Risk Of Female Breast Cancer Research Articles

Adulthood dietary and lifestyle patterns and risk of breast cancer: Global Cancer Update Programme (CUP Global) systematic literature review

BackgroundAn increasing number of studies in recent years investigate various dietary and lifestyle patterns and associated breast cancer (BC) risk. ObjectivesThis study aimed to comprehensively synthesize and grade the evidence on dietary and lifestyle patterns and BC risk. MethodsDatabases were systematically searched up to 31 March, 2022, for evidence from RCTs and prospective cohort studies on adherence to a dietary pattern alone or in combination with lifestyle behaviors and incidence of or mortality from primary BC in adult females. Findings in all, premenopausal, and postmenopausal females were descriptively synthesized instead of meta-analyzed due to patterns heterogeneity. An independent Global Cancer Update Programme Expert Panel graded the strength of the evidence. ResultsA total of 84 publications were included. Results for patterns reflecting both a healthy diet and lifestyle were more consistent than for patterns that included diet only. There was strong-probable evidence that a priori World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) and American Cancer Society (ACS) dietary and lifestyle scores may reduce BC risk in all and postmenopausal females, whereas in premenopausal females, less evidence was found contributing to limited-suggestive grade. There was also a limited-suggestive evidence that adherence to the Healthy Lifestyle Index and other diet and lifestyle scores may reduce BC risk in postmenopausal females; a posteriori Western/meat/alcohol dietary patterns may increase BC risk in postmenopausal females; and prudent/vegetarian/Mediterranean dietary patterns may reduce BC risk in all females. For the remaining patterns, evidence was graded as limited-no conclusions. ConclusionsAdvice to adopt combined aspects of a healthy diet and lifestyle according to WCRF/AICR and ACS scores, encouraging a healthy weight, physical activity, alcohol and smoking avoidance, and a healthy diet rich in fruits, vegetables, (whole)grains and cereals and discouraging red and processed meat, can be proposed to females to lower BC risk.This review was registered at PROSPERO as ID CRD42021270129 (https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42021270129) on 28 August, 2021, and further updated on 4 May, 2022, in order to extend the search period.

Night shift work and female breast cancer: a two-stage dose-response meta-analysis for the correct risk definition

IntroductionThe hypothesis of this study is night shift work exposure can increase the risk of female breast cancer. To validate this hypothesis, the authors conducted a two-stage dose-response meta-analysis with improved quality on this topic.MethodsThe medical librarian searched PubMed, EMBASE, and the Cochrane Library on December 30th, 2022. The eight inclusion criteria were determined and strictly applied to the selection process. A reliable dose-response meta-analysis methodology was applied.ResultsReliable 10 cohort (total cases: 15,953, and total person-years: 6,812,138) and 11 case-control reports (total cases: 9196, and total controls:12,210) were included in the final analysis. The pooled risk ratio (RR) of female breast cancer (from cohort studies) for 1, 10, 20, and 30 years of night shift work exposure was 1.0042 (95% CI 1.0014–1.0070), 1.0425 (95% CI 1.0138–1.0719), 1.0867 (95% CI 1.0278–1.1490), and 1.1328 (95% CI 1.0419–1.2317), respectively. The pooled odds ratio (OR) of female breast cancer (from case-control studies) for 1, 10, 20, and 30 years of night shift work exposure was 1.0213 (95% CI 1.0108–1.0319), 1.2346 (95% CI 1.1129–1.3695), 1.5242 (95% CI 1.2386–1.8756), and 1.8817 (95% CI 1.3784–2.5687), respectively.DiscussionThis study has several strengths from the perspective of a dose-response meta-analysis: Strictly applied eight inclusion criteria, separately synthesized RRs from cohort studies and ORs from case-control studies, clearly defined exposure dose, years of night shift work for each risk estimate, a reliable dose-response meta-analysis methodology, and careful considering of selection, exposure, and outcome biases and confounder adjustment for each study. This careful consideration of potential biases and confounding led to the exclusion of unreliable two cohort and five case-control studies.

