scholarly journals MTHFR C677T and A1298C Polymorphisms in Breast Cancer, Gliomas and Gastric Cancer: A Review

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 587
Author(s):  
Igor Petrone ◽  
Paula Sabbo Bernardo ◽  
Everton Cruz dos Santos ◽  
Eliana Abdelhay
Keyword(s):  
Breast Cancer ◽  
Gastric Cancer ◽  
Dna Methylation ◽  
Mthfr C677t ◽  
Water Soluble ◽  
Mthfr Polymorphisms ◽  
Methyl Donor ◽  
Vitamin B9 ◽  
Increased Risk ◽  
The Impact

Folate (vitamin B9) is found in some water-soluble foods or as a synthetic form of folic acid and is involved in many essential biochemical processes. Dietary folate is converted into tetrahydrofolate, a vital methyl donor for most methylation reactions, including DNA methylation. 5,10-methylene tetrahydrofolate reductase (MTHFR) is a critical enzyme in the folate metabolism pathway that converts 5,10-methylenetetrahydrofolate into 5-methyltetrahydrofolate, which produces a methyl donor for the remethylation of homocysteine to methionine. MTHFR polymorphisms result in reduced enzyme activity and altered levels of DNA methylation and synthesis. MTHFR polymorphisms have been linked to increased risks of several pathologies, including cancer. Breast cancer, gliomas and gastric cancer are highly heterogeneous and aggressive diseases associated with high mortality rates. The impact of MTHFR polymorphisms on these tumors remains controversial in the literature. This review discusses the relationship between the MTHFR C677T and A1298C polymorphisms and the increased risk of breast cancer, gliomas, and gastric cancer. Additionally, we highlight the relevance of ethnic and dietary aspects of population-based studies and histological stratification of highly heterogeneous tumors. Finally, this review discusses these aspects as potential factors responsible for the controversial literature concerning MTHFR polymorphisms.

scholarly journals PITX2 DNA-Methylation: Predictive versus Prognostic Value for Anthracycline-Based Chemotherapy in Triple-Negative Breast Cancer Patients

Breast Care ◽  
2020 ◽  
pp. 1-9
Author(s):  
Rudolf Napieralski ◽  
Gabriele Schricker ◽  
Gert Auer ◽  
Michaela Aubele ◽  
Jonathan Perkins ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Cancer Patients ◽  
Triple Negative Breast Cancer ◽  
Predictive Value ◽  
Untreated Patient ◽  
Triple Negative ◽  
Statistical Significance ◽  
Breast Cancer Patients ◽  
The Impact

<b><i>Background:</i></b> PITX2 DNA methylation has been shown to predict outcomes in high-risk breast cancer patients after anthracycline-based chemotherapy. To determine its prognostic versus predictive value, the impact of PITX2 DNA methylation on outcomes was studied in an untreated cohort vs. an anthracycline-treated triple-negative breast cancer (TNBC) cohort. <b><i>Material and Methods:</i></b> The percent DNA methylation ratio (PMR) of paired-like homeodomain transcription factor 2 (PITX2) was determined by a validated methylation-specific real-time PCR test. Patient samples of routinely collected archived formalin-fixed paraffin-embedded (FFPE) tissue and clinical data from 144 TNBC patients of 2 independent cohorts (i.e., 66 untreated patients and 78 patients treated with anthracycline-based chemotherapy) were analyzed. <b><i>Results:</i></b> The risk of 5- and 10-year overall survival (OS) increased continuously with rising PITX2 DNA methylation in the anthracycline-treated population, but it increased only slightly during 10-year follow-up time in the untreated patient population. PITX2 DNA methylation with a PMR cutoff of 2 did not show significance for poor vs. good outcomes (OS) in the untreated patient cohort (HR = 1.55; <i>p</i> = 0.259). In contrast, the PITX2 PMR cutoff of 2 identified patients with poor (PMR &#x3e;2) vs. good (PMR ≤2) outcomes (OS) with statistical significance in the anthracycline-treated cohort (HR = 3.96; <i>p</i> = 0.011). The results in the subgroup of patients who did receive anthracyclines only (no taxanes) confirmed this finding (HR = 5.71; <i>p</i> = 0.014). <b><i>Conclusion:</i></b> In this hypothesis-generating study PITX2 DNA methylation demonstrated predominantly predictive value in anthracycline treatment in TNBC patients. The risk of poor outcome (OS) correlates with increasing PITX2 DNA methylation.

