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Fernández-Aparicio Á, Schmidt-RioValle J, García PA, González-Jiménez E. Short Breastfeeding Duration is Associated With Premature Onset of Female Breast Cancer. Clin Nurs Res 2022; 31:901-908. [PMID: 35075913 DOI: 10.1177/10547738211069725] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]
Abstract
Currently, there is controversy concerning potential factors that contribute to the development of breast cancer. Our study analyzed the possible association between weight status, cigarette consumption, lactation period, serum estrogen levels, family history of breast cancer, and age at breast cancer diagnosis. We conducted a retrospective study at a University Hospital in Granada (Spain) by consulting the medical records of 524 women aged 19 to 91 years, all of them diagnosed and treated for breast cancer from 2011 to 2019. Our findings indicated that in non-morbidly obese females who were also non-smokers, a maternal lactation period of more than 3 months (p = .013) and the absence of family antecedents of cancer (p = .025) were statistically significant factors that led to a more advanced age at breast cancer diagnosis. Thus, maternal lactation seems to have a potential protective effect on breast cancer.
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Kinlen LJ, Gilham C, Ray R, Thomas DB, Peto J. Cohabitation, infection and breast cancer risk. Int J Cancer 2020; 148:1408-1418. [PMID: 32984953 DOI: 10.1002/ijc.33319] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/27/2020] [Revised: 08/20/2020] [Accepted: 09/15/2020] [Indexed: 11/09/2022]
Abstract
For 50 years, the effect of age at first birth (AFB) has been thought to explain the strong association between breast cancer risk and age at first marriage (AFM), which was first reported in 1926. The independent effects of AFM, AFB and number of sexual partners adjusted for parity and other risk factors were estimated in reanalysis of a large international case-control study conducted in 1979 to 1982 (2274 breast cancers, 18209 controls) by unconditional logistic regression. Respective AFB and AFM breast cancer odds ratios (ORs) for ≥31 years relative to ≤18 years were 3.01 (95% CI 2.44-3.71; P(trend) < .0001) and 3.24 (95% CI 2.62-4.01; P(trend) < .0001) in univariate analyses. Among married parous women, these ORs fell to 1.38 (95% CI 0.98-1.95; P(trend) < .03) for AFB and 1.70 (95% CI 1.17-2.46; P(trend) < .002) for AFM when fitted together in multivariate analysis including other risk factors. A similar adjusted OR for AFM ≥ 31 years relative to ≤18 years was seen among married nulliparous women (OR 1.71, 95% CI 0.98-2.98; P(trend) < .001). AFM (a surrogate for age at starting prolonged cohabitation) is thus strongly associated with breast cancer risk. This suggests an effect of close contact. Identifying the (probably infective) mechanism might lead to effective prevention of breast cancer. The independent effect of AFB is smaller and could be due to residual confounding.
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Affiliation(s)
- Leo J Kinlen
- Cancer Research UK Cancer Epidemiology Unit, Nuffield Department of Population Medicine, University of Oxford, Oxford, UK
| | - Clare Gilham
- Faculty of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, UK
| | - Roberta Ray
- Fred Hutchinson Cancer Research Center, Seattle, Washington, USA
| | - David B Thomas
- Fred Hutchinson Cancer Research Center, Seattle, Washington, USA
| | - Julian Peto
- Faculty of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, UK
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Parity reduces mammary repopulating activity but does not affect mammary stem cells defined as CD24 + CD29/CD49fhi in mice. Breast Cancer Res Treat 2020; 183:565-575. [PMID: 32696317 DOI: 10.1007/s10549-020-05804-1] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/23/2020] [Accepted: 07/11/2020] [Indexed: 12/19/2022]
Abstract
BACKGROUND Breast cancer (BCa) mortality is decreasing with early detection and improvement in therapies. The incidence of BCa, however, continues to increase, particularly estrogen-receptor-positive (ER +) subtypes. One of the greatest modifiers of ER + BCa risk is childbearing (parity), with BCa risk halved in young multiparous mothers. Despite convincing epidemiological data, the biology that underpins this protection remains unclear. Parity-induced protection has been postulated to be due to a decrease in mammary stem cells (MaSCs); however, reports to date have provided conflicting data. METHODS We have completed rigorous functional testing of repopulating activity in parous mice using unfractionated and MaSC (CD24midCD49fhi)-enriched populations. We also developed a novel serial transplant method to enable us to assess self-renewal of MaSC following pregnancy. Lastly, as each pregnancy confers additional BCa protection, we subjected mice to multiple rounds of pregnancy to assess whether additional pregnancies impact MaSC activity. RESULTS Here, we report that while repopulating activity in the mammary gland is reduced by parity in the unfractionated gland, it is not due to a loss in the classically defined MaSC (CD24+CD49fhi) numbers or function. Self-renewal was unaffected by parity and additional rounds of pregnancy also did not lead to a decrease in MaSC activity. CONCLUSIONS Our data show instead that parity impacts on the stem-like activity of cells outside the MaSC population.