A closer look at utilized radiation doses during chest CT for COVID-19 patients

This study examined radiation exposure from CT scans performed on 500 adult COVID-19 patients at two major university hospitals in Morocco. A robust correlation (r = 0.82) was found between patient size and Size-Specific Dose Estimate (SSDE), which ranged from 10.11 to 17.87 mGy. The mean CTDIvol was 6.7 mGy, contrasting markedly with the mean SSDE of 12.81 mGy. This highlights a substantial difference, with the SSDE-to-CTDIvol ratio being approximately 1.91. Notably, the SSDE was nearly twice as high as the CTDIvol, underscoring the vulnerability of obese COVID-19 patients. Evaluation of different CT scanner models showed higher radiation doses associated with the Siemens Somaton Emotion 16 compared to the GE Optima CT520 Series, emphasizing the need to account for scanner-specific factors in dose optimization protocols. A comparison of chest CT reference doses (DRL) from this study with international data showed a lower mean CTDIvol here (6.7 mGy) than reported in other countries. However, the DRL in terms of DLP is in the same range or lower as compared to others. Using the BEIR VII model, the lifetime attributable risk (LAR) of cancer from COVID-19 chest CTs was estimated. Elevated risks of lung cancer in both genders and increased breast cancer risk in females were projected, albeit with limitations regarding overestimated cancer incidence. The high effective dose values, approaching 15.3 mSv, underscore the need for dose optimization, especially in obese COVID-19 patients receiving chest CTs.

Fraction of cancers attributable to and prevented by reproductive factors and exogenous hormones use in Italy

ObjectiveEndogenous and exogenous hormonal factors have been associated with female breast, genital, and colorectal cancer risk. The aim of the present study is to conduct an evidence-based evaluation of the fraction of cancers attributable to and prevented by exogenous hormonal (i.e., combined oral contraceptives [COC] and combined estrogen-progestogen menopausal therapy [CEPMT]) and reproductive factors (i.e., parity and breastfeeding) in Italy. Study designWe calculated the population attributable and prevented fractions combining relative risks and prevalence of exposure in Italian women. Italian cancer incidence and mortality data were extracted from national sources and used to estimate the number of cancer cases and deaths attributable to reproductive factors and exogenous hormones in Italy in 2020. For long-term effects, a 20-year latency period was considered. ResultsCOC were responsible for 4.4 % of breast and 10.9 % of cervical cancers in women aged 15–44, but also avoided 6.4 % of endometrial, 5.6 % of ovarian, and 2.9 % of colorectal cancers in women of all ages. Overall, COC use prevented 1174 cancer diagnoses and 577 cancer deaths. CEPMT caused 0.4 % of breast cancers at age 45–69. Low parity accounted for 8.1 %, 11.8 % and 15.5 % of breast, endometrial and ovarian cancers, respectively (6267 cases, 1796 deaths). Breastfeeding avoided 6.4 % of breast cancers (3775 cases, 897 deaths). ConclusionsOur analysis quantified the complex effects of hormonal and reproductive factors on cancer burden in Italian women.

Association Between Polymorphisms in DNA Damage Repair Pathway Genes and Female Breast Cancer Risk.

Breast cancer risk have been discussed to be associated with polymorphisms in genes as well as abnormal DNA damage repair function. This study aims to assess the relationship between genes single nucleotide polymorphisms (SNPs) related to DNA damage repair and female breast cancer risk in Chinese population. A case-control study containing 400 patients and 400 healthy controls was conducted. Genotype was identified using the sequence MassARRAY method and expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor-2 (HER-2) in tumor tissues was analyzed by immunohistochemistry assay. The results revealed that ATR rs13091637 decreased breast cancer risk influenced by ER, PR (CT/TT vs. CC: adjusted odds ratio [OR] = 1.54, 95% confidence interval [CI]: 1.04-2.27, p = 0.032; CT/TT vs. CC: adjusted OR = 1.63, 95%CI: 1.14-2.35, p = 0.008) expression. Stratified analysis revealed that PALB2 rs16940342 increased breast cancer risk in response to menstrual status (AG/GG vs. AA: adjusted OR = 1.72, 95%CI: 1.13-2.62, p = 0.011) and age of menarche (AG/GG vs. AA: adjusted OR = 1.54, 95%CI: 1.03-2.31, p = 0.037), whereas ATM rs611646 and Ku70 rs132793 were associated with reduced breast cancer risk influenced by menarche (GA/AA vs. GG: adjusted OR = 0.50, 95%CI: 0.30-0.95, p = 0.033). In a summary, PALB2 rs16940342, ATR rs13091637, ATM rs611646, and Ku70 rs132793 were associated with breast cancer risk.