Impact of Medicaid expansion on two-year mortality among stage IV breast cancer (BC) patients according to race.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 6525-6525
Author(s):  
Catalina Malinowski ◽  
Xiudong Lei ◽  
Hui Zhao ◽  
Sharon H. Giordano ◽  
Mariana Chavez Mac Gregor
Keyword(s):  
Breast Cancer ◽  
Low Income ◽  
Stage Iv ◽  
Medicaid Expansion ◽  
Risk Of Death ◽  
Stage Iv Breast Cancer ◽  
Increased Risk ◽  
The Impact ◽  
Expansion Period ◽  
White Patients

6525 Background: Inadequate access to healthcare services is associated with worse outcomes. Disparities in access to cancer care are more frequently seen among racial/ethnic minorities, uninsured patients, and those with low socioeconomic status. A provision in the Affordable Care Act called for expansion of Medicaid eligibility in order to cover more low-income Americans. In this study, we evaluate the impact of Medicaid expansion in 2-year mortality among metastatic BC patients according to race. Methods: Women (aged 40-64) diagnosed with metastatic BC (stage IV de novo) between 01/01/2010 and 12/31/2015 and residing in states that underwent Medicaid expansion in 01/2014 were identified in the National Cancer Database. For comparison purposes, 2010-2013 was considered the pre-expansion period and 2014-2015 the post-expansion period. We calculated 2-year mortality difference-in-difference (DID) estimates between White and non-White patients using multivariable linear regression models. Results are presented as adjusted differences (in % points) between groups in the pre- and post-expansion periods and as adjusted DID with 95%CI. Covariates included age, comorbidity, BC subtype, insurance type, transfer of care, distance to hospital, region, residence area, education, income quartile, facility type and facility volume. In addition, overall survival (OS) was evaluated in pre- and post-expansion periods via Kaplan-Meier method and Cox proportional hazards models; results are presented as 2-year OS estimates, hazard ratios (HRs), and 95% CIs. Results: Among 7,675 patients included, 4,942 were diagnosed in the pre- and 2,733 in the post-expansion period. We observed a reduction in 2-year mortality rates in both groups according to Medicaid expansion. Among Whites 2-year mortality decreased from 42.5% to 38.7% and among non-Whites from 45.4% to 36.4%, resulting in an adjusted DID of -5.2% (95%CI -9.8 to -0.6, p = 0.027). A greater reduction in 2-year mortality was observed among non-Whites in a sub-analysis of patients who resided in the poorest quartile (n = 1372), with an adjusted DID of -14.6% (95%CI -24.8 to -4.4, p = 0.005). In the multivariable Cox model, during the pre-expansion period there was an increased risk of death for non-Whites compared to Whites (HR 1.14, 95% CI 1.03 to 1.26, P = 0.04), however no differences were seen in the post-expansion period between the two groups (HR 0.93, 95% CI 0.80 to 1.07, P = 0.31). Conclusions: Medicaid expansion reduced racial disparities by decreasing the 2-year mortality of non-White patients with metastatic breast cancer and reducing the gap when compared to Whites. These results highlight the positive impact of policies aimed at improving equity and increasing access to health care.

scholarly journals Association Between MTHFR Polymorphisms and the Risk of Essential Hypertension: An Updated Meta-analysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Hao Meng ◽  
Shaoyan Huang ◽  
Yali Yang ◽  
Xiaofeng He ◽  
Liping Fei ◽  
...  
Keyword(s):  
Sensitivity Analysis ◽  
Essential Hypertension ◽  
Methylenetetrahydrofolate Reductase ◽  
Meta Analysis ◽  
Mthfr C677t ◽  
Cochrane Library ◽  
Mthfr Polymorphisms ◽  
Southeast Asians ◽  
Increased Risk ◽  
Meta Analyses

