Publications by authors named "Maria Elena Martinez"

188 Publications

Association of germline genetic variants with breast cancer-specific survival in patient subgroups defined by clinic-pathological variables related to tumor biology and type of systemic treatment.

Breast Cancer Res 2021 Aug 18;23(1):86. Epub 2021 Aug 18.

Department of Medicine, Huntsman Cancer Institute, Salt Lake City, UT, USA.

Background: Given the high heterogeneity among breast tumors, associations between common germline genetic variants and survival that may exist within specific subgroups could go undetected in an unstratified set of breast cancer patients.

Methods: We performed genome-wide association analyses within 15 subgroups of breast cancer patients based on prognostic factors, including hormone receptors, tumor grade, age, and type of systemic treatment. Analyses were based on 91,686 female patients of European ancestry from the Breast Cancer Association Consortium, including 7531 breast cancer-specific deaths over a median follow-up of 8.1 years. Cox regression was used to assess associations of common germline variants with 15-year and 5-year breast cancer-specific survival. We assessed the probability of these associations being true positives via the Bayesian false discovery probability (BFDP < 0.15).

Results: Evidence of associations with breast cancer-specific survival was observed in three patient subgroups, with variant rs5934618 in patients with grade 3 tumors (15-year-hazard ratio (HR) [95% confidence interval (CI)] 1.32 [1.20, 1.45], P = 1.4E-08, BFDP = 0.01, per G allele); variant rs4679741 in patients with ER-positive tumors treated with endocrine therapy (15-year-HR [95% CI] 1.18 [1.11, 1.26], P = 1.6E-07, BFDP = 0.09, per G allele); variants rs1106333 (15-year-HR [95% CI] 1.68 [1.39,2.03], P = 5.6E-08, BFDP = 0.12, per A allele) and rs78754389 (5-year-HR [95% CI] 1.79 [1.46,2.20], P = 1.7E-08, BFDP = 0.07, per A allele), in patients with ER-negative tumors treated with chemotherapy.

Conclusions: We found evidence of four loci associated with breast cancer-specific survival within three patient subgroups. There was limited evidence for the existence of associations in other patient subgroups. However, the power for many subgroups is limited due to the low number of events. Even so, our results suggest that the impact of common germline genetic variants on breast cancer-specific survival might be limited.
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http://dx.doi.org/10.1186/s13058-021-01450-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8371820PMC
August 2021

Association between Sugar-Sweetened Beverage Intake and Mortality Risk in Women: The California Teachers Study.

J Acad Nutr Diet 2021 Aug 10. Epub 2021 Aug 10.

professor and Dean of the Herbert Wertheim School of Public Health and Human Longevity Science at University of California San Diego, La Jolla, CA. Electronic address:

Background: The evidence linking sugar-sweetened beverage (SSB) intake and mortality risk is conflicting, and associations between various SSB subtypes and mortality remain unclear.

Objective: To examine the association between baseline SSB intake, subtypes of SSB intake, and mortality risk in women.

Design: Prospective cohort study.

Participants/setting: Participants of the California Teachers Study (n=100,314; median age 53) free of cardiovascular disease (CVD), cancer, and diabetes at baseline (1995-1996) were followed from 1995 to 2015. Baseline SSB intake was defined as caloric soft drinks (regular soft drinks, not diet soda), sweetened bottled waters or teas, and fruit drinks; and was derived from a self-administered food frequency questionnaire.

Main Outcome Measure: Mortality was ascertained via annual linkage with state- and nationwide mortality records and the National Death Index over 20-years.

Statistical Analysis: Multivariable-adjusted Cox proportional hazards models were used to generate hazard ratios (HR) and 95% confidence intervals (CI) for assessing associations between SSB intake and mortality. Rare/never consumers were the comparator group.

Results: There were a total of 14,143 deaths over 20 years (30.5% from CVD; 29.2% from cancer). In women who consumed ≥7 servings/week of SSBs at baseline (4% of participants), the multivariable-adjusted HRs were not significant for all-cause, CVD-specific, or cancer-specific mortality. Consuming ≥7 servings/week of baseline caloric soft drink was associated with a higher risk of all-cause (HR = 1.26, 95% CI 1.10, 1.46; P trend = 0.02) and cancer-specific (HR = 1.33, 95% CI 1.08, 1.63; P trend = 0.08) mortality. In secondary analyses, consuming ≥1.5 cups/day of baseline SSBs was associated with all-cause mortality (HR = 1.12, 95% CI 1.02, 1.24; P trend = 0.01).