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Niehoff NM, Gammon MD, Keil AP, Nichols HB, Engel LS, Sandler DP, White AJ. Airborne mammary carcinogens and breast cancer risk in the Sister Study. ENVIRONMENT INTERNATIONAL 2019; 130:104897. [PMID: 31226564 PMCID: PMC6679994 DOI: 10.1016/j.envint.2019.06.007] [Citation(s) in RCA: 21] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 02/06/2019] [Revised: 05/10/2019] [Accepted: 06/03/2019] [Indexed: 05/04/2023]
Abstract
INTRODUCTION Potentially carcinogenic hazardous air pollutants (air toxics) have been inconsistently associated with breast cancer. Whether metabolic factors modify these associations is unknown. We studied 29 non-metallic air toxics classified as mammary gland carcinogens in animal studies in relation to breast cancer risk. METHODS Participants included 49,718 women from the Sister Study. Census tract air toxic concentration estimates from the 2005 National Air Toxics Assessment were linked to enrollment residential addresses. Adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for individual air toxics were estimated using Cox regression. Body mass index (BMI) was considered a potential modifier. Relevant mixtures were identified using classification trees. RESULTS Over follow-up (average = 8.4 years), 2975 women were newly diagnosed with breast cancer (invasive or ductal carcinoma in situ). Several air toxics, including methylene chloride, polycyclic organic matter, propylene dichloride, and styrene, were associated with increased risk. Of these, methylene chloride was most consistently associated with risk across multiple analyses. It was associated with overall (HRquintile 4vs1 = 1.21 (95%CI = 1.07-1.38)) and estrogen receptor positive (ER+) invasive breast cancer (HRquintile 4vs1 = 1.28 (95%CI = 1.08-1.52)) in individual pollutant models, although no dose-response was observed. Associations were stronger among overweight/obese (vs. non-overweight/obese) women (p < 0.05) for six air toxics. The classification tree identified combinations of age, methylene chloride, BMI, and four other toxics (propylene dichloride, ethylene dibromide, ethylidene dichloride, styrene) related to overall breast cancer. CONCLUSIONS Some non-metallic air toxics, particularly methylene chloride, were associated with the hazard for overall and ER+ breast cancer. Overweight/obese women may be particularly susceptible to air toxics.
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Affiliation(s)
- Nicole M Niehoff
- Department of Epidemiology, University of North Carolina, 135 Dauer Drive, Chapel Hill, NC 27599, United States of America.
| | - Marilie D Gammon
- Department of Epidemiology, University of North Carolina, 135 Dauer Drive, Chapel Hill, NC 27599, United States of America
| | - Alexander P Keil
- Department of Epidemiology, University of North Carolina, 135 Dauer Drive, Chapel Hill, NC 27599, United States of America
| | - Hazel B Nichols
- Department of Epidemiology, University of North Carolina, 135 Dauer Drive, Chapel Hill, NC 27599, United States of America
| | - Lawrence S Engel
- Department of Epidemiology, University of North Carolina, 135 Dauer Drive, Chapel Hill, NC 27599, United States of America
| | - Dale P Sandler
- Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, United States of America
| | - Alexandra J White
- Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, United States of America
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Press DJ, Ibraheem A, Dolan ME, Goss KH, Conzen S, Huo D. Racial disparities in omission of oncotype DX but no racial disparities in chemotherapy receipt following completed oncotype DX test results. Breast Cancer Res Treat 2017; 168:207-220. [PMID: 29181717 DOI: 10.1007/s10549-017-4587-8] [Citation(s) in RCA: 28] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/13/2017] [Accepted: 11/18/2017] [Indexed: 12/31/2022]
Abstract
PURPOSE To examine racial/ethnic disparities in Oncotype DX (ODX) testing among patients with node-negative, estrogen receptor (ER)-positive, human epidermal growth factor receptor 2 (HER2)-negative breast cancers and possible racial/ethnic disparities in chemotherapy receipt following ODX testing within Recurrence Score (RS) category (Not Done, Low, Intermediate, High), as well as chemotherapy receipt time trends within RS categories. METHODS A retrospective cohort list of 125,288 women who were potentially indicated for ODX testing from 2010 to 2014 was obtained using the National Cancer Database. We fit multivariate logistic regression predicting chemotherapy receipt, adjusting for clinical factors, patient demographic factors, and hospital-level factors, separately by RS category, and calculated odds ratios (OR) and 95% confidence intervals (CI), as well as time trends. RESULTS Overall, ODX testing was completed for 46.1% of Non-Hispanic (NH) Whites, 43.9% of NH Blacks, and 41.7% of Hispanics. Among patients who did not receive ODX testing, NH Black and Hispanic women both experienced statistically significant increases in chemotherapy receipt relative to NH White women (NH Black OR 1.23; 95% CI 1.11-1.37; Hispanic OR 1.23; 95% CI 1.07-1.42). However, among patients with ODX results, no statistically significant racial/ethnic differences in chemotherapy receipt were observed within strata of RS category. Trend analyses demonstrated increasing adherence to national guidelines for ODX testing. CONCLUSIONS We identified racial disparities in omission of ODX testing but no differences in chemotherapy receipt if ODX test results were obtained, suggesting increasing access to ODX testing may improve racial equality in efficacious use of adjuvant chemotherapy for ER-positive HER2-negative breast cancer.
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Affiliation(s)
- David J Press
- Department of Public Health Sciences, The University of Chicago, 5841 S. Maryland Ave., MC2000, Chicago, IL, 60637, USA.