Background: Since the 1990s, there have been a lot of research on single-nucleotide polymorphism (SNP) and different diseases, including many studies on 5,10-methylenetetrahydrofolate reductase (MTHFR) polymorphism and essential hypertension (EH). Nevertheless, their conclusions were controversial. So far, six previous meta-analyses discussed the internal relationship between the MTHFR polymorphism and EH, respectively. However, they did not evaluate the credibility of the positive associations. To build on previous meta-analyses, we updated the literature by including previously included papers as well as nine new articles, improved the inclusion criteria by also considering the quality of the papers, and applied new statistical techniques to assess the observed associations. Objectives: This study aims to explore the degree of risk correlation between two MTHFR polymorphisms and EH. Methods: PubMed, EMBASE, the Cochrane Library, CNKI, and Wan Fang electronic databases were searched to identify relevant studies. We evaluated the relation between the MTHFR C677T (rs1801133) and A1298C (rs1801131) polymorphisms and EH by calculating the odds ratios (OR) as well as 95% confidence intervals (CI). Here we used subgroup analysis, sensitivity analysis, cumulative meta-analysis, assessment of publication bias, meta-regression meta, False-positive report probability (FPRP), Bayesian false discovery probability (BFDP), and Venice criterion. Results: Overall, harboring the variant of MTHFR C677T was associated with an increased risk of EH in the overall populations, East Asians, Southeast Asians, South Asians, Caucasians/Europeans, and Africans. After the sensitivity analysis, positive results were found only in the overall population (TT vs. CC: OR = 1.14, 95% CI: 1.00–1.30, Ph = 0.032, I2 = 39.8%; TT + TC vs. CC: OR = 1.15, 95% CI: 1.01–1.29, Ph = 0.040, I2 = 38.1%; T vs. C: OR = 1.14, 95% CI: 1.04–1.25, Ph = 0.005, I2 = 50.2%) and Asian population (TC vs. CC: OR = 1.14, 95% CI: 1.01–1.28, Ph = 0.265, I2 = 16.8%; TT + TC vs. CC: OR = 1.17, 95% CI: 1.04–1.30, Ph = 0.105, I2 = 32.9%; T vs. C: OR = 1.10, 95% CI: 1.02–1.19, Ph = 0.018, I2 = 48.6%). However, after further statistical assessment by FPRP, BFDP, and Venice criteria, the positive associations reported here could be deemed to be false-positives and present only weak evidence for a causal relationship. In addition, when we performed pooled analysis and sensitivity analysis on MTHFR A1298C; all the results were negative. Conclusion: The positive relationships between MTHFR C677T and A1298C polymorphisms with the susceptibility to present with hypertension were not robust enough to withstand statistical interrogation by FPRP, BFDP, and Venice criteria. Therefore, these SNPs are probably not important in EH etiology.

Epigenetic modifications and human pathologies: cancer and CVD

2010 ◽  
Vol 70 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Susan J. Duthie
Keyword(s):  
Dna Methylation ◽  
Human Cancer ◽  
Dna Methyltransferases ◽  
Water Soluble ◽  
Leafy Vegetables ◽  
Dna Hypomethylation ◽  
Human Diet ◽  
Human Colon Cancer ◽  
Increased Risk ◽  
Risk Of Cancer