Conclusions: Although the baseline frequency of total SSB intake was not significantly associated with mortality, consuming ≥7 servings/week of caloric soft drinks was associated with higher risk of all-cause and cancer-specific mortality. Findings support public health efforts to reduce caloric soft drink consumption.
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http://dx.doi.org/10.1016/j.jand.2021.08.099DOI Listing
August 2021

Mendelian randomisation study of smoking exposure in relation to breast cancer risk.

Br J Cancer 2021 Aug 2. Epub 2021 Aug 2.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA.

Background: Despite a modest association between tobacco smoking and breast cancer risk reported by recent epidemiological studies, it is still equivocal whether smoking is causally related to breast cancer risk.

Methods: We applied Mendelian randomisation (MR) to evaluate a potential causal effect of cigarette smoking on breast cancer risk. Both individual-level data as well as summary statistics for 164 single-nucleotide polymorphisms (SNPs) reported in genome-wide association studies of lifetime smoking index (LSI) or cigarette per day (CPD) were used to obtain MR effect estimates. Data from 108,420 invasive breast cancer cases and 87,681 controls were used for the LSI analysis and for the CPD analysis conducted among ever-smokers from 26,147 cancer cases and 26,072 controls. Sensitivity analyses were conducted to address pleiotropy.

Results: Genetically predicted LSI was associated with increased breast cancer risk (OR 1.18 per SD, 95% CI: 1.07-1.30, P = 0.11 × 10), but there was no evidence of association for genetically predicted CPD (OR 1.02, 95% CI: 0.78-1.19, P = 0.85). The sensitivity analyses yielded similar results and showed no strong evidence of pleiotropic effect.

Conclusion: Our MR study provides supportive evidence for a potential causal association with breast cancer risk for lifetime smoking exposure but not cigarettes per day among smokers.
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http://dx.doi.org/10.1038/s41416-021-01432-8DOI Listing
August 2021

The Type 3 Deiodinase Is a Critical Modulator of Thyroid Hormone Sensitivity in the Fetal Brain.

Front Neurosci 2021 29;15:703730. Epub 2021 Jun 29.

Center for Molecular Medicine, Maine Medical Center Research Institute, MaineHealth, Scarborough, ME, United States.

Thyroid hormones (TH) are critical for the development and function of the central nervous system (CNS). Although their effects on the rodent brain peak within 2-3 weeks postnatally, the fetal brain has been found largely insensitive to exogenously administrated TH. To address this issue, here we examined gene expression in brains from mouse fetuses deficient in the type 3 deiodinase (DIO3), the selenoenzyme responsible for clearing TH. At embryonic day E18.5 qPCR determinations indicated a marked increase in the mRNA expression of T3-responsive genes and . The increased expression of these genes was confirmed by hydridization in multiple areas of the cortex and in the striatum. RNA sequencing revealed 246 genes differentially expressed (70% up-regulated) in the brain of E18.5 -/- male fetuses. Differential expression of 13 of these genes was confirmed in an extended set of samples that included females. Pathway analyses of differentially expressed genes indicated enrichment in glycolysis and signaling related to axonal guidance, synaptogenesis and hypoxia inducible factor alpha. Additional RNA sequencing identified 588 genes differentially expressed (35% up-regulated) in the brain of E13.5 -/- male fetuses. Differential expression of 13 of these genes, including , and , was confirmed in an extended set of samples including females. Although pathway analyses of differentially expressed genes at E13.5 also revealed significant enrichment in axonal guidance and synaptogenesis signaling, top enrichment was found for functions related to the cell cycle, aryl hydrocarbon receptor signaling, PCP and kinetochore metaphase signaling pathways and mitotic roles of polo-like kinase. Differential expression at E13.5 was confirmed by qPCR for additional genes related to collagen and extracellular matrix and for selected transcription factors. Overall, our results demonstrate that the rodent fetal brain is sensitive to TH as early as E13.5 of gestational age, and suggest that TH distinctly affects brain developmental programs in early and late gestation. We conclude that DIO3 function is critical to ensure an adequate timing for TH action in the developing brain and is probably the main factor underlying the lack of effects on the fetal brain observed in previous studies after TH administration.
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http://dx.doi.org/10.3389/fnins.2021.703730DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8265566PMC
June 2021

Performance of African-ancestry-specific polygenic hazard score varies according to local ancestry in 8q24.

Prostate Cancer Prostatic Dis 2021 Jun 14. Epub 2021 Jun 14.

School of Public Health, Louisiana State University Health Sciences Center, New Orleans, LA, USA.

