One proposed mechanism by which alcohol may influence breast cancer risk is by increasing circulating estradiol levels, as has been observed in controlled feeding studies in both premenopausal and postmenopausal women [6,7]. A second potential mechanism is that alcohol may function as a cocar- cinogen, inhibiting detoxification of carcinogens, or by impair- ing clearance of carcinogens [3,8-10]. There are data suggesting that alcohol may act early in the carcinogenic proc- ess [6-9], as well as later, functioning as a tumor promoter . The current study failed to support our a priori hypothesis and suggests that recent alcohol consumption does not contribute additional risk to women with proliferative breast disease. One explanation may be that women with proliferative breast dis- eases are further along on the continuum to breast cancer, and Table 3
Benign breast disease is an important risk factor for breast cancer. In our analysis, we observed a modest risk of biopsy confirmed BBD, both proliferative and nonproliferative lesions, among women with endometriosis. The strongest increased risk of proliferative BBD in women with endometriosis was observed among women with a history of infertility. Contrary to our a priori hypothesis, we found that endometriosis was associated with an increased risk of both proliferative and nonproliferative lesions. This finding is difficult to interpret given the lack of uniformity for classifying nonproliferative benign lesions across studies. In their seminal study, Dupont and Page found no increased breast cancer risk among women with nonproliferative BBD . However, more recent research has found modest increased risk of breast cancer among nonproliferative lesions [9, 17, 41]. Wang et al. in a companion study to the National Surgical Adjuvant Breast and Bowel Project (NSABP) Breast Cancer Prevention Trail found that women in the “lower category” of BBD had 1.6 times the risk of breast cancer compared to healthy women . Hartman et. al. found that women with nonproliferative BBD had a 1.27 (95% CI: 1.15–1.41) fold risk of breast cancer among a cohort of women from the Mayo Clinic . And most recently, Castells et. al. found nonproliferative lesions conferred a 2.23 fold (95% CI: 1.86–2.68) increased risk of breast cancer in a population based screening cohort . Few studies have investigated risk factors for both proliferative and nonproliferative lesions given the mixed findings among nonproliferative lesions related to breast cancer risk.
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We also noted a positive association between MBD and CCH/FEA. In the literature, columnar cell lesions have been reported to include changes such as proliferation of columnar shaped epithelial cells within enlarged TDLUs and have been classified with or without atypia [30, 31]. Turasvili et al. conducted a study of histologic features from bilateral subcutaneous mastectomies from forensic autopsy, and reported an association between columnar cell (CC) lesions and radiographic breast density measured as high Faxitron Wolfe density (OR = 2.1, 95% CI 1.01–4.6; p = 0.04) . They also showed that CC lesions are asso- ciated with higher tissue collagen, suggesting that stromal composition and epithelial stromal interaction may poten- tially contribute to the association between CC lesions and breast density. In a study of 282 women with FEA in a co- hort with benign breast disease, FEA has been associated with AH in half the cases, with ADH more commonly so than ALH . Further research is warranted to under- stand the molecular mechanisms underlying early epithe- lial changes in mammary glandular tissue that may provide insight into mechanisms for breast cancer development.
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Fibrocystic breast disease or change is a most common benign lesion of the breast consisting of cystic dilation of intra lobular glands. It occurs between the ages of 25 and 45 years. More than 50 % of women present with illdefined palpable mass, cyclical pain, and tenderness. The exact cause of FCD is not known, but hormones may have role in its development.
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Mean participant age at baseline was 12.0 (SD: 1.6; range: 9.0 – 15.9) years. Al- though some of these dietary data were collected before adolescence, and some as young as age 9 years, we shall here- after refer to this as a study of adoles- cent diet. Mean (SD) carotenoid intakes were 491 (349) m g/day for a -carotene, 2417 (1467) m g/day for b -carotene, 153 (94) m g/day for b -cryptoxanthin, 2058 (1850) m g/day for lutein/zeaxanthin, 5418 (2073) m g/day for lycopene, and 1137 (571) m g/day for RAE of vitamin A. Girls with higher b -carotene intake were more physically active (12.9 hours/week of moderate to vigorous activity in the highest quartile com- pared with 11.1 hours/week in the lowest quartile; Table 1) and were more likely to have a family history of breast cancer (10.0% vs 7.5%) and BBD (26.0% vs 23.9%). One hundred twenty-two girls reported biopsy- con ﬁ rmed BBD over the study follow- up period.