| | - Abiola Ibraheem
- Section of Hematology/Oncology, Department of Medicine Chicago, University of Chicago, Chicago, IL, USA
| | - M Eileen Dolan
- Section of Hematology/Oncology, Department of Medicine Chicago, University of Chicago, Chicago, IL, USA
| | - Kathleen H Goss
- University of Chicago Comprehensive Cancer Center, University of Chicago, Chicago, IL, USA
| | - Suzanne Conzen
- Section of Hematology/Oncology, Department of Medicine Chicago, University of Chicago, Chicago, IL, USA
| | - Dezheng Huo
- Department of Public Health Sciences, The University of Chicago, 5841 S. Maryland Ave., MC2000, Chicago, IL, 60637, USA
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Bado I, Gugala Z, Fuqua SAW, Zhang XHF. Estrogen receptors in breast and bone: from virtue of remodeling to vileness of metastasis. Oncogene 2017; 36:4527-4537. [PMID: 28368409 PMCID: PMC5552443 DOI: 10.1038/onc.2017.94] [Citation(s) in RCA: 20] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/28/2016] [Revised: 02/28/2017] [Accepted: 02/28/2017] [Indexed: 12/11/2022]
Abstract
Bone metastasis is a prominent cause of morbidity and mortality in cancer. High rates of bone colonization in breast cancer, especially in the subtype expressing estrogen receptors (ERs), suggest tissue-specific proclivities for metastatic tumor formation. The mechanisms behind this subtype-specific organ-tropism remains largely elusive. Interestingly, as the major driver of ER+ breast cancer, ERs also have important roles in bone development and homeostasis. Thus, any agents targeting ER will also inevitably affect the microenvironment, which involves the osteoblasts and osteoclasts. Yet, how such microenvironmental effects are integrated with direct therapeutic responses of cancer cells remain poorly understood. Recent findings on ER mutations, especially their enrichment in bone metastasis, raised even more provocative questions on the role of ER in cancer-bone interaction. In this review, we evaluate the importance of ERs in bone metastasis and discuss new avenues of investigation for bone metastasis treatment based on current knowledge.
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Affiliation(s)
- Igor Bado
- Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030
- Dan L. Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030
- Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030
| | - Zbigniew Gugala
- Department of Orthopaedic Surgery and Rehabilitation, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555
| | - Suzanne A. W. Fuqua
- Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030
- Dan L. Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030
| | - Xiang H.-F. Zhang
- Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030
- Dan L. Duncan Cancer Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030
- Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030
- McNair Medical Institute, Baylor College of Medicine, One Baylor Plaza, Houston, TX, 77030
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Chien L, Tseng T, Chen C, Jiang H, Tsai F, Liu T, Hsiung CA, Chang I. Comparison of annual percentage change in breast cancer incidence rate between Taiwan and the United States-A smoothed Lexis diagram approach. Cancer Med 2017; 6:1762-1775. [PMID: 28560749 PMCID: PMC5504335 DOI: 10.1002/cam4.1102] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/12/2017] [Revised: 03/07/2017] [Accepted: 04/25/2017] [Indexed: 11/29/2022] Open
Abstract
Recent studies compared the age effects and birth cohort effects on female invasive breast cancer (FIBC) incidence in Asian populations with those in the US white population. They were based on age-period-cohort model extrapolation and estimated annual percentage change (EAPC) in the age-standardized incidence rates (ASR). It is of interest to examine these results based on cohort-specific annual percentage change in rate (APCR) by age and without age-period-cohort model extrapolation. FIBC data (1991-2010) were obtained from the Taiwan Cancer Registry and the U.S. SEER 9 registries. APCR based on smoothed Lexis diagrams were constructed to study the age, period, and cohort effects on FIBC incidence. The patterns of age-specific rates by birth cohort are similar between Taiwan and the US. Given any age-at-diagnosis group, cohort-specific rates increased overtime in Taiwan but not in the US; cohort-specific APCR by age decreased with birth year in both Taiwan and the US but was always positive and large in Taiwan. Given a diagnosis year, APCR decreased as birth year increased in Taiwan but not in the US. In Taiwan, the proportion of APCR attributable to cohort effect was substantial and that due to case ascertainment was becoming smaller. Although our study shows that incidence rates of FIBC have increased rapidly in Taiwan, thereby confirming previous results, the rate of increase over time is slowing. Continued monitoring of APCR and further investigation of the cause of the APCR decrease in Taiwan are warranted.
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Affiliation(s)
- Li‐Hsin Chien
- Division of Biostatistics and BioinformaticsInstitute of Population Health SciencesNational Health Research InstitutesTaiwan
| | - Tzu‐Jui Tseng
- Center of Biomedical ResourcesNational Health Research InstitutesTaiwan
| | - Chung‐Hsing Chen
- National Institute of Cancer ResearchNational Health Research InstitutesTaiwan
| | - Hsin‐Fang Jiang
- National Institute of Cancer ResearchNational Health Research InstitutesTaiwan
| | - Fang‐Yu Tsai
- National Institute of Cancer ResearchNational Health Research InstitutesTaiwan
| | - Tsang‐Wu Liu
- National Institute of Cancer ResearchNational Health Research InstitutesTaiwan
| | - Chao A. Hsiung
- Division of Biostatistics and BioinformaticsInstitute of Population Health SciencesNational Health Research InstitutesTaiwan
| | - I‐Shou Chang
- Division of Biostatistics and BioinformaticsInstitute of Population Health SciencesNational Health Research InstitutesTaiwan
- Center of Biomedical ResourcesNational Health Research InstitutesTaiwan
- National Institute of Cancer ResearchNational Health Research InstitutesTaiwan
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Thivyah Prabha A, Sekar D. Deciphering the molecular signaling pathways in breast cancer pathogenesis and their role in diagnostic and treatment modalities. GENE REPORTS 2017; 7:1-17. [DOI: 10.1016/j.genrep.2017.01.003] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/23/2022]
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Dall G, Risbridger G, Britt K. Mammary stem cells and parity-induced breast cancer protection- new insights. J Steroid Biochem Mol Biol 2017; 170:54-60. [PMID: 26907964 DOI: 10.1016/j.jsbmb.2016.02.018] [Citation(s) in RCA: 21] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/08/2016] [Revised: 02/09/2016] [Accepted: 02/18/2016] [Indexed: 11/26/2022]
Abstract
Parity (childbearing) significantly decreases a woman's risk of breast cancer and the protective effect is greater if the woman is younger and has more children. The mechanism/s of parity-induced protection are not known. Although several factors are postulated to play a role, we discuss how a reduction in the number of mammary stem cells (MaSCs) may lead to a reduction in breast cancer risk in parous women. Firstly we review the epidemiology linking childbearing to reduced breast cancer risk and discuss how additional births, a young age at first full term birth, and breastfeeding impact the protection. We then detail the mouse and human studies implicating MaSC in parity induced protection and the in-vivo work being performed in mice to directly investigate the effect of parity on MaSC. Finally we discuss the transplant and lineage tracing experiments assessing MaSC activity according to parity and the need to define if MaSC are indeed more carcinogen sensitive than mature mammary epithelial cells. Continuing and future studies attempting to define the parity induced mechanisms will aid in the development of preventative therapies.