Background: We previously developed an African-ancestry-specific polygenic hazard score (PHS46+African) that substantially improved prostate cancer risk stratification in men with African ancestry. The model consists of 46 SNPs identified in Europeans and 3 SNPs from 8q24 shown to improve model performance in Africans. Herein, we used principal component (PC) analysis to uncover subpopulations of men with African ancestry for whom the utility of PHS46+African may differ.

Materials And Methods: Genotypic data were obtained from the PRACTICAL consortium for 6253 men with African genetic ancestry. Genetic variation in a window spanning 3 African-specific 8q24 SNPs was estimated using 93 PCs. A Cox proportional hazards framework was used to identify the pair of PCs most strongly associated with the performance of PHS46+African. A calibration factor (CF) was formulated using Cox coefficients to quantify the extent to which the performance of PHS46+African varies with PC.

Results: CF of PHS46+African was strongly associated with the first and twentieth PCs. Predicted CF ranged from 0.41 to 2.94, suggesting that PHS46+African may be up to 7 times more beneficial to some African men than others. The explained relative risk for PHS46+African varied from 3.6% to 9.9% for individuals with low and high CF values, respectively. By cross-referencing our data set with 1000 Genomes, we identified significant associations between continental and calibration groupings.

Conclusion: We identified PCs within 8q24 that were strongly associated with the performance of PHS46+African. Further research to improve the clinical utility of polygenic risk scores (or models) is needed to improve health outcomes for men of African ancestry.
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http://dx.doi.org/10.1038/s41391-021-00403-7DOI Listing
June 2021

Gene-Environment Interactions Relevant to Estrogen and Risk of Breast Cancer: Can Gene-Environment Interactions Be Detected Only among Candidate SNPs from Genome-Wide Association Studies?

Cancers (Basel) 2021 May 14;13(10). Epub 2021 May 14.

Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, 2730 Herlev, Denmark.

In this study we aim to examine gene-environment interactions (GxEs) between genes involved with estrogen metabolism and environmental factors related to estrogen exposure. GxE analyses were conducted with 1970 Korean breast cancer cases and 2052 controls in the case-control study, the Seoul Breast Cancer Study (SEBCS). A total of 11,555 SNPs from the 137 candidate genes were included in the GxE analyses with eight established environmental factors. A replication test was conducted by using an independent population from the Breast Cancer Association Consortium (BCAC), with 62,485 Europeans and 9047 Asians. The GxE tests were performed by using two-step methods in GxEScan software. Two interactions were found in the SEBCS. The first interaction was shown between rs13035764 of NCOA1 and age at menarche in the GE|2df model (-2df = 1.2 × 10). The age at menarche before 14 years old was associated with the high risk of breast cancer, and the risk was higher when subjects had homozygous minor allele G. The second GxE was shown between rs851998 near ESR1 and height in the GE|2df model (-2df = 1.1 × 10). Height taller than 160 cm was associated with a high risk of breast cancer, and the risk increased when the minor allele was added. The findings were not replicated in the BCAC. These results would suggest specificity in Koreans for breast cancer risk.
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http://dx.doi.org/10.3390/cancers13102370DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8156547PMC
May 2021

The Influence of Patient-Provider Language Concordance in Cancer Care: Results of the Hispanic Outcomes by Language Approach (HOLA) Randomized Trial.

Int J Radiat Oncol Biol Phys 2021 May 29. Epub 2021 May 29.

Department of Radiation Medicine and Applied Sciences, University of California, San Diego, California. Electronic address:

Purpose: Delivering linguistically competent care is critical to serving patients who have limited English proficiency (LEP) and represents a key national strategy to help reduce health disparities. Current acceptable standards of communication with patients who have LEP include providers communicating through professional interpretive services or bilingual providers speaking the patients' preferred language directly. This randomized clinical trial tests the effect of patient-provider language concordance on patient satisfaction.

Methods And Materials: Eighty-three adult Spanish-speaking patients with cancer were randomly assigned to receive care from either (1) 1 of 2 bilingual physicians speaking to the patient directly in Spanish or (2) the same physicians speaking English and using a professional interpreter service. Validated questionnaires were administered to assess patient-reported satisfaction with both provider communication and overall care. Transcripts of initial consultations were analyzed for content variations.