This means that it can be transmitted through either sex and that some family members may transmit the abnormal gene without developing cancer themselves. It is not yet known how many breast cancer genes there may be. Two breast cancer genes, BRCA1 and BRCA2, which are located on the long arms of chromosomes 17 and 13 respectively, have been identified and account for a substantial proportion of very high risk families—ie those with four or more breast cancers among close relatives. Both genes are very large and mutations can occur at almost any position, so that molecular screening to detect mutation for the first time in an affected individual or family is technically demanding. Certain mutations occur at high frequency in defined populations. For instance, some 2% of Ashkenazi Jewish women carry either BRCA1 185 del AG
In this study, the majority of the benign breast disease samples represented non-proliferative breast conditions. Although the study design and cohort number are both limiting factors in evaluating the role of ANX A3 in reducing benign breast biopsies rate, as such, this could be a venue for further exploration. An interesting phenomenon demonstrated in this work was the over expression of ANX A3 in benign breast conditions as well as breast cancer samples compared to healthy women. Here, the benign disease group ANX A3 expression was shown to be higher than the cancer group both on the serum and tissue levels. The cancer serum and tissue samples on the other hand had higher ANX A3 expression compared to controls. Although the molecular mechanism explaining such trend remains unclear, a similar benign disease tissue ANX A3 over expression trend was found in benign prostate hypertrophy (BPH) relative to prostatic in situ neoplasms (PIN) and invasive prostatic carcinoma tissue samples [27, 28]. Secreted ANX A3 has also been shown to correlate with ovarian cancer chemotherapy resistance .
Breast cancer patients’ samples and data were collected from the Department of Biochemistry and Histopathology, Grant Medical College and Sir J J Group of Hospitals, Mumbai, India. Of 256 selected patients, 207 female patients had histopathologically confirmed breast cancer, and 15 patients had benign breast disease (BBD). The remaining 34 patients were excluded from the study, as they were treated cases. His- topathologic examination confirmed invasive breast cancer in different stages of disease in 207 patients, aged 25 to 75 years. A group of 175 age matched ( ± 2 years) healthy female controls were arbitrarily selected from patients’ relatives. Information on patients’ age, menopausal status, disease stage, ER and PgR status, and clinical nodes was noted from case files.
The BCFR and kConFab used the same risk factor ques- tionnaire . At baseline, questionnaires were inter- viewer administered, either in person or by telephone, or administered by mail. The risk factor questionnaire asked about each participant’s demographic characteris- tics, height, weight, history of benign breast disease, breast and ovarian surgeries, reproductive history, and lifestyle factors. The cancer family history questionnaire asked about breast and other cancers (excluding non-melanoma skin cancer) in the participants and their first-degree and second-degree relatives. Each partici- pant’s cancer information was obtained from one or more sources and was usually self-reported or reported by a first-degree relative. Where possible, verification of cancer diagnosis was sought through pathologist review of tissue samples, pathology reports, cancer registries, medical records, or death certificates [28–30].
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A group of newly diagnosed breast cancer patients who were admitted to a university hospital or attending a breast clinic in Tehran, Iran were interviewed following their surgery or first course of chemotherapy between Sep- tember 2001 and March 2002. After obtaining oral con- sent from each patient, data were collected using a structured questionnaire including socio-demographic factors, date of first symptom recognition and first medi- cal consultation. Delay was defined as time intervals of more than 12 weeks from first symptom recognition to first medical consultation and thus patients were divided into two groups: those who presented at three months or less and those who delayed more than three months. Patients were excluded if their data concerning delay were unreliable. If patients were not sure of the date of first symptom recognition or could not recall the date, data considered unreliable. Clinical data including stage of dis- ease, tumor size and lymph node status also were extracted from patients' medical records. Statistical analy- sis was performed using univariate and multivariate logis- tic regression models to calculate odds ratios (OR). Age, marital status, educational level, family history of breast cancer, history of benign breast disease, number of chil- dren and the nature of first symptom have been selected as potential explanatory factors. The Statistical Package for Social Sciences (SPSS) was used to analyze data . Results
There are already target groups in Germany, for which risk-adapted screening has been implemented (40). Currently women who fulfill the inclusion criteria for the German Consortium for Hereditary Breast and Ovarian Cancer, and who carry a mutation in a known cancer gene, have access to an intensified surveillance program. The crucial point is the detection of a high risk gene (BRCA1, BRCA2, CDH1 or TP53) or a moderate gene (CHEK2, PALB2, RAD51C/D, NBN or ATM) (59). Another target group are women who were treated for Hodgkin´s disease (HD) in childhood or adolescence and who have an increased risk to develop breast cancer due to prior radiotherapy. These women also have access to an intensified surveillance program (58). Families who fulfill the inclusion criteria for the German Consortium for Hereditary Breast and Ovarian Cancer, where no mutation in any known risk gene can be identified, are more challenging. In this constellation, the decision to recommend intensified surveillance is based on the calculated risk (heterozygous risk > 20% or lifetime risk > 30%) based on Cyrillic (40).