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Affiliation(s)
- Genevieve Dall
- Metastasis Research Laboratory, Peter MacCallum Cancer Centre, 7 St Andrews Place, East Melbourne 3002, Australia; Department of Anatomy and Developmental Biology, Monash University Clayton, Wellington Rd 3800, Australia
| | - Gail Risbridger
- Department of Anatomy and Developmental Biology, Monash University Clayton, Wellington Rd 3800, Australia
| | - Kara Britt
- Metastasis Research Laboratory, Peter MacCallum Cancer Centre, 7 St Andrews Place, East Melbourne 3002, Australia; Department of Anatomy and Developmental Biology, Monash University Clayton, Wellington Rd 3800, Australia; The Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Australia.
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10
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Dall GV, Britt KL. Estrogen Effects on the Mammary Gland in Early and Late Life and Breast Cancer Risk. Front Oncol 2017; 7:110. [PMID: 28603694 PMCID: PMC5445118 DOI: 10.3389/fonc.2017.00110] [Citation(s) in RCA: 87] [Impact Index Per Article: 10.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/14/2016] [Accepted: 05/10/2017] [Indexed: 12/16/2022] Open
Abstract
A woman has an increased risk of breast cancer if her lifelong estrogen exposure is increased due to an early menarche, a late menopause, and/or an absence of childbearing. For decades, it was presumed that the number of years of exposure drove the increased risk, however, recent epidemiological data have shown that early life exposure (young menarche) has a more significant effect on cancer risk than late menopause. Thus, rather than the overall exposure it seems that the timing of hormone exposure plays a major role in defining breast cancer risk. In support of this, it is also known that aberrant hormonal exposure prior to puberty can also increase breast cancer risk, yet the elevated estrogen levels during pregnancy decrease breast cancer risk. This suggests that the effects of estrogen on the mammary gland/breast are age-dependent. In this review article, we will discuss the existing epidemiological data linking hormone exposure and estrogen receptor-positive breast cancer risk including menarche, menopause, parity, and aberrant environmental hormone exposure. We will discuss the predominantly rodent generated experimental data that confirm the association with hormone exposure and breast cancer risk, confirming its use as a model system. We will review the work that has been done attempting to define the direct effects of estrogen on the breast, which are beginning to reveal the mechanism of increased cancer risk. We will then conclude with our views on the most pertinent questions to be addressed experimentally in order to explore the relationship between age, estrogen exposure, and breast cancer risk.
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Affiliation(s)
| | - Kara Louise Britt
- Peter MacCallum Cancer Centre, Melbourne, VIC, Australia
- The Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, VIC, Australia
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Horn J, Vatten LJ. Reproductive and hormonal risk factors of breast cancer: a historical perspective. Int J Womens Health 2017; 9:265-272. [PMID: 28490905 PMCID: PMC5414577 DOI: 10.2147/ijwh.s129017] [Citation(s) in RCA: 22] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/23/2022] Open
Abstract
The complexity of breast cancer etiology has puzzled scientists for more than 300 years. In this brief review, we emphasize the importance of reproductive and hormonal factors in relation to the risk of breast cancer. By following the historical course of how various risk factors have been determined, this study attempts to illustrate the origin of hypotheses, their subsequent rejection, and development of new hypotheses. Starting with the contributions of Italian physicians in the 18th century and covering the activity of British epidemiologists before World War II, this review ends up with the international collaboration that became increasingly important in the second half of the 20th century.
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Affiliation(s)
- Julie Horn
- Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway.,Department of Gynecology and Obstetrics, Levanger Hospital, Nord-Trøndelag Hospital Trust, Levanger, Norway
| | - Lars J Vatten
- Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway
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12
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Lukong KE. Understanding breast cancer - The long and winding road. BBA CLINICAL 2017; 7:64-77. [PMID: 28194329 PMCID: PMC5300293 DOI: 10.1016/j.bbacli.2017.01.001] [Citation(s) in RCA: 132] [Impact Index Per Article: 16.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/03/2016] [Revised: 12/28/2016] [Accepted: 01/24/2017] [Indexed: 12/24/2022]
Abstract
Background Despite a remarkable increase in the depth of our understanding and management of breast cancer in the past 50 years, the disease is still a major public health problem worldwide and poses significant challenges. The palpability of breast tumors has facilitated diagnosis and documentation since ancient times. The earliest descriptions of breast cancer date back to around 3500 BCE. For centuries to follow, theories by Hippocrates (460 BCE) and Galen (200 CE), attributing the cause of breast cancer to an “excess of black bile” and treatment options including the use of opium and castor oil, prevailed. Surgical resection was introduced in the 18th century. The advent of modern medicine led to the development of novel treatment options that include hormonal, targeted and chemo-therapies. There are still several therapeutic challenges including the treatment of triple negative breast cancer (TNBC), and overcoming drug resistance. Scope of review The increased incidence and awareness of breast cancer has led to significant changes in diagnosis and treatment in recent decades. But, mankind has come a long way. Herein, I have traced how our understanding of breast cancer has evolved from the early description of the disease around 460 BCE as “black bile-containing crab-like tumors” to the conventional as a heterogeneous disease with high degree of diversity between and within tumors, as well as among breast cancer patients. How is breast cancer treated today and how do risk factors, breast cancer subtype and drug resistance contribute to the therapeutic challenges at the turn of the 21st century? Major conclusions Breast cancer remains a serious public health issue worldwide. However, appreciable growth in our understanding of breast cancer in the past century has led to remarkable progress in the early detection, treatment and prevention of the disease. The clinical focus is shifting more towards tailored therapy as more targets are characterized and novel highly innovative approaches are developed. General significance Tracing the history of breast cancer, highlights how increased awareness of the disease, and progress in research and development have enhance our understanding of the disease.
