pract. 2011 Dec 16;36(12):20-6; quiz 722089837
Cites: Sleep Med Rev. 2013 Aug;17(4):273-8423137527
Cites: Cancer. 2012 Feb 15;118(4):937-4621773969
Cites: Cancer Res. 2006 May 15;66(10):5521-516707482
Cites: Cancer Sci. 2006 Jul;97(7):589-9616827798
Cites: Am J Epidemiol. 2006 Aug 15;164(4):358-6616777931
Cites: Reproduction. 2006 Sep;132(3):379-9216940279
Cites: Scand J Work Environ Health. 2007 Feb;33(1):66-7317353967
Cites: Am J Hum Genet. 2007 Aug;81(2):208-2717668372
Cites: Scand J Work Environ Health. 2007 Oct;33(5):336-4317973059
Cites: Cold Spring Harb Symp Quant Biol. 2007;72:459-6418419305
Cites: Mol Cancer Res. 2008 Sep;6(9):1461-818819933
Cites: Lancet Oncol. 2007 Dec;8(12):1065-619271347
Cites: Eur J Cancer. 2009 May;45(7):1218-3119091545
Cites: BMC Psychiatry. 2009;9:7019909500
Cites: Cancer Res. 2009 Dec 15;69(24):9315-2219934327
Cites: Cancer Res. 2010 Feb 15;70(4):1459-6820124474
Cites: Science. 2002 Dec 13;298(5601):2213-612481141
Cites: J Natl Cancer Inst. 2004 Mar 17;96(6):434-4215026468
Cites: Cancer Lett. 1992 Jul 10;64(3):249-561638517
Cites: Science. 2004 Dec 24;306(5705):2187-91; author reply 2187-9115622558
Cites: Epidemiology. 2005 Mar;16(2):254-815703542
Cites: J Natl Cancer Inst. 2005 Apr 20;97(8):567-7615840879
Cites: Nat Struct Mol Biol. 2005 May;12(5):441-815821743
Cites: Epidemiology. 2006 Jan;17(1):108-1116357603
Cites: Cancer Causes Control. 2006 Feb;17(1):39-4416411051
Cites: Cancer Prev Res (Phila). 2010 Apr;3(4):539-4820233903
Cites: PLoS One. 2010;5(4):e1000720368993
Cites: BMC Cancer. 2010;10:11020334671
Cites: Scand J Work Environ Health. 2010 Mar;36(2):134-4120039012
Cites: Alcohol Alcohol. 2010 Jul-Aug;45(4):303-1120554694
Cites: IARC Monogr Eval Carcinog Risks Hum. 2010;98:9-76421381544
Cites: Breast Cancer Res Treat. 2011 Jun;127(2):531-4020978934
Cites: Am J Epidemiol. 2011 Jun 1;173(11):1272-921454824
Cites: Chronobiol Int. 2011 Oct;28(8):653-621929297
Cites: J Pineal Res. 2011 Oct;51(3):259-6921605163
Cites: Cell Death Differ. 2012 Mar;19(3):397-40521818120
Cites: Chronobiol Int. 2012 Mar;29(2):203-1022324558
Cites: JAMA. 2012 Feb 15;307(7):666; author reply 66622337674
Cites: Mol Cell Endocrinol. 2012 Apr 4;351(2):152-6622245784
Cites: Nat Genet. 2012 Mar;44(3):312-822267197
Cites: Cancer Epidemiol Biomarkers Prev. 2012 Apr;21(4):609-1822315366
Cites: Chem Res Toxicol. 2012 Apr 16;25(4):811-2422303888
Cites: Br J Cancer. 2012 Jun 19;107 Suppl 1:S3-722710676
Cites: Eur J Cancer. 2012 Jul;48(11):1722-921852111
Cites: Occup Environ Med. 2012 Aug;69(8):551-622645325
Cites: Int J Cancer. 2012 Dec 1;131(11):2547-5222473669
Cites: J Pineal Res. 2012 Nov;53(4):366-7322582944
Cites: Int J Cancer. 2012 Dec 15;131(12):2886-9722447246
Cites: Int J Cancer. 2013 Feb 15;132(4):924-3122689255
Cites: Endocr J. 2013;60(1):1-1323171705
Cites: Am J Epidemiol. 2013 Feb 15;177(4):316-2723324334
Cites: PLoS One. 2013;8(2):e5691523437270
Cites: Scand J Work Environ Health. 2013 Mar 1;39(2):178-8622517501
Cites: Scand J Work Environ Health. 2013 Mar 1;39(2):187-9422552736
Cites: Bioorg Med Chem Lett. 2013 Apr 1;23(7):1929-3423481644
Cites: Hum Mol Genet. 2012 Feb 15;21(4):958-6222072393
PubMed ID
23822714 View in PubMed
Less detail

Analysis of Swedish male breast cancer family data: a simple way to incorporate a common sibling effect.