A deep intronic recurrent CHEK2 variant c.1009-118_1009-87delinsC affects pre-mRNA splicing and contributes to hereditary breast cancer predisposition

Germline CHEK2 pathogenic variants confer an increased risk of female breast cancer (FBC). Here we describe a recurrent germline intronic variant c.1009-118_1009-87delinsC, which showed a splice acceptor shift in RNA analysis, introducing a premature stop codon (p.Tyr337PhefsTer37).The variant was found in 21/10,204 (0.21%) Czech FBC patients compared to 1/3250 (0.03%) controls (p = 0.04) and in 4/3639 (0.11%) FBC patients from an independent German dataset. In addition, we found this variant in 5/2966 (0.17%) Czech (but none of the 443 German) ovarian cancer patients, three of whom developed early-onset tumors.Based on these observations, we classified this variant as likely pathogenic.

Interaction between body mass index and family history of cancer on the risk of female breast cancer

Both body mass index (BMI) and family history of cancer are established risk factors for female breast cancer. However, few studies explored the potential interaction between both factors. We assessed the association of BMI and its interaction with family cancer history on the risk of female breast cancer in Shanghai, China. Based on a population-based prospective cohort study started from 2008 to 2012 with 15,055 Chinese female participants in Minhang district, Shanghai. Cox regression models were used to estimate the association of BMI and its interaction with a family history of cancer on breast cancer risk. The additive interaction was evaluated by the relative excess risk due to interaction (RERI) and the attributable proportion due to interaction (AP), and the multiplicative interaction was assessed by the product term (BMI* family history of cancer) in the Cox regression model. Compared with BMI of < 24 kg/m2 and no family history of cancer, women with BMI of ≥ 24 kg/m2 and a family history of cancer had a higher risk for breast cancer with HR 2.06 (95% CI 1.39, 3.06). There was an additive interaction between BMI and family history of cancer on breast cancer incidence, with the RERI being 0.29 (95% CI 0.08, 0.51) and the AP being 0.37 (95% CI 0.08, 0.66). The coexistence of obesity and cancer family history may exacerbate breast cancer incidence risk, highlighting the importance of weight management in women with a family history of cancer.

An investigation of the relationship between female university students' breast cancer risk factors and their health beliefs about breast self-examination.

The purpose of this study is to determine the relationship between female university students' breast cancer risk factors and their health beliefs about breast self-examination (BSE). The sample of this descriptive and correlational study was 389 female students who were determined by stratified sampling method. Data were collected through the Socio-demographic Characteristics and Breast Cancer Risk Factors Determination Form and the Champion's Health Belief Model Scale (CHBMS). Data obtained from the study were analysed using SPSS for Windows 16.0 program. Data analysis was performed using percentage distributions, z test, and Spearman correlation analysis. Statistical significance was accepted p<0.05. While a positive correlation was detected between students' perceived breast cancer risk for themselves and perceived susceptibility, severity, benefit, self-efficacy related to BSE and health motivation mean scores, a negative and significant correlation was detected with perceived barriers to BSE mean score (p<0.05). Results showed that although female university students had some risk factors in terms of breast cancer, they have low levels of perceived risk factors for themselves.

Causal association of nonalcoholic fatty liver disease with 22 extrahepatic cancers: A Mendelian randomization study.