The humoral, lymphatic and anti-hormonal theories of breast cancer Introduction of radical mastectomy, radiotherapy, mammography, and targeted therapy The introduction of randomized trial Breast cancer foundations, awareness and the Angelina Jolie effect Promising future for tailored therapy
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Blackadar CB. Historical review of the causes of cancer. World J Clin Oncol 2016; 7:54-86. [PMID: 26862491 PMCID: PMC4734938 DOI: 10.5306/wjco.v7.i1.54] [Citation(s) in RCA: 168] [Impact Index Per Article: 18.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/20/2015] [Revised: 10/31/2015] [Accepted: 11/24/2015] [Indexed: 02/06/2023] Open
Abstract
In the early 1900s, numerous seminal publications reported that high rates of cancer occurred in certain occupations. During this period, work with infectious agents produced only meager results which seemed irrelevant to humans. Then in the 1980s ground breaking evidence began to emerge that a variety of viruses also cause cancer in humans. There is now sufficient evidence of carcinogenicity in humans for human T-cell lymphotrophic virus, human immunodeficiency virus, hepatitis B virus, hepatitis C virus, human papillomavirus, Epstein-Barr virus, and human herpes virus 8 according to the International Agency for Research on Cancer (IARC). Many other causes of cancer have also been identified by the IARC, which include: Sunlight, tobacco, pharmaceuticals, hormones, alcohol, parasites, fungi, bacteria, salted fish, wood dust, and herbs. The World Cancer Research Fund and the American Institute for Cancer Research have determined additional causes of cancer, which include beta carotene, red meat, processed meats, low fibre diets, not breast feeding, obesity, increased adult height and sedentary lifestyles. In brief, a historical review of the discoveries of the causes of human cancer is presented with extended discussions of the difficulties encountered in identifying viral causes of cancer.
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14
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Islami F, Liu Y, Jemal A, Zhou J, Weiderpass E, Colditz G, Boffetta P, Weiss M. Breastfeeding and breast cancer risk by receptor status--a systematic review and meta-analysis. Ann Oncol 2015; 26:2398-407. [PMID: 26504151 DOI: 10.1093/annonc/mdv379] [Citation(s) in RCA: 139] [Impact Index Per Article: 13.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/29/2015] [Accepted: 08/06/2015] [Indexed: 12/29/2022] Open
Abstract
BACKGROUND Breastfeeding is inversely associated with overall risk of breast cancer. This association may differ in breast cancer subtypes defined by receptor status, as they may reflect different mechanisms of carcinogenesis. We conducted a systematic review and meta-analysis of case-control and prospective cohort studies to investigate the association between breastfeeding and breast cancer by estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) status. DESIGN We searched the PubMed and Scopus databases and bibliographies of pertinent articles to identify relevant articles and used random-effects models to calculate summary odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS This meta-analysis represents 27 distinct studies (8 cohort and 19 case-control), with a total of 36 881 breast cancer cases. Among parous women, the risk estimates for the association between ever (versus never) breastfeeding and the breast cancers negative for both ER and PR were similar in three cohort and three case-control studies when results were adjusted for several factors, including the number of full-term pregnancies (combined OR 0.90; 95% CI 0.82-0.99), with little heterogeneity and no indication of publication bias. In a subset of three adjusted studies that included ER, PR, and HER2 status, ever breastfeeding showed a stronger inverse association with triple-negative breast cancer (OR 0.78; 95% CI 0.66-0.91) among parous women. Overall, cohort studies showed no significant association between breastfeeding and ER+/PR+ or ER+ and/or PR+ breast cancers, although one and two studies (out of four and seven studies, respectively) showed an inverse association. CONCLUSIONS This meta-analysis showed a protective effect of ever breastfeeding against hormone receptor-negative breast cancers, which are more common in younger women and generally have a poorer prognosis than other subtypes of breast cancer. The association between breastfeeding and receptor-positive breast cancers needs more investigation.
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Affiliation(s)
- F Islami
- Surveillance and Health Services Research, American Cancer Society, Atlanta Institute for Translational Epidemiology and the Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York
| | - Y Liu
- Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St Louis, USA
| | - A Jemal
- Surveillance and Health Services Research, American Cancer Society, Atlanta
| | - J Zhou
- Institute for Translational Epidemiology and the Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York
| | - E Weiderpass
- Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø Cancer Registry of Norway, Oslo, Norway Department of Genetic Epidemiology, Folkhälsan Research Center, Helsinki, Finland
| | - G Colditz
- Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St Louis, USA Siteman Cancer Center, Washington University School of Medicine, St Louis
| | - P Boffetta
- Institute for Translational Epidemiology and the Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York
| | - M Weiss
- Breastcancer.org/breasthealth.org, Lankenau Medical Center, Wynnewood, USA
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Hurst JH. Pioneering geneticist Mary-Claire King receives the 2014 Lasker~Koshland Special Achievement Award in Medical Science. J Clin Invest 2014; 124:4148-51. [PMID: 25196046 DOI: 10.1172/jci78507] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/27/2023] Open
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Morabia A. Snippets from the past: is Flint, Michigan, the birthplace of the case-control study? Am J Epidemiol 2013; 178:1687-90. [PMID: 24064743 DOI: 10.1093/aje/kwt221] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/14/2022] Open
Abstract
In the summer of 1924, an outbreak of scarlet fever occurred in Flint, Michigan. Unable to trace it to the usual causes, particularly fresh milk, the Michigan Department of Health used a novel approach to disentangle the enigma: The 116 cases of scarlet fever were compared with 117 "controls" selected from neighbors of the quarantined cases and from patients at the City Health Center who had been treated for ailments unrelated to scarlet fever. The extraordinary culprit was ice cream, which had a frequent/occasional/none consumption prevalence of 60%, 34%, and 6% among the cases and 24%, 51%, and 25% among the controls, respectively. The 1925 report reads, "Detailed epidemiological investigation, by means of case histories and control histories on well persons, confirmed early suspicions and established the fact that the epidemic was spread by ice cream" (Am J Hyg. 1925;5(5):669-681). This forgotten epidemiologic study is the oldest study using the case-control design to have been resurrected thus far. The case-control study design may have been conceived simultaneously, but independently and for different purposes, in England (Janet Lane-Claypon's 1926 report on the determinants of breast cancer) and the United States.