https://arctichealth.org/en/permalink/ahliterature21693
Source
Genet Epidemiol. 1998;15(2):201-12
Publication Type
Article
Date
1998
Author
P M Karunaratne
R C Elston
N. Loman
H. Olsson
J. Ranstam
Author Affiliation
Department of Epidemiology and Biostatistics, Rammelkamp Center for Education and Research, Case Western Reserve University, Cleveland, Ohio 44109, USA.
Source
Genet Epidemiol. 1998;15(2):201-12
Date
1998
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
BRCA2 Protein
Breast Neoplasms - epidemiology - genetics
Breast Neoplasms, Male - epidemiology - genetics
Cohort Studies
Data Interpretation, Statistical
Family Health
Female
Follow-Up Studies
Humans
Incidence
Male
Middle Aged
Models, Genetic
Models, Statistical
Mutation
Neoplasm Proteins - genetics
Prevalence
Regression Analysis
Research Support, U.S. Gov't, P.H.S.
Risk assessment
Sweden - epidemiology
Transcription Factors - genetics
Abstract
Based on a population-based cohort study, Olsson et al. [1993] found significant evidence for elevated incidence of breast and ovarian cancers among female first-degree relatives of men with breast cancer. Using an extension of logistic regressive models we investigate whether, after allowing for multifactorial familial correlations, single locus segregation could be the cause of the elevated incidence in these families. The logit for a given sib in the class D logistic regressive model depends on the order in which affected sibs occur in a sibship. That makes the model less appropriate for the situation where a polygenic component or a common sibling environment may be present, as well as being computationally cumbersome. In this paper, we propose to use the proportion of siblings in a sibship who are affected to quantify a sibling correlation. That not only relaxes the interchangeability problem but also makes the model computationally efficient. We then use this modified class D logistic regressive model for our segregation analysis. Using the proportion of siblings in a sibship who are affected as a covariate resulted in a significantly higher likelihoods in all the models we investigated. We found evidence for a dominant Mendelian gene leading to early age of onset of breast and/or ovarian cancer. This could either be a germline mutation of BRCA2 or a mutation in a gene different from BRCA2.
PubMed ID
9554557 View in PubMed
Less detail

Androgen receptor expression and breast cancer mortality in a population-based prospective cohort.

https://arctichealth.org/en/permalink/ahliterature292708
Source
Breast Cancer Res Treat. 2017 Oct; 165(3):645-657
Publication Type
Journal Article
Date
Oct-2017
Author
Karin Elebro
Pär-Ola Bendahl
Helena Jernström
Signe Borgquist
Author Affiliation
Division of Oncology and Pathology, Clinical Sciences Lund, Lund University, Lund, Sweden. Karin.Elebro@med.lu.se.
Source
Breast Cancer Res Treat. 2017 Oct; 165(3):645-657
Date
Oct-2017
Language
English
Publication Type
Journal Article
Keywords
Adult
Aged
Biomarkers, Tumor
Breast Neoplasms - epidemiology - genetics - mortality - pathology
Cause of Death
Combined Modality Therapy
Female
Gene Expression
Humans
Immunohistochemistry
Middle Aged
Neoplasm Grading
Neoplasm Staging
Population Surveillance
Prognosis
Receptors, Androgen - genetics - metabolism
Sweden - epidemiology
Abstract
The increase in clinical trials with androgen receptor (AR)-targeting drugs emphasizes the need of clarifying the role of AR expression in different breast cancer subtypes. AR confers good prognosis in estrogen receptor positive (ER+) breast cancer, but its role in ER-negative (ER-) breast cancer is unclear. The aim of this study was to elaborate on previous findings of a differential prognostic role for AR depending on ER status, using breast cancer mortality (BCM) as endpoint, in a population-based cohort from the Malmö Diet and Cancer Study.