It is unclear whether nonalcoholic fatty liver disease (NAFLD) acts as a direct contributing factor to multiple extrahepatic cancers. We aimed to systematically investigate the causal relationships of NAFLD with extrahepatic cancers. We conducted a two-sample Mendelian randomization analysis to assess the causal effects of NAFLD on 22 extrahepatic cancers. We examined the association of NAFLD with extrahepatic cancers using multiple methods in the largest genome-wide association study meta-analysis to date. We also replicated the analyses and performed two independent sensitivity analysis in the largest genome-wide association study of UK Biobank. Using the weighted median method, genetically predicted NAFLD was significantly associated with female breast cancer risk (odds ratio [OR] 15.99; 95% confidence interval [CI] 9.58-26.69). Genetically predicted NAFLD is associated with cervical and laryngeal cancers using the inverse variance weighting method, and the ORs were 2.44 (95% CI 1.43-4.14) and 1.94 (95% CI 1.35-2.78), respectively. We observed that patatin-like phospholipase domain-containing protein 3-driven and transmembrane 6 superfamily member 2-driven NAFLD were associated with increased risks of leukemia, lung cancer, and prostate cancers (all with p<0.05). Furthermore, we confirmed the causal association between NAFLD and breast cancer using five known single-nucleotide polymorphisms of NAFLD and six genome-wide association study-identified variants. The ORs of the weighted median estimator was 10.76 (95% CI 8.27-13.98) and 10.76 (95% CI 8.25-14.04), respectively (p<0.001). Genetically predicted NAFLD is associated with an increased risk of female breast cancer, as well as cervical, laryngeal, leukemia, lung, and prostate cancers.

Assessing the Relationship Between Persistent Organic Pollutants in Adipose Tissue and Female Breast Cancer Risk in Taiwan: A Prioritization Study

Assessing the Relationship Between Persistent Organic Pollutants in Adipose Tissue and Female Breast Cancer Risk in Taiwan: A Prioritization Study

Subsequent female breast cancer risk associated with anthracycline chemotherapy for childhood cancer

Anthracycline-based chemotherapy is associated with increased subsequent breast cancer (SBC) risk in female childhood cancer survivors, but the current evidence is insufficient to support early breast cancer screening recommendations for survivors treated with anthracyclines. In this study, we pooled individual patient data of 17,903 survivors from six well-established studies, of whom 782 (4.4%) developed a SBC, and analyzed dose-dependent effects of individual anthracycline agents on developing SBC and interactions with chest radiotherapy. A dose-dependent increased SBC risk was seen for doxorubicin (hazard ratio (HR) per 100 mg m−2: 1.24, 95% confidence interval (CI): 1.18–1.31), with more than twofold increased risk for survivors treated with ≥200 mg m−2 cumulative doxorubicin dose versus no doxorubicin (HR: 2.50 for 200–299 mg m−2, HR: 2.33 for 300–399 mg m−2 and HR: 2.78 for ≥400 mg m−2). For daunorubicin, the associations were not statistically significant. Epirubicin was associated with increased SBC risk (yes/no, HR: 3.25, 95% CI: 1.59–6.63). For patients treated with or without chest irradiation, HRs per 100 mg m−2 of doxorubicin were 1.11 (95% CI: 1.02–1.21) and 1.26 (95% CI: 1.17–1.36), respectively. Our findings support that early initiation of SBC surveillance may be reasonable for survivors who received ≥200 mg m−2 cumulative doxorubicin dose and should be considered in SBC surveillance guidelines for survivors and future treatment protocols.

Exposure to Organochlorine Pesticides and Female Breast Cancer Risk According to Molecular Receptors Expression: a Systematic Review and Meta-analysis of Epidemiological Evidence.

Organochlorine pesticides (OCP) have been proposed as potential mammary carcinogens since they interact with steroid signaling pathways. However, the epidemiological results are not conclusive. Most studies have evaluated breast cancer (BC) as a single entity without considering the different molecular expressions, including estrogen receptor (ER), progesterone receptor (PR), and HER2, that could differ in their association with these contaminants. Hence, we assessed the association between biological concentration of OCP and BC, according to its molecular receptor expression, based on a systematic review and meta-analysis. Of the 141 articles eligible for full-text review, nine met the inclusion criteria. The way in which molecular expression was reported was heterogeneous; therefore, the inclusion of studies in the meta-analysis was limited to eight articles. A negative association was identified for β-hexachlorocyclohexane and trans-nonachlor with ER + tumors and between hexachlorobenzene and ER - tumors. No associations were observed for p,p'-dichlorodiphenyldichloroethylene, cis-nonachlor, and dieldrin, and it was not possible to evaluate the associations between OCP with HER2 expression or triple-negative tumors due to lack of data. The results suggest that some OCP might be associated with BC depending on the expression of ER. However, the evidence is not conclusive due to the scarce data. We identified several methodological aspects to fill the gaps in knowledge and increase the comparability among studies.