Results: Compared with patients receiving care through professional interpretive services, patients cared for in direct Spanish reported significantly improved general satisfaction, technical quality of care (mean composite score [MCS], 4.41 vs 4.06; P = .005), care team interpersonal manner (MCS, 4.37 vs 3.88; P = .004), communication (MCS, 4.50 vs 4.25; P = .018), and time spent with patient,(MCS, 4.30 vs 3.92; P = .028). Specific to physician communication, patients rated direct-Spanish care more highly in perceived opportunity to disclose concerns (MCS 4.91 vs 4.62; P = .001), physician empathy (MCS, 4.94 vs 4.59; P <.001), confidence in physician abilities (MCS, 4.84 vs 4.51; P = .001), and general satisfaction with their physician (MCS, 4.88 vs 4.59; P <.001). Analyzing the content of consultation encounters revealed differences between study arms, with the direct-Spanish arm having more physician speech related to patient history verification (mean number of utterances, 13 vs 9; P = .01) and partnering activities (mean utterances, 16 vs 5; P <.001). Additionally, patients in the direct-Spanish arm were more likely to initiate unprompted speech (mean utterances, 11 vs 3; P <.001) and asked their providers more questions (mean utterances, 11 vs 4; P = .007).

Conclusions: This study shows improved patient-reported satisfaction among patients with cancer who had LEP and were cared for in direct Spanish compared with interpreter-based communication. Further research into interventions to mitigate the patient-provider language barrier is necessary to optimize care for this population.
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http://dx.doi.org/10.1016/j.ijrobp.2021.05.122DOI Listing
May 2021

Assessment of Factors Associated With Parental Perceptions of Voluntary Decisions About Child Participation in Leukemia Clinical Trials.

JAMA Netw Open 2021 May 3;4(5):e219038. Epub 2021 May 3.

Population Sciences, Disparities and Community Engagement, University of California San Diego Moores Cancer Center, La Jolla.

Importance: Obtaining voluntary informed consent prior to enrollment in clinical trials is a fundamental ethical requirement.

Objective: To assess whether health literacy, contextual factors, or sociodemographic characteristics are associated with perception of voluntariness among parents who had consented for their child's participation in a leukemia therapeutic clinical trial.

Design, Setting, And Participants: This cross-sectional study prospectively enrolled 97 parents of children diagnosed as having leukemia at Rady Children's Hospital San Diego, a large tertiary academic center in California, from 2014 to 2017. Health literacy, contextual factors (acculturation, decisional regret, and satisfaction with informed consent), sociodemographic characteristics, and perception of voluntariness after consenting for a therapeutic clinical trial were measured. Univariable and multivariable regression were used to determine significant associations. The analyses for the present study were conducted from May 2019 to May 2020.

Exposures: Informed consent for a therapeutic leukemia clinical trial.

Main Outcomes And Measures: The primary outcome of interest was perception of voluntariness and its associations with health literacy and other contextual factors (acculturation, decisional regret, and satisfaction with informed consent) and sociodemographic characteristics, including age, race/ethnicity, parental language, educational level, insurance type, marital status, and socioeconomic status.

Results: Of 97 parents included, the majority were women (65 [67%]), married (71 [73%]), and of self-reported Hispanic ethnicity (50 [52%]). Lower perception of voluntariness was significantly associated with lower health literacy (r = 0.30; 95% CI, 0.11-0.47; P = .004), Spanish language (x̅ = -4.50, P = .05), lower acculturation if of Hispanic ethnicity (r = 0.30; 95% CI, 0.02-0.54; P = .05), greater decisional regret (r = -0.54; 95% CI, -0.67 to -0.38; P < .001), and lower satisfaction with informed consent (r = 0.39; 95% CI, 0.21-0.54; P < .001) in univariable analysis. Lower health literacy remained significantly associated with lower perception of voluntariness in multivariable analysis after adjustment for contextual factors and sociodemographic characteristics (β = 4.06; 95% CI, 1.60-6.53; P = .001). Lower health literacy was significantly associated with Hispanic ethnicity (mean, 4.16; 95% CI, 3.75-4.57; P < .001), Spanish language spoken at home (mean, 3.17; 95% CI, 1.94-4.40; P < .001), high school or less educational level (mean, 3.41; 95% CI, 2.83-3.99; P < .001), public insurance (mean, 4.00; 95% CI, 3.55-4.45; P < .001), and unmarried status (mean, 3.71; 95% CI, 2.91-4.51; P = .03).

Conclusions And Relevance: Among parents of children with newly diagnosed leukemia who had consented for their child's participation in a therapeutic clinical trial, lower perception of voluntariness was significantly associated with lower health literacy. These results suggest that parents with low health literacy may perceive external influences in their decision for their child's participation in clinical trials. This finding highlights the potential role of recruitment interventions tailored to the participant's health literacy level to improve voluntary informed consent in underserved populations.
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http://dx.doi.org/10.1001/jamanetworkopen.2021.9038DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8097494PMC
May 2021

Association of Health-Care System with Prostate Cancer-Specific Mortality in African American and Non-Hispanic White Men.