Immunohistochemical AR expression was assessed in 910 women with invasive breast cancer diagnosed 1991-2010, supplemented with clinicopathological information, vital status, and cause of death, with the last follow-up in December 2014 (median 10 years). Survival analyses according to AR status and AR/ER combinations were performed.
AR expression was available for 671 tumors. AR+ (n = 573, 85%) was associated with favorable established tumor markers and lower BCM in univariable analysis, especially during the first 5 years following diagnosis [HR 0.4; 95% confidence intervals (CI) 0.2-0.7]. Multivariable analysis for short-term follow-up indicated higher BCM among patients with AR+ER- tumors (HR 3.5; 95% CI 1.4-9.1) than other AR and ER combinations.
AR expression added prognostic information to ER expression with respect to short-term prognosis. The worst prognosis was seen for patients with AR+/ER- tumors in short-term follow-up, supporting the pre-specified hypothesis. However, larger cohorts are needed for further characterization of the role of AR expression in ER- breast cancer.
Notes
Cites: J Natl Cancer Inst. 2014 Jan;106(1):djt319 PMID 24273215
Cites: Cancer Res. 2009 Aug 1;69(15):6131-40 PMID 19638585
Cites: J Clin Invest. 2011 Jul;121(7):2750-67 PMID 21633166
Cites: Clin Cancer Res. 2017 Jun 1;23 (11):2702-2712 PMID 28151718
Cites: Ann Surg Oncol. 2015 Jan;22(1):82-9 PMID 25145503
Cites: J Intern Med. 1993 Jan;233(1):45-51 PMID 8429286
Cites: J Breast Cancer. 2015 Jun;18(2):134-42 PMID 26155289
Cites: Breast Cancer Res. 2014 Jan 22;16(1):R7 PMID 24451109
Cites: Endocr Relat Cancer. 2016 Oct;23(10):R485-98 PMID 27528625
Cites: Ann Oncol. 2016 May;27(5):812-8 PMID 27052658
Cites: Breast Cancer Res Treat. 2012 May;133(1):311-20 PMID 22231421
Cites: Lancet. 1998 May 16;351(9114):1451-67 PMID 9605801
Cites: Br J Cancer. 2016 Feb 2;114(3):248-55 PMID 26742006
Cites: Clin Cancer Res. 2013 Oct 1;19(19):5533-40 PMID 23948975
Cites: J Clin Epidemiol. 2009 Nov;62(11):1202-9 PMID 19364635
Cites: Breast Cancer Res Treat. 2010 May;121(1):1-11 PMID 19533338
Cites: Histopathology. 1991 Nov;19(5):403-10 PMID 1757079
Cites: Endocr Relat Cancer. 2014 Aug;21(4):T161-81 PMID 24951107
Cites: Mol Cancer Ther. 2017 Jul;16(7):1389-1400 PMID 28468774
Cites: Eur J Cancer Prev. 2001 Dec;10(6):489-99 PMID 11916347
Cites: Breast Cancer Res. 2013 Oct 01;15(5):R92 PMID 24286369
Cites: Oncogene. 2005 Jul 7;24(29):4660-71 PMID 15897907
Cites: Oncotarget. 2016 Jul 5;7(27):41285-41293 PMID 27285752
Cites: Clin Cancer Res. 2013 Oct 1;19(19):5505-12 PMID 23965901
Cites: Cancer. 2017 May 15;123(10 ):1686-1688 PMID 28406524
Cites: Clin Cancer Res. 2011 Apr 1;17(7):1867-74 PMID 21325075
Cites: Scand J Public Health. 2002;30(2):103-12 PMID 12028859
Cites: Acta Oncol. 2009;48(1):27-33 PMID 18767000
Cites: Am J Cancer Res. 2012;2(4):434-45 PMID 22860233
Cites: Oncogene. 2006 Jun 29;25(28):3994-4008 PMID 16491124
Cites: Int J Cancer. 2008 Sep 1;123(5):1146-53 PMID 18528862
Cites: Curr Opin Endocrinol Diabetes Obes. 2016 Jun;23(3):249-56 PMID 26945136
Cites: Breast Cancer Res Treat. 2006 Nov;100(2):229-35 PMID 16932852
Cites: Clin Cancer Res. 2015 Aug 15;21(16):3640-50 PMID 25904752
Cites: Mol Cancer Res. 2016 Nov;14 (11):1054-1067 PMID 27565181
Cites: Horm Cancer. 2015 Dec;6(5-6):206-13 PMID 26201402
Cites: Endocr Relat Cancer. 2015 Jun;22(3):R87-R106 PMID 25722318
Cites: J Natl Cancer Inst. 2013 Oct 2;105(19):1504-11 PMID 24029245
Cites: Breast Cancer Res Treat. 2015 Nov;154(2):225-37 PMID 26487496
Cites: Ann Oncol. 2010 Mar;21(3):488-92 PMID 19887463
Cites: Breast Cancer Res Treat. 2014 Oct;147(3):473-85 PMID 25178514
Cites: Mol Cancer Ther. 2015 Mar;14(3):769-78 PMID 25713333
PubMed ID
28643022 View in PubMed
Less detail

An evaluation of genetic heterogeneity in 145 breast-ovarian cancer families. Breast Cancer Linkage Consortium.