Integrating somatic CNV and gene expression in breast cancers from women with PTEN hamartoma tumor syndrome

Women with germline PTEN variants (PTEN hamartoma tumor syndrome, PHTS) have up to 85% lifetime risk of female breast cancer (BC). We previously showed that PHTS-derived BCs are distinct from sporadic BCs both at the clinical and genomic levels. In this study, we examined somatic copy number variations (CNV) and transcriptome data to further characterize the somatic landscape of PHTS-derived BCs. We analyzed exome sequencing data from 44 BCs from women with PHTS for CNV. The control group comprised of 558 women with sporadic BCs from The Cancer Genome Atlas (TCGA) dataset. Here, we found that PHTS-derived BCs have several distinct CNV peaks compared to TCGA. Furthermore, RNA sequencing data revealed that PHTS-derived BCs have a distinct immunologic cell type signature, which points toward cancer immune evasion. Transcriptomic data also revealed PHTS-derived BCs with pathogenic germline PTEN variants appear to have vitamin E degradation as a key pathway associated with tumorigenesis. In conclusion, our study revealed distinct CNV x transcript features in PHTS-derived BCs, which further facilitate understanding of BC biology arising in the setting of germline PTEN mutations.

Lifestyle Quality Indices and Female Breast Cancer Risk: A Systematic Review and Meta-Analysis.

Breast cancer (BC) poses an important burden of disease, which probably could be reduced by adopting healthy lifestyles like healthy body weight, healthy diet, and physical activity, among others. Many studies have reported that adherence to healthy lifestyles may decrease BC risk. The main objective of this study was to estimate a summary association of studies evaluating a healthy lifestyle index and BC risk. A systematic review and meta-analysis following the Cochrane methodology were carried out. Observational studies, including healthy lifestyle indices and their association with BC, were searched from 4 databases. For the meta-analysis, random-effectsmodel was used to evaluate overall BC risk, BC by molecular subtype and menopausal status. Thirty-one studies were included in the systematic review, and 29 studies in the meta-analysis. When the highest vs. the lowest category to a healthy lifestyle index were compared, the study identified a 20% risk reduction for BC in prospective studies (hazard ratio [HR] 0.80 95% CI: 0.78, 0.83) and an odds ratio (OR) of 0.74 (95% CI: 0.63, 0.86) for retrospective studies. The inverse association remained statistically significant when stratified by menopausal status, except for premenopausal BC in prospective studies. Furthermore, an inverse association was found for molecular subtypes estrogen receptor (ER+)/progesterone receptor (PR+): HR = 0.68 (95%CI: 0.63, 0.73), ER+/PR-: HR = 0.78 (95% CI: 0.67, 0.90) and ER-/PR-: HR = 0.77 (95% CI: 0.64, 0.92). Most studies scored at a low risk of bias and a moderate score for the certainty of the evidence. Adherence to a healthy lifestyle reduces the risk of BC, regardless of its molecular subtypes, which should be considered a priority to generate recommendations for BC prevention at a population level. International prospective register of systematic reviews (PROSPERO) ID: CRD42021267759.

Association of education level with the risk of female breast cancer: a prospective cohort study

BackgroundBreast cancer is a serious threat to female health, and its incidence varies with education level (EL). In the present study, the association between EL and the risk of developing female breast cancer was investigated.MethodsFrom May 2006 to December 2007, 20,400 observation subjects in Kailuan Cohort received questionnaires and were subjected to clinical examinations for data collection on baseline population characteristics, height, weight, lifestyle and past disease history. Then, these participants were followed up with from the date of recruitment to December 31, 2019. Cox proportional risk regression models were used to analyse the association between EL and the risk of developing female breast cancer.ResultsThe cumulative follow-up period of 20,129 observation subjects that meet the inclusion criteria of this study was 254,386.72 person-years, and the median follow-up time was 12.96 years. During the follow-up period, 279 cases of breast cancer were diagnosed. In comparison with the low EL group, the risk of developing breast cancer was significantly higher in the medium (hazard ratio [HR] (95% confidence interval [CI]) = 2.23 (1.12–4.64)] and high [HRs (95% CI) = 2.52 (1.12–5.70)] EL group.ConclusionAn increased risk of breast cancer was associated with a higher EL, and some certain factors, such as alcohol use and hormone therapy, may play a mediating role.