Epigenetic changes are inherited alterations in DNA that affect gene expression and function without altering the DNA sequence. DNA methylation is one epigenetic process implicated in human disease that is influenced by diet. DNA methylation involves addition of a 1-C moiety to cytosine groups in DNA. Methylated genes are not transcribed or are transcribed at a reduced rate. Global under-methylation (hypomethylation) and site-specific over-methylation (hypermethylation) are common features of human tumours. DNA hypomethylation, leading to increased expression of specific proto-oncogenes (e.g. genes involved in proliferation or metastasis) can increase the risk of cancer as can hypermethylation and reduced expression of tumour suppressor (TS) genes (e.g. DNA repair genes). DNA methyltransferases (DNMT), together with the methyl donor S-adenosylmethionine (SAM), facilitate DNA methylation. Abnormal DNA methylation is implicated not only in the development of human cancer but also in CVD. Polyphenols, a group of phytochemicals consumed in significant amounts in the human diet, effect risk of cancer. Flavonoids from tea, soft fruits and soya are potent inhibitors of DNMT in vitro, capable of reversing hypermethylation and reactivating TS genes. Folates, a group of water-soluble B vitamins found in high concentration in green leafy vegetables, regulate DNA methylation through their ability to generate SAM. People who habitually consume the lowest level of folate or with the lowest blood folate concentrations have a significantly increased risk of developing several cancers and CVD. This review describes how flavonoids and folates in the human diet alter DNA methylation and may modify the risk of human colon cancer and CVD.

Fine particulate matter PM2.5 generated by building demolition increases the malignancy of breast cancer MDA-MB-231 cells

2020 ◽  
Author(s):  
Chun-Wen Cheng ◽  
Gwo-Tarng Sheu ◽  
Jing-Shiuan Chou ◽  
Pei-Han Wang ◽  
Yu-Chun Cheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Wound Healing ◽  
Cancer Cells ◽  
Fine Particulate Matter ◽  
Water Soluble ◽  
Migration And Invasion ◽  
Control Group ◽  
Increased Risk ◽  
Freeze Dried ◽  
Building Demolition

Abstract Background PM2.5 is associated with increased risk of mortality for a variety of cancers and all subjects, including breast cancer in females, and lung cancer in males. This study investigates the effects of water-extracted PM2.5 on a triple-negative breast cancer (TNBC) cell line, MDA-MB-231, by sampling suspended particulates around a building demolition site.Methods PM2.5 particles were obtained using a high-flow TISCH sampler. Being water-soluble, they were extracted from sampled filters using an ultrasonic oscillator and then freeze-dried. The heavy metal components of soluble PM2.5 particle was analyzed by ICP-MS. Cell viability was evaluated by MTT assay for cells that were exposed to PM2.5. Wound healing and transwell cell migration and invasion assays were used to measure cell motility and the invasiveness of cancer cells that had been exposed to PM2.5 into a chemo-attractant substance. Possible mechanisms of cancer malignancy were analyzed by Western blot analysis.Results The results revealed that nearby PM2.5 concentrations increased significantly during the deconstruction of buildings, and the Cd, Cu, Pb, Zn and Cr contents of soluble PM2.5 also significantly increased. Following exposure to PM2.5, the survival rate of breast cancer cells was significantly higher than that of the control group. Soluble PM2.5-treated cells also had a higher migration capacity, as determined by wound healing and transwell migration assays. The signaling pathway of FAK/PI3K/AKT proteins was more activated in PM2.5-treated cells than the control group. The data show that increased levels of Aurora B and Bcl-2 were associated with cell proliferation. Elevated levels of cathepsins D, β-catenin, N-cadherin, vimentin and MMP-9 were associated with breast cancer cell metastasisConclusion Soluble PM2.5 that is generated in building demolition may have a role in the promotion/progression of surviving in TNBC cells, increasing the malignancy of breast cancer. The prevention of environmental PM2.5 from deconstruction is strongly recommended.

scholarly journals Methylation-Based Biological Age and Breast Cancer Risk

2019 ◽  
Vol 111 (10) ◽  
pp. 1051-1058 ◽  
Author(s):  
Jacob K Kresovich ◽  
Zongli Xu ◽  
Katie M O’Brien ◽  
Clarice R Weinberg ◽  
Dale P Sandler ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Cox Regression ◽  
Disease Risk ◽  
Statistical Tests ◽  
Biological Age ◽  
Cancer Case ◽  
Increased Risk