J Natl Cancer Inst 2021 Apr 21. Epub 2021 Apr 21.

Department of Radiation Medicine and Applied Sciences, University of California San Diego School of Medicine, La Jolla, California.

Background: Disparities in prostate cancer-specific mortality (PCSM) between African American and non-Hispanic White (White) patients have been attributed to biological and systemic factors. We evaluated drivers of these disparities in the Surveillance, Epidemiology and End Results (SEER) national registry and an equal-access system, the Veterans Health Administration (VHA).

Methods: We identified African American and White patients diagnosed with prostate cancer between 2004-2015 in SEER (N = 311,691) and the VHA (N = 90,749). We analyzed the association between race and metastatic disease at presentation using multivariable logistic regression adjusting for sociodemographic factors, and PCSM using sequential competing-risks regression adjusting for disease and sociodemographic factors.

Results: The median follow-up was 5.3 years in SEER and 4.7 years in the VHA. African American men were more likely than White men to present with metastatic disease in SEER (adjusted odds ratio = 1.23, 95% confidence interval [CI] = 1.17-1.30), but not in the VHA (adjusted odds ratio = 1.07, 95% CI = 0.98-1.17). African American versus White race was associated with an increased risk of PCSM in SEER (subdistribution hazard ratio [SHR] = 1.32, 95% CI = 1.10-1.60), but not in the VHA (SHR = 1.00, 95% CI: 0.93-1.08). Adjusting for disease extent, PSA, and Gleason score eliminated the association between race and PCSM in SEER (aSHR 1.04, 95% CI 0.93-1.16).

Conclusions: Racial disparities in PCSM were present in a nationally representative registry, but not in an equal-access healthcare system, due to differences in advanced disease at presentation. Strategies to increase healthcare access may bridge the racial disparity in outcomes. Longer follow-up is needed to fully assess mortality outcomes.Disparities between African American and non-Hispanic White (White) patients in cancer-specific mortality have been described across numerous cancer types and healthcare systems[1-5]. The survival gap between African American and White patients with prostate cancer has been well-characterized, with two-fold higher prostate cancer-specific mortality (PCSM) rates among African American patients depending on the setting[1, 6-10]. This disparity has been attributed to differences in prostate cancer biology in African American men, in addition to systemic factors in mediating this disparity, such as differential access to healthcare, Prostate-Specific Antigen (PSA) screening, and distrust in the healthcare system[1, 11-16].The Veterans Health Administration (VHA) is a relatively equal-access healthcare system that treats a large, ethnically diverse population of veterans. The Surveillance, Epidemiology and End Results (SEER) program is a national cancer registry program that collects data from the general United States (US) population. The goals of the present investigation were to 1) Compare PCSM between African American and White men within SEER and the VHA and 2) Identify modifiable system-level contributors to these disparities. We hypothesized that PCSM would be comparable among African American and White men in an equal-access setting, the VHA, but not in a national registry, SEER, and that this disparity in SEER would be in part driven by more advanced disease at presentation.
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http://dx.doi.org/10.1093/jnci/djab062DOI Listing
April 2021

Polygenic hazard score is associated with prostate cancer in multi-ethnic populations.

Nat Commun 2021 02 23;12(1):1236. Epub 2021 Feb 23.

Division of Cancer Sciences, University of Manchester, Manchester Academic Health Science Centre, Radiotherapy Related Research, The Christie Hospital NHS Foundation Trust, Manchester, UK.

Genetic models for cancer have been evaluated using almost exclusively European data, which could exacerbate health disparities. A polygenic hazard score (PHS) is associated with age at prostate cancer diagnosis and improves screening accuracy in Europeans. Here, we evaluate performance of PHS (PHS, adapted for OncoArray) in a multi-ethnic dataset of 80,491 men (49,916 cases, 30,575 controls). PHS is associated with age at diagnosis of any and aggressive (Gleason score ≥ 7, stage T3-T4, PSA ≥ 10 ng/mL, or nodal/distant metastasis) cancer and prostate-cancer-specific death. Associations with cancer are significant within European (n = 71,856), Asian (n = 2,382), and African (n = 6,253) genetic ancestries (p < 10). Comparing the 80/20 PHS percentiles, hazard ratios for prostate cancer, aggressive cancer, and prostate-