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Cancer is a group of diseases characterized by uncontrolled growth and spread of abnormal cells. If the spread is not controlled, it can result in death. It is caused by both external factors like tobacco, chemicals, radiation, and infectious organisms etc & internal factors like mutations, genetic factors, hormones, altered metabolic consequences etc. These factors may act together or in sequence to initiate or promote carcinogenesis. Breast cancer is a malignant (cancerous) tumor that starts from cells of the breast. It is the second commonest cancer of the world which comprises approx 19% of the total female cancers. According to American Cancer Society Report there will be more than 12 million new cancer cases every year worldwide, of which
The breast is composed of approximately 20 lobes made up of epithelial and stromal elements. In each lobe there are 10 -100 lobules that drain through ductules into a sub-segmental duct and finally into a segmental duct. Near the nipple these ducts expand into lactiferous sinuses which converge into the collecting duct and finally open into the nipple. Close to the end of the collecting duct, the epithelium is stratified squamous as in the nipple skin, but elsewhere along the ductal system, extending to and including the acini of the lobule, the epithelium is composed of two layers; an inner columnar cell layer and an outer and often incomplete layer of myoepithelial cells. Both of the latter cell types border the basement membrane. A lobule, with its draining ductule, is termed a terminal duct lobular unit (Fig 1.2). The lobule itself consists of 10 to 100 acini bound together in fine vascular connective tissue. The periductal stroma or connective tissue is distinct from that of the interlobular and intersegmental spaces in being loose, vascular and more cellular. Within the lobule this stroma is more abundant and even more cellular, but, unlike the periductal tissue, it lacks elastic fibres. Elastic tissue surrounds the extralobular ductal system and increases in amount with age and parity.
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Breasts are the integral part of the female reproductive system. Breast tissues, due to abnormal hormonal variations, are subjected to a number of pathological conditions - both benign and malignant. Benign diseases form the majority of pathologies. In India, cancer of breast is the second most common cancer in women.  It is sometimes difficult to determine clinically whether a suspicious lump is benign or malignant. FNAC can provide cytomorphological diagnosis of palpable breast lumps.  The aim of the study is to establish the role of FNAC as “one-stop”diagnostic procedure for breast lumps.
The vital status of the study group was assessed as of September 30, 2012, by passive follow-up, using data from the population registry. The disease- free survival (DFS) and overall survival (OS) were estimated by the Kaplan-Meier method. DFS was calculated from the date of the start of primary therapy to the date of breast cancer recurrence, the date of death from any cause, or the date of the last follow-up. OS was calculated from the date of the start of primary therapy and death of any cause. The Log- rank test was used for survival comparison between the groups. P < 0.05 indicated a significant statistical difference. All statistical analyses were performed using Stata Statistical Software version 11.0 (StataCorp. 2009. Stata Statistical Software: Release 11.0 College Station, TX, USA).
Methods: Patients receiving drug therapies for metastatic breast cancer between 2004 and 2015 at our institution were reviewed. The survival time after NL and IS was compared and the frequency of NL with each drug calculated. Results: For the 107 eligible patients, the survival time after NL at second-line chemotherapy was significantly worse than after IS (median survival time 4.3 months vs. 20.3 months, p = 0.0048). Maintenance therapy with bevacizumab or trastuzumab had a high frequency of NL (88.9%), and third-line eribulin had a low frequency of NL (16.7%). A multivariate analysis showed that NL at second-line chemotherapy was not an independent risk factor (hazard ratio 1.02, 95%; confidence interval 0.54 – 1.93, p = 0.95) for the total survival time.