Abstract Background Age is one of the strongest predictors of cancer, chronic disease, and mortality, but biological responses to aging differ among people. Epigenetic DNA modifications have been used to estimate “biological age,” which may be a useful predictor of disease risk. We tested this hypothesis for breast cancer. Methods Using a case-cohort approach, we measured baseline blood DNA methylation of 2764 women enrolled in the Sister Study, 1566 of whom subsequently developed breast cancer after an average of 6 years. Using three previously established methylation-based “clocks” (Hannum, Horvath, and Levine), we defined biological age acceleration for each woman by comparing her estimated biological age with her chronological age. Hazard ratios and 95% confidence intervals for breast cancer risk were estimated using Cox regression models. All statistical tests were two-sided. Results Each of the three clocks showed that biological age acceleration was statistically significantly associated with increased risk of developing breast cancer (5-year age acceleration, Hannum’s clock: hazard ratio [HR] = 1.10, 95% confidence interval [CI] = 1.00 to 1.21, P = .04; Horvath’s clock: HR = 1.08, 95% CI = 1.00 to 1.17, P = .04; Levine’s clock: HR = 1.15, 95% CI = 1.07 to 1.23, P < .001). For Levine’s clock, each 5-year acceleration in biological age corresponded with a 15% increase in breast cancer risk. Although biological age may accelerate with menopausal transition, age acceleration in premenopausal women independently predicted breast cancer. Case-only analysis suggested that, among women who develop breast cancer, increased age acceleration is associated with invasive cancer (odds ratio for invasive = 1.09, 95% CI = 0.98 to 1.22, P = .10). Conclusions DNA methylation-based measures of biological age may be important predictors of breast cancer risk.

scholarly journals Mortality and Risk of Cancer After Prophylactic Bilateral Oophorectomy in Women With a Family History of Cancer

2018 ◽  
Vol 2 (3) ◽  
Author(s):  
Julie Abildgaard ◽  
Magnus Glindvad Ahlström ◽  
Gedske Daugaard ◽  
Dorte Lisbet Nielsen ◽  
Anette Tønnes Pedersen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Family History ◽  
Rate Ratio ◽  
Bilateral Oophorectomy ◽  
Family History Of Cancer ◽  
Increased Risk ◽  
History Of ◽  
Risk Of Cancer ◽  
The Impact ◽  
History Of Cancer

Abstract Background Current international guidelines recommend systemic hormone therapy (HT) to oophorectomized women until the age of natural menopause. Despite an inherited predisposition to estrogen-dependent malignancies, the guidelines also apply to women oophorectomized because of a family history of cancer. The objective of this study was to investigate the impact of HT on mortality and risk of cancer in women oophorectomized because of a family history of cancer. Methods A nationwide, population-based cohort was used to study women oophorectomized because of a family history of cancer (n = 2002). Comparison cohorts included women from the background population individually matched on age (n = 18 018). Oophorectomized women were subdivided into three groups: oophorectomized at 1) age 45 years or younger not using HT, 2) age 45 years or younger using HT, 3) older than age 45 years, and their respective population comparison cohorts. Results Women oophorectomized at age 45 years or younger using HT had increased overall mortality (mortality rate ratio [MRR] = 3.45, 95% confidence interval [CI] = 1.53 to 7.79), mortality because of cancer (MRR = 5.67, 95% CI = 1.86 to 17.34), and risk of overall cancer (incidence rate ratio [IRR] = 3.68, 95% CI = 1.93 − 6.98), primarily reflected in an increased risk of breast cancer (IRR = 4.88, 95% CI = 2.19 − 10.68). Women oophorectomized at age 45 years or younger not using HT and women oophorectomized at older than age 45 years did not have increased mortality, mortality because of cancer, or risk of overall cancer, but they had increased risk of breast cancer (IRR = 2.64, 95% CI = 1.14 to 6.13, and IRR = 1.72, 95% CI = 1.14 to 2.59, respectively). Conclusions Use of HT in women oophorectomized at age 45 years or younger with a family history of cancer is associated with increased mortality and risk of overall cancer and breast cancer. Our study warrants further investigation to establish the impact of HT on mortality and cancer risk in oophorectomized women with a family history of cancer.