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Anothaisintawee T, Wiratkapun C, Lerdsitthichai P, Kasamesup V, Wongwaisayawan S, Srinakarin J, Hirunpat S, Woodtichartpreecha P, Boonlikit S, Teerawattananon Y, Thakkinstian A. Risk factors of breast cancer: a systematic review and meta-analysis. Asia Pac J Public Health 2013; 25:368-87. [PMID: 23709491 DOI: 10.1177/1010539513488795] [Citation(s) in RCA: 113] [Impact Index Per Article: 9.4] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Abstract
The etiology of breast cancer might be explained by 2 mechanisms, namely, differentiation and proliferation of breast epithelial cells mediated by hormonal factors. We performed a systematic review and meta-analysis to update effects of risk factors for both mechanisms. MEDLINE and EMBASE were searched up to January 2011. Studies that assessed association between oral contraceptives (OC), hormonal replacement therapy (HRT), diabetes mellitus (DM), or breastfeeding and breast cancer were eligible. Relative risks with their confidence intervals (CIs) were extracted. A random-effects method was applied for pooling the effect size. The pooled odds ratios of OC, HRT, and DM were 1.10 (95% CI = 1.03-1.18), 1.23 (95% CI = 1.21-1.25), and 1.14 (95% CI = 1.09-1.19), respectively, whereas the pooled odds ratio of ever-breastfeeding was 0.72 (95% CI = 0.58-0.89). Our study suggests that OC, HRT, and DM might increase risks, whereas breastfeeding might lower risks of breast cancer.
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Morabia A, Rubenstein B, Victora CG. Epidemiology and public health in 1906 England: Arthur Newsholme's methodological innovation to study breastfeeding and fatal diarrhea. Am J Public Health 2013; 103:e17-22. [PMID: 23678939 DOI: 10.2105/ajph.2013.301227] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/04/2022]
Abstract
In 1906 Arthur Newsholme linked artificial feeding and fatal diarrhea in infants aged one year and younger on the basis of two independent sources of information: mortality registration and a three-year (1903-1905) census of infants from Brighton, United Kingdom. Artificial feeding was more common in the infants who had died (89.3%) than in those in the survey (22.3%). However, boldly assuming the two data sources were nested, Newsholme computed the risks of fatal diarrhea: these were 48 times greater for infants fed fresh cow's milk and 94 times greater for those fed condensed milk than for infants who were exclusively breastfed. This mode of computing risks and risk ratios before the invention of the cohort study design was more innovative than was the usual investigation techniques of his contemporary epidemiologists. Newsholme's conclusions were consistent with the current knowledge that breastfeeding protects against fatal diarrhea.
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Affiliation(s)
- Alfredo Morabia
- Center for Biology of Natural Systems, Queens College, City University of New York, New York, NY 11367, USA.
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Morabia A. 'Lung cancer and tobacco consumption': technical evaluation of the 1943 paper by Schairer and Schoeniger published in Nazi Germany. J Epidemiol Community Health 2013; 67:208-12. [PMID: 23155058 PMCID: PMC3618958 DOI: 10.1136/jech-2012-201853] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/03/2022]
Affiliation(s)
- Alfredo Morabia
- Center for the Biology of Natural Systems, Queens College, City University of New York, New York, NY 11367, USA.
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Krieger N. Who and what is a "population"? Historical debates, current controversies, and implications for understanding "population health" and rectifying health inequities. Milbank Q 2012; 90:634-81. [PMID: 23216426 PMCID: PMC3530737 DOI: 10.1111/j.1468-0009.2012.00678.x] [Citation(s) in RCA: 61] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022] Open
Abstract
CONTEXT The idea of "population" is core to the population sciences but is rarely defined except in statistical terms. Yet who and what defines and makes a population has everything to do with whether population means are meaningful or meaningless, with profound implications for work on population health and health inequities. METHODS In this article, I review the current conventional definitions of, and historical debates over, the meaning(s) of "population," trace back the contemporary emphasis on populations as statistical rather than substantive entities to Adolphe Quetelet's powerful astronomical metaphor, conceived in the 1830s, of l'homme moyen (the average man), and argue for an alternative definition of populations as relational beings. As informed by the ecosocial theory of disease distribution, I then analyze several case examples to explore the utility of critical population-informed thinking for research, knowledge, and policy involving population health and health inequities. FINDINGS Four propositions emerge: (1) the meaningfulness of means depends on how meaningfully the populations are defined in relation to the inherent intrinsic and extrinsic dynamic generative relationships by which they are constituted; (2) structured chance drives population distributions of health and entails conceptualizing health and disease, including biomarkers, as embodied phenotype and health inequities as historically contingent; (3) persons included in population health research are study participants, and the casual equation of this term with "study population" should be avoided; and (4) the conventional cleavage of "internal validity" and "generalizability" is misleading, since a meaningful choice of study participants must be in relation to the range of exposures experienced (or not) in the real-world societies, that is, meaningful populations, of which they are a part. CONCLUSIONS To improve conceptual clarity, causal inference, and action to promote health equity, population sciences need to expand and deepen their theorizing about who and what makes populations and their means.