As discussed above, reduced iodide concentration, ele- vated levels of the thyroid hormones and antibodies con- tributed to an increased risk of breast cancer in previous reports and in our study. However, some authors sug- gested also the possible impact of breast cancer on the thyroid with the resulting increased level of thyroid hor- mones and the autoimmune response with the detect- able thyroid antibodies . In our series we found shift of about 15–20 years between the primary peak of the diagnosed Graves' disease and the secondary maximal incidence of breast cancer (Figure 4). However, the ob- served long shift is partially affected by the fact that par- ticipants in our study were younger than the general population of patients with Graves’ disease, as they were hospitalized due to the more prominent symptoms. Older patients with usually more subtle clinical course of Graves’ disease are treated as outpatients . Despite some possible level of bias, we claim that it is the Graves’ disease which could contribute to the subse- quently observed development of breast cancer.
Abstract: REGgamma (REGγ) has been recently found in several types of human cancer, however, its clinical signifi- cance in metastasis and prognosis of breast cancer remains unknown. In this study, immunohistochemical staining and western blot analysis were performed to evaluate REGγ expression in both mouse and human breast cancer specimens. We found that in MMTV-PyMT mice, 14 out of 20 (70%) mouse mammary carcinomas were REGγ positive, which was significantly higher than control (0/20, 0%, P < 0.001) and lower than metastatic lung tumour (20/20, 100%, P = 0.027). Further investigation for REGγ expression in 136 human breast cancer tissues with the paired peritumoural normal breast tissues and 140 breast benign disease tissue samples showed that REGγ was undetectable in normal breast tissues and nonmetastatic axillary lymph nodes (ALNs), whereas 111 out of 136 (81.6%) breast cancer tissue samples were REGγ positive, which was significantly higher than breast benign disease tissues (9/140, 6.4%, P < 0.001) and lower than metastatic ALNs (116/116, 100%, P < 0.001). The 5-year disease-free and overall survivals of patients with negative/low level of REGγ were significantly higher than those of patients with high level of REGγ (P < 0.05). Cox regression analyses further indicated that REGγ could serve as a novel independent prognostic factor for breast cancer (OR = 4.369, P = 0.008). Our results suggest that the high expression of REGγ might predict metastasis and poor prognosis in breast cancer.
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Male breast cancer accounts for only 1% of all breast cancer diagnoses in the United Kingdom, yet it still claimed responsibility for 353 new cases and 73 deaths in 2012 (Office of National Statistics, 2014; Northern Ireland Cancer Registry, 2014; Welsh Cancer Intelligence and Surveillance Unit, 2014; ISD Scotland, 2014). Though rare, outcomes for breast cancer tend to be worse for men than for women, due to delayed detection occasioned partly by lower disease awareness (Thomas et al., 2010). Both diagnosis and treatment are the same across the genders, with treatment often bringing appearance-altering side effects (Giordarno, 2005; Harlan et al., 2010). Despite these similarities, the disparity between incidence rates has led to the perception of breast cancer as a disease affecting only women, with campaigns and interventions further maintaining gendered ideas through the ‘pink ribbon culture’ (Sulik, 2011). Low levels of awareness of male breast cancer among health professionals and the general public place men at a disadvantage (France et al., 2000) What is the psychosocial impact of male breast cancer?
Stock cultures of all three breast cancer cell lines were grown as a monolayer in RPMI 1640 (given in appendix 2) supplemented with 2mM glutamine and 10% FCS in 75ml plastic flat bottomed flasks (Nunc). The bottles with loosened tops were kept at 37°C in a humidified incubator gassed with a mixture of 95% air and 5% carbon dioxide (BOC Ltd). Cells were subcultured once or twice a week to maintain exponential growth. To subculture the cells, 5ml of trypsin-EDTA (Gibco) was added to the flask after removing the culture medium. After several minutes, the cells were detached from the flask by gentle agitation. The trypsin-EDTA was
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