Multi-Morbidity and Risk of Breast Cancer among Women in the UK Biobank Cohort.

(Multi-)Morbidity shares common biological mechanisms or risk factors with breast cancer. This study aimed to investigate the association between the number of morbidities and patterns of morbidity and the risk of female breast cancer. Among 239,436 women (40-69 years) enrolled in the UK Biobank cohort who had no cancer history at baseline, we identified 35 self-reported chronic diseases at baseline. We assigned individuals into morbidity patterns using agglomerative hierarchical clustering analysis. We fitted Cox models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for breast cancer risk. In total, 58.4% of women had at least one morbidity, and the prevalence of multi-morbidity was 25.8%. During a median 7-year follow-up, there was no association between breast cancer risk (5326 cases) and either the number of morbidities or the identified clinically relevant morbidity patterns: no-predominant morbidity (reference), psychiatric morbidities (HR = 1.04, 95%CI 0.94-1.16), respiratory/immunological morbidities (HR = 0.98, 95%CI 0.90-1.07), cardiovascular/metabolic morbidities (HR = 0.93, 95%CI 0.81-1.06), and unspecific morbidities (HR = 0.98, 95%CI 0.89-1.07), overall. Among women younger than 50 years of age only, however, there was a significant association with psychiatric morbidity patterns compared to the no-predominant morbidity pattern (HR = 1.25, 95%CI 1.02-1.52). The other associations did not vary when stratifying by age at baseline and adherence to mammography recommendations. In conclusion, multi-morbidity was not a key factor to help identify patients at an increased risk of breast cancer.

Digital Screen Time and the Risk of Female Breast Cancer: A Retrospective Matched Case-Control Study.

As the use of electronic devices such as mobile phones, tablets, and computers continues to rise globally, concerns have been raised about their potential impact on human health. Exposure to high energy visible (HEV) blue light, emitted from digital screens, particularly the so-called artificial light at night (ALAN), has been associated with adverse health effects, ranging from disruption of circadian rhythms to cancer. Breast cancer incidence rates are also increasing worldwide. This study aimed at finding a correlation between breast cancer and exposure to blue light from mobile phone. In this retrospective matched case-control study, we aimed to investigate whether exposure to blue light from mobile phone screens is associated with an increased risk of female breast cancer. We interviewed 301 breast cancer patients (cases) and 294 controls using a standard questionnaire and performed multivariate analysis, chi-square, and Fisher's exact tests for data analysis. Although heavy users in the case group of our study had a statistically significant higher mean 10-year cumulative exposure to digital screens compared to the control group (7089±14985 vs 4052±12515 hours, respectively, P=0.038), our study did not find a strong relationship between exposure to HEV and development of breast cancer. Our findings suggest that heavy exposure to HEV blue light emitted from mobile phone screens at night might constitute a risk factor for promoting the development of breast cancer, but further large-scale cohort studies are warranted.

Association between Urinary Lead and Female Breast Cancer: A Population-Based Cross-Sectional Study.

Previous studies have explored the relationship between serum lead levels and the risk of female breast cancer (FBC). However, it is still uncertain whether urinary lead levels are associated with FBC. This study aimed to investigate the potential association between urinary lead and FBC. A cross-sectional case-control study was conducted using the National Health and Nutrition Examination Survey (NHANES), which is a series of cross-sectional, nationally representative surveys of the United States population consisting of 10 survey waves from 1999 to 2018. This study analyzed a total of 2795 female participants (≥20 years), consisting of 210 participants with FBC and 2585 healthy controls. Urinary lead was detected using Inductively Coupled Plasma-Mass Spectrometry, which was divided into four levels by using quartiles-defining cut points. Multivariate logistic regression was used to analyze the association between urinary lead and FBC. Multivariate logistic regression revealed that urinary lead was positively correlated with FBC (Odds ratio [OR], 2.16; 95% confidence interval [CI]: [1.18, 3.95], p < 0.05) in a fully adjusted model. There were significantly increased ORs of FBC in quartile 4 (Q4) and quartile 3 (Q3), compared with the lowest quartile 1 (Q1) (Q4, OR = 1.48, 95% CI [0.89, 2.48]; Q3: OR = 1.01, 95% CI [0.59, 1.73], p for trend = 0.021). No significant interaction effects were observed between urinary lead levels and FBC between the subgroups (age, race, educational status, body mass index (BMI), marital status, family income to poverty ratio, hypertension status, diabetes status, renal function status, smoking history, ever been pregnant, oral contraceptive use, occupation classification, etc.) (All interaction p-value > 0.05). Urinary lead is likely positively associated with FBC in the US population.