Molecular Analysis Of Patients With Deep Venous Thrombosis

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4799-4799
Author(s):  
Soudabeh Hosseeini ◽  
Ebrahim Kalantari ◽  
Akbar Dorgalaleh ◽  
Arash Rozei ◽  
Marzieh Jafari ◽  
...  
Keyword(s):  
Risk Factors ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Mthfr C677t ◽  
Control Group ◽  
Mthfr A1298c ◽  
Increased Risk ◽  
Fv Leiden ◽  
The Impact ◽  
Pai 1

Background Deep venous thrombosis (DVT) refers to the formation of a thrombus within a deep vein that frequently occurs after surgical procedures, trauma, in the presence of cancer and immobilization conditions. DVT is a major health problem that causes high rate of morbidity and mortality in the general population. Hyper coagulation states such as antithrombin-III, protein-C and protein-S deficiencies, contribute to formation of DVT. Congenital and acquired gene mutations are other risk factors that stimulate formation of thrombus. Our aims in this study was to molecularly analyze the patients with DVT and assess the impact of common mutations of MTHFR (C677T) (A1298C), PAI-1, Prothrombin 20210 and FV Leiden mutation on occurrence of deep venous thrombosis. Methods This long-term study was conducted from June 2009 to July 2013 on 221 patients with deep venues thrombosis. Two hundred and twenty-one age and sex matched individuals were also chosen as control group. The diagnosis of venous thromboembolic disease was based on patient’s history, clinical findings and D-dimer test. Finally deep venous thrombosis was confirmed with Doppler ultrasonography. In addition, all participants were asked to complete a standardized questionnaire on acquired risk factors for venous thrombosis. After confirmation of DVT, both groups were assessed molecularly for five mutations including, MTHFR C677T, MTHFR A1298C, PAI-1 4G/5G, Prothrombin 20210 and FV Leiden. The relationship between these mutations and the risk of DVT was calculated using logistic regression and expressed as an OR with a 95% confidence interval (CI). Results The mean age of patients and control group were 38±0.8 and 3.7± 0.7 years. Our results revealed that the MTHFR C677T (OR 2.9, 95% 95% CI 1.1 to 7.5) and MTHFR A1298C in heterozygote manner (OR 4.3, 95% CI 1.4 to 13.7) were each associated with an increased risk of DVT. The OR associated with being a carrier of the PAI-1 4G/5G genotype was 2.9 (95% CI 1.14 to 7.5). There was a 4-fold increased risk of DVT associated with Prothrombin 20210 mutation in heterozygote manner (OR 4.3, 95% CI 1.4 to 13.7). For patients who were heterozygous for FV Leiden mutation OR DVT was 2.6 (95% CI 1.3 to 5.0). Conclusion Our findings suggest that genetic risk factors have a contributory role on occurrence of DVT. Disclosures: No relevant conflicts of interest to declare.

Association of core needle biopsies with increase in metastatic dissemination of breast cancer.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e21090-e21090
Author(s):  
Carman A. Giacomantonio ◽  
Cheryl A. Dean ◽  
Edward G. Mathenge ◽  
Amber A. Black ◽  
Wendy Schulte ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Extrinsic Factors ◽  
Core Needle ◽  
Metastatic Dissemination ◽  
Increased Risk ◽  
Alu Sequence ◽  
Significant Difference ◽  
The Impact