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Affiliation(s)
- Nancy Krieger
- Department of Society, Human Development and Health, Harvard School of Public Health, Boston, MA 02115, USA.
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Zhang Y, Liu C, Peng H, Zhang J, Feng Q. IL1 receptor antagonist gene IL1-RN variable number of tandem repeats polymorphism and cancer risk: a literature review and meta-analysis. PLoS One 2012; 7:e46017. [PMID: 23049925 PMCID: PMC3457944 DOI: 10.1371/journal.pone.0046017] [Citation(s) in RCA: 34] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/03/2012] [Accepted: 08/27/2012] [Indexed: 12/13/2022] Open
Abstract
IL1 receptor antagonist (IL1RA) and IL1beta (IL1β), members of the pro-inflammatory cytokine interleukin-1 (IL1) family, play a potential role against infection and in the pathogenesis of cancers. The variable number of tandem repeats (VNTR) polymorphism in the second intron of the IL1 receptor antagonist gene (IL1-RN) and a polymorphism in exon 5 of IL1B (IL1B+3954C>T, rs1143634) have been suggested in predisposition to cancer risk. However, studies have shown inconsistent results. To validate any association, a meta-analysis was performed with 14,854 cases and 19,337 controls from 71 published case–control studies for IL1-RN VNTR and 33 eligible studies contained 7,847 cases and 8917 controls for IL1B +3954. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated from comparisons to assess the strength of the association. There was significant association between the IL1-RN VNTR polymorphism and the risk of cancer for any overall comparison. Furthermore, cancer type stratification analysis revealed that there were significantly increased risks of gastric cancer, bladder cancer and other cancer groups. Infection status analysis indicated that the H. pylori or HBV/HCV infection and IL1-RN VNTR genotypes were independent factors for developing gastric or hepatocellular cancers. In addition, a borderline significant association was observed between IL1B+3954 polymorphism and the increased cancer risk. Although some modest bias could not be eliminated, this meta-analysis suggested that the IL1-RN VNTR polymorphisms may contribute to genetic susceptibility to gastric cancer. More studies are needed to further evaluate the role of the IL1B+3954 polymorphism in the etiology of cancer.
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Affiliation(s)
- Ying Zhang
- Inspection Division, Kunshan Hospital Affiliated to Nanjing University of Chinese Medicine, Kunshan, Jiangsu, China
| | - Changming Liu
- Inspection Division, Kunshan Hospital Affiliated to Nanjing University of Chinese Medicine, Kunshan, Jiangsu, China
| | - Huiping Peng
- Department of Gastroenterology, Kunshan Hospital Affiliated to Nanjing University of Chinese Medicine, Kunshan, Jiangsu, China
| | - Jianzhi Zhang
- Inspection Division, Kunshan Hospital Affiliated to Nanjing University of Chinese Medicine, Kunshan, Jiangsu, China
| | - Quanlin Feng
- Department of Surgical Oncology, Kunshan Hospital Affiliated to Nanjing University of Chinese Medicine, Kunshan, Jiangsu, China
- * E-mail:
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Moffat RE, Eichholzer M, Myrick ME, Schmid SM, Raggi A, de Geyter C, Schötzau A, Güth U. Menopausal state in breast cancer: how reliable is the data? Clin Breast Cancer 2011; 11:390-4. [PMID: 21903481 DOI: 10.1016/j.clbc.2011.07.002] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/09/2011] [Revised: 07/13/2011] [Accepted: 07/15/2011] [Indexed: 10/17/2022]
Abstract
UNLABELLED Despite the high importance of the menopausal state for the management of breast cancer, above all, when planning antihormonal adjuvant therapy, the menopausal state cannot be defined at the time of diagnosis ina significant proportion of women. The scope of uncertainties regarding the recording of the menopausal state in a cohort of patients with breast cancer is evaluated. INTRODUCTION Menopause is a cornerstone both in breast cancer (BC) pathophysiology and in clinical management. The scope of uncertainties regarding the recording of the menopausal state in a cohort of patients with BC is evaluated in this study. PATIENTS AND METHODS The data of a Swiss prospective relational BC database that covered a 20-year period (1990-2009; n=1457) was analyzed. For the definition of menopause, the guidelines of the National Comprehensive Cancer Network were used. RESULTS The menopausal state was unclear in 150 patients (10.2%). Of these, 122 (81.3%) had undergone a hysterectomy before menopause; in 28 women (18.7%), an endocrine therapy obscured the patient's actual endocrine status. When taking only the subgroup of women in which menopause usually occurs (45-55 years) into consideration, the menopausal state was unclear in 91 cases of 337 women (27.0%). From the entire cohort, the date of last menstruation remained obscure in 450 patients (30.9%). CONCLUSION Despite the high importance of the menopausal state for the management of BC, above all, when planning antihormonal adjuvant therapy, the menopausal state was unable to be defined at the time of BC diagnosis in a significant proportion of women. The dilemma that menopause cannot be assessed in some BC cases is increasingly being recognized. Close cooperation between oncologists and endocrinologists is desirable to establish an optimal, individually tailored therapy for women with an unclear menopausal state due to hormonal therapies, hysterectomy, or chemotherapy.