https://arctichealth.org/en/permalink/ahliterature23409
Source
Am J Hum Genet. 1995 Jan;56(1):254-64
Publication Type
Article
Date
Jan-1995
Author
S A Narod
D. Ford
P. Devilee
R B Barkardottir
H T Lynch
S A Smith
B A Ponder
B L Weber
J E Garber
J M Birch
Author Affiliation
Department of Medicine, McGill University, Montreal, Quebec, Canada.
Source
Am J Hum Genet. 1995 Jan;56(1):254-64
Date
Jan-1995
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
BRCA1 Protein
Breast Neoplasms - epidemiology - genetics
Breast Neoplasms, Male - epidemiology - genetics
Chromosomes, Human, Pair 17
Female
Genetic Heterogeneity
Genetic Predisposition to Disease
Humans
Iceland - epidemiology
Lod Score
Male
Middle Aged
Neoplasm Proteins - genetics
Neoplasms, Multiple Primary - epidemiology - genetics
Neoplastic Syndromes, Hereditary - epidemiology - genetics
Netherlands - epidemiology
Ovarian Neoplasms - epidemiology - genetics
Pedigree
Transcription Factors - genetics
Abstract
The breast-ovary cancer-family syndrome is a dominant predisposition to cancer of the breast and ovaries which has been mapped to chromosome region 17q12-q21. The majority, but not all, of breast-ovary cancer families show linkage to this susceptibility locus, designated BRCA1. We report here the results of a linkage analysis of 145 families with both breast and ovarian cancer. These families contain either a total of three or more cases of early-onset (before age 60 years) breast cancer or ovarian cancer. All families contained at least one case of ovarian cancer. Overall, an estimated 76% of the 145 families are linked to the BRCA1 locus. None of the 13 families with cases of male breast cancer appear to be linked, but it is estimated that 92% (95% confidence interval 76%-100%) of families with no male breast cancer and with two or more ovarian cancers are linked to BRCA1. These data suggest that the breast-ovarian cancer-family syndrome is genetically heterogeneous. However, the large majority of families with early-onset breast cancer and with two or more cases of ovarian cancer are likely to be due to BRCA1 mutations.
PubMed ID
7825586 View in PubMed
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Association between 8-oxo-7,8-dihydro-2'-deoxyguanosine excretion and risk of postmenopausal breast cancer: nested case-control study.

https://arctichealth.org/en/permalink/ahliterature114047
Source
Cancer Epidemiol Biomarkers Prev. 2013 Jul;22(7):1289-96
Publication Type
Article
Date
Jul-2013
Author
Steffen Loft
Anja Olsen
Peter Møller
Henrik E Poulsen
Anne Tjønneland
Author Affiliation
Department of Public Health, Section of Enviromental Health, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. stl@sund.ku.dk
Source
Cancer Epidemiol Biomarkers Prev. 2013 Jul;22(7):1289-96
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Breast Neoplasms - epidemiology - genetics - metabolism - urine
Case-Control Studies
Cohort Studies
DNA Damage
Denmark - epidemiology
Deoxyguanosine - analogs & derivatives - urine
Diet
Female
Follow-Up Studies
Humans
Middle Aged
Oxidative Stress - genetics - physiology
Postmenopause - genetics - urine
Prospective Studies
Receptors, Estrogen - biosynthesis
Risk factors
Tumor Markers, Biological - urine
Abstract
Oxidative stress may be important in carcinogenesis and a possible risk factor for breast cancer. The urinary excretion of oxidatively generated biomolecules, such as 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), represents biomarkers of oxidative stress, reflecting the rate of global damage to DNA in steady state.