e21090 Background: Given the reported association between incisional procedures performed on cancer patients and subsequent increases in metastasis, as well as the established inverse relationship between metastasis and patient survival, this study establishes the extent to which incisional core needle biopsies (CNB) affects tumor growth and metastatic dissemination in two distinct breast cancer animal models. Methods: Using the chick embryo system (CES) and murine breast cancer model (MuBC)the impact of CNB on cancer metastases was evaluated. Human MDA-MB-231 and MDA-MB-435 cancer cells were used in the xenograft / CES, and murine 4T1 Breast cancer cells for the syngeneic MuBC . In each model, tumors were biopsied in half of the animals while the other half were left undisturbed (CES:n=40, MuBC:n=40). The impact of CNB on tumor growth, necrosis and metastases was assessed. Metastases levels in the CES was determined by quantitative PCR for human alu sequence DNA in chick tissue extracts. Metastatic burden in the MuBC model was evaluated by microscopic quantification of metastatic areas in sectioned and H-E stained mouse organs. Results: When biopsied and un-biopsied groups were compared, both models showed significant difference in pulmonary metastasis. MDA-MB-435 CES (p=0.025) and 4T1 MuBC (p=0.026). MDA-MB-231 CES showed no significant change in lung metastases in the CES but did however show increased Chorioallantoic Membrane (CAM) metastasis (p=0.018) and both cell lines showed statistically significant alteration in Liver metastasis, (MDA-MB-231 CES (p=0.006); MDA-MB-435 CES (p=0.004)). Interestingly only MDA-MB-435 (CES) tumor growth was significantly increased after CNB (p=0.002). Conclusions: These results offer the first experimental evidence that core needle biopsies result in an increased risk of metastatic dissemination and affect metastatic tropic behavior. They also reinforce the concept of a multi-step metastatic pathway and suggest involvement of extrinsic factors that influence the extravastion and intravasation steps. The clinical implications are considerable and follow-up studies examining potential mechanisms and countermeasures are urgently required

Association of baseline cardiovascular risk factors and health care utilization and costs in elderly breast cancer patients enrolled in SWOG clinical trials.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 11508-11508
Author(s):  
Dawn L. Hershman ◽  
Cathee Till ◽  
Jason Dennis Wright ◽  
Melissa Kate Accordino ◽  
Riha Vaidya ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Risk Factors ◽  
Clinical Trials ◽  
Cancer Patients ◽  
Healthcare Costs ◽  
Disease Risk ◽  
Breast Cancer Patients ◽  
Increased Risk ◽  
Clinical Records ◽  
The Impact

11508 Background: Cardiovascular-disease risk factors (CVD-RFs) increase the risk of cardiac events in women undergoing chemotherapy. Less is known about the impact of CVD-RFs on healthcare utilization and costs. Methods: We examined breast cancer patients treated uniformly on SWOG clinical trials from 1999-2011. We identified baseline diabetes, hypertension, hypercholesterolemia, and coronary artery disease (CAD) by linking trial records to Medicare claims; obesity was identified using clinical records. The outcomes were emergency room visits (ER), hospitalizations and costs. Multivariable logistic and linear regression were used. Results: Among the 708 patients included in the analysis, 160 (22.6%) experienced 234 separate hospitalizations, and 193 (27.3%) experienced 311 separate ER visits. Diabetes, hypertension, hypercholesterolemia, and CAD were all associated with increased risk of hospitalizations and ER visit. Hypertension had the strongest association, with more than a threefold risk of hospitalization for those with hypertension compared to those without (OR [95% CI], 3.16 [1.85-5.40], p<0.001). For those with ≥3 CVD-RFs, the risk of hospitalization was greater compared to 0 or 1 CVD-RFs (OR [95% CI], 2.74 [1.71-4.38], p<0.001). Similar results were seen for ER visits. In the first 12 months after trial registration, patients with diabetes ($38,324 vs $30,923, 23.9% increase, p=0.05), hypercholesterolemia ($34,168 vs $30,661, 11.4% increase, p=0.02), and CAD ($37,781 vs $31,698, 19.2% increase, p=0.04) had statistically significantly higher total healthcare costs. Additionally, those with 2 significant CVD-RFs ($35,353 vs. $28,899, 22.3% increase, p=.005) had higher total healthcare costs. Conclusions: Our study demonstrates that the presence of both CVD-RFs and ER visits and hospitalizations are frequent among elderly BC patients. The risk of ER visits and hospitalizations is higher among patients with CVD-RFs, and increases with the number of RFs. Better management of CVD-RFs and more aggressive symptom management may be required to reduce both physical and financial toxicities to elderly patients undergoing BC therapy.

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