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Opdahl S, Alsaker MDK, Janszky I, Romundstad PR, Vatten LJ. Joint effects of nulliparity and other breast cancer risk factors. Br J Cancer 2011; 105:731-6. [PMID: 21811252 PMCID: PMC3188938 DOI: 10.1038/bjc.2011.286] [Citation(s) in RCA: 34] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023] Open
Abstract
Background: Pregnancy may reduce breast cancer risk through induction of persistent changes of the mammary gland that make the breast less susceptible to carcinogenic factors. It is not known to what extent the effects of parity are independent of other breast cancer risk factors. Methods: In a Norwegian cohort of 58 191 women (2890 breast cancers), we assessed whether the effects of parity on postmenopausal breast cancer risk may be modified by menstrual and anthropometric factors. We calculated attributable proportions due to interaction as a measure of synergism. Results: Parity, height, body mass index (BMI), age at menarche and menopause were all associated with breast cancer risk in the expected directions. For BMI, follow-up was stratified into two age groups because of non-proportional hazards. We found that nulliparity and overweight may amplify each other's effect on breast cancer risk among women after 70 years of age (attributable proportion 0.21, 95% confidence interval 0.04–0.39). There was some indication that parity and age at menopause may antagonise each other's effect. Effects of parity were largely unaffected by age at menarche and height. Conclusion: Nulliparity and overweight may have a synergistic effect on breast cancer risk in elderly women. If confirmed by others, the findings may help disentangle the interplay of different causes of breast cancer.
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Affiliation(s)
- S Opdahl
- Department of Public Health and Community Medicine, Faculty of Medicine, Norwegian University of Science and Technology, MTFS, Trondheim N-7491, Norway.
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He B, Zhang Y, Pan Y, Xu Y, Gu L, Chen L, Wang S. Interleukin 1 beta (IL1B) promoter polymorphism and cancer risk: evidence from 47 published studies. Mutagenesis 2011; 26:637-42. [PMID: 21653279 DOI: 10.1093/mutage/ger025] [Citation(s) in RCA: 31] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022] Open
Abstract
Interleukin 1β (IL-1B) is a pro-inflammatory cytokine against infection, playing an important role in the pathogenesis of cancers. The -31T/C polymorphism of the interleukin 1β gene (IL1B) has been implicated in cancer risk through its influence on the IL1B transcription. However, results from studies are conflicting. To clarify the association, a meta-analysis was performed for 11 125 cases and 14 415 controls from 47 published case-control studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association. No significant associations were observed for total cancer from all the comparisons. Through the stratified analyses, there was a statistically significant decreased risk of hepatocellular cancer in carriers of the C allele than non-carriers (CC versus TT: OR = 0.87, 95% CI: 0.77-0.98, P(heterogeneity) = 0.103; TC versus TT: OR = 0.77, 95% CI: 0.62-0.95, P(heterogeneity) = 0.734; TC + CC versus TT: OR = 0.74, 95% CI: 0.61-0.91, P(heterogeneity) = 0.472). Similarly, decreased risk was observed for gastric cancer of the C/C genotype compared with the T/T genotype (OR = 0.87, 95% CI: 0.77-0.98, P(heterogeneity) = 0.103). Using the recessive model, a significantly decreased risk was observed for gastric cancer (OR = 0.88, 95% CI: 0.80-0.97, P(heterogeneity) = 0.158), European population (OR = 0.84, 95% CI: 0.73-0.97, P(heterogeneity) = 0.070) and positive infection-matched studies (OR = 0.75, 95% CI: 0.60-0.94, P(heterogeneity) = 0.220); however, an increased risk was found for breast cancer (OR = 1.34, 95% CI: 1.18-1.61, P(heterogeneity) = 0.116). Although some modest bias could not be eliminated, this meta-analysis suggests that the IL1B -31C allele is a low-penetrance protective factor for the development of cancer, in particular for that associated with infection.
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Affiliation(s)
- Bangshun He
- Central Laboratory, Nanjing First Hospital Affiliated to Nanjing Medical University, 68 Changle Road, Nanjing 210006, Jiangsu, China
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Deficiency in trefoil factor 1 (TFF1) increases tumorigenicity of human breast cancer cells and mammary tumor development in TFF1-knockout mice. Oncogene 2011; 30:3261-73. [PMID: 21358676 PMCID: PMC3141110 DOI: 10.1038/onc.2011.41] [Citation(s) in RCA: 85] [Impact Index Per Article: 6.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/13/2023]
Abstract
Although trefoil factor 1 (TFF1; previously named pS2) is abnormally expressed in about 50% of human breast tumors, its physiopathological role in this disease has been poorly studied. Moreover, controversial data have been reported. TFF1 function in the mammary gland therefore needs to be clarified. In this study, using retroviral vectors, we performed TFF1 gain- or loss-of-function experiments in four human mammary epithelial cell lines: normal immortalized TFF1-negative MCF10A, malignant TFF1-negative MDA-MB-231 and malignant TFF1-positive MCF7 and ZR75.1. The expression of TFF1 stimulated the migration and invasion in the four cell lines. Forced TFF1 expression in MCF10A, MDA-MB-231 and MCF7 cells did not modify anchorage-dependent or -independent cell proliferation. By contrast, TFF1 knockdown in MCF7 enhanced soft-agar colony formation. This increased oncogenic potential of MCF7 cells in the absence of TFF1 was confirmed in vivo in nude mice. Moreover, chemically induced tumorigenesis in TFF1-deficient (TFF1-KO) mice led to higher tumor incidence in the mammary gland and larger tumor size compared with wild-type mice. Similarly, tumor development was increased in the TFF1-KO ovary and lung. Collectively, our results clearly show that TFF1 does not exhibit oncogenic properties, but rather reduces tumor development. This beneficial function of TFF1 is in agreement with many clinical studies reporting a better outcome for patients with TFF1-positive breast primary tumors.
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