In a nested case-control design, we examined associations between urinary excretion of 8-oxodG and risk of breast cancer in a population-based cohort of 24,697 postmenopausal women aged 50 to 64 years with 3 to 7 years follow-up. The accruing cases of breast cancer were matched to controls by age at diagnosis, baseline age, and hormone replacement therapy (HRT). Spot urine samples collected at entry was analyzed for 8-oxodG by high-performance liquid chromatography with electrochemical detection. Incidence rate ratio (IRR; 95% confidence intervals) based on 336 matched pairs with all information was estimated per unit increase in 8-oxodG divided by creatinine for all and estrogen receptor (ER) positive and negative breast cancers.
There was a borderline significant positive association between 8-oxodG and risk of all breast cancer (IRR: 1.08; 1.00-1.17 per unit increase in nmol/mmol creatinine). This association was significant with respect to the risk of ER-positive cancer (IRR: 1.11; 1.01-1.23) and among women not using HRT (IRR: 1.11; 0.97-1.26) or with low dietary iron intake (IRR: 1.10; 1.06-1.37 per unit increase) for all breast cancer.
We observed positive association between 8-oxodG excretion and risk of especially ER-positive breast cancer.
Our results suggest that oxidative stress with damage to DNA is important for the development of breast cancer.
PubMed ID
23658396 View in PubMed
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Association between CYP17 gene polymorphism and risk of breast cancer in young women.

https://arctichealth.org/en/permalink/ahliterature20946
Source
Int J Cancer. 1999 Aug 20;84(4):350-3
Publication Type
Article
Date
Aug-20-1999
Author
M. Bergman-Jungeström
M. Gentile
A C Lundin
S. Wingren
Author Affiliation
Department of Biomedicine and Surgery, Division of Oncology, Faculty of Health Sciences, University Hospital, Linköping, Sweden.
Source
Int J Cancer. 1999 Aug 20;84(4):350-3
Date
Aug-20-1999
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Alleles
Base Sequence
Breast Neoplasms - epidemiology - genetics - mortality - pathology
Cell Cycle
Confidence Intervals
Female
Heterozygote Detection
Humans
Lymphatic Metastasis
Odds Ratio
Point Mutation
Polymorphism, Genetic
Predictive value of tests
Promoter Regions (Genetics)
Receptors, Estrogen - analysis
Receptors, Progesterone - analysis
Research Support, Non-U.S. Gov't
Risk factors
Steroid 17-alpha-Hydroxylase - genetics
Survival Analysis
Sweden - epidemiology
Abstract
Long-term exposure to oestrogens is a well-recognised risk factor for breast cancer, whereas little is known about the influence of polymorphisms of genes involved in oestrogen biosynthesis and metabolism. A candidate, containing a single bp polymorphism, T-->C, (designated, A2 allele), might be the CYP17 gene, which codes for an enzyme involved in oestrogen synthesis. This polymorphism creates an additional Sp1-type promoter site (CCACC box), which has been shown to be associated with increased serum oestrogen levels. We performed a case-control study, to evaluate association of the CYP17 gene polymorphism with risk of breast cancer in young women (younger than 37 years). We found a statistically significant increased risk in carriers of at least 1 A2 allele [odds ratio (OR), 2.0; 95% confidence interval (CI), 1.1-3.5, p = 0.027], and a trend toward a gene-dose effect illustrated by a slightly higher risk for A2-homozygous subjects (OR, 2.8) than for heterozygous women (OR, 1. 9). Furthermore, when we investigated the CYP17 genotype in relation to tumour characteristics, breast cancer patients with 1 or 2 A2 alleles tended to have lower oestrogen receptor levels (risk ratio, 0.70; CI, 0.41-1.2, p = 0.44). Our findings suggest that CYP17 gene polymorphism influences breast carcinogenesis in young women. Int. J. Cancer (Pred. Oncol.) 84:350-353, 1999.
PubMed ID
10404084 View in PubMed
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