Cancer Risk Associated With PTEN Pathogenic Variants Identified Using Multigene Hereditary Cancer Panel Testing.

PTEN-associated clinical syndromes such as Cowden syndrome (CS) increase cancer risk and have historically been diagnosed based upon phenotypic criteria. Because not all patients clinically diagnosed with CS have PTEN pathogenic variants (PVs), and not all patients with PTEN PVs have been clinically diagnosed with CS, the cancer risk conferred by PTEN PVs calculated from cohorts of patients with clinical diagnoses of CS/CS-like phenotypes may be inaccurate. We assessed a consecutive cohort of 727,091 individuals tested clinically for hereditary cancer risk, with a multigene panel between September 2013 and February 2022. Multivariable logistic regression models accounting for personal and family cancer history, age, sex, and ancestry were used to quantify disease risks associated with PTEN PVs. PTEN PVs were detected in 0.027% (193/727,091) of the study population, and were associated with a high risk of female breast cancer (odds ratio [OR], 7.88; 95% CI, 5.57 to 11.16; P = 2.3 × 10-31), endometrial cancer (OR, 13.51; 95% CI, 8.77 to 20.83; P = 4.2 × 10-32), thyroid cancer (OR, 4.88; 95% CI, 2.64 to 9.01; P = 4.0 × 10-7), and colon polyposis (OR, 31.60; CI, 15.60 to 64.02; P = 9.0 × 10-22). We observed modest evidence suggesting that PTEN PVs may be associated with ovarian cancer risk (OR, 3.77; 95% CI, 1.71 to 8.32; P = 9.9 × 10-4). Among patients with similar personal/family history and ancestry, every 5-year increase in age of diagnosis decreased the likelihood of detecting a PTEN PV by roughly 60%. We demonstrate that PTEN PVs are associated with significantly increased risk for a range of cancers. Together with the observation that PTEN PV carriers had earlier disease onset relative to otherwise comparable noncarriers, our results may guide screening protocols, inform risk-management strategies, and warrant enhanced surveillance approaches that improve clinical outcomes for PTEN PV carriers, regardless of their clinical presentation.

Evaluation of AURKA rs2273535 and CDKN1B rs34330 Polymorphisms Association with the Risk of Breast Cancer

Background &amp; Objective: Breast cancer consists of a heterogeneous group of tumours with different prognosis and is the most common cause of cancer-related mortality among women. In this study, our goal was to evaluate the association of AURKA rs2273535 and CDKN1B rs34330 polymorphisms with risk of female breast cancer in southwest part of Iran.&#x0D; Materials &amp; Methods: This case-control study was done on 50 women with breast cancer and 50 healthy women without any symptoms or family history of breast cancer as the case and control group, respectively. Restriction fragment length polymorphism (RFLP- PCR) technique was designed to determine the AURKA rs2273535 and CDKN1B rs34330 gene polymorphisms. Afterwards, statistical analysis was done by means of SPSS (version 17).&#x0D; Results: In current research, our finding showed that rs2273535 T allele increased the susceptibility of breast cancer (OR:2.58, 95%CI:1.5-31.09, P=0.006). Moreover, T allele in dominant phase could raise the risk of the breast cancer (OR:3.01, 65%CI:1.31-6.92, P=0.009). However, the other polymorphism, CDKN1B rs34330, revealed no associations with increased risk of breast cancer.&#x0D; Conclusion: These findings suggest that AURKA rs2273535 may influence individual’s susceptibility to breast cancer. But we found no associations regarding CDKN1B rs34330 polymorphism and this type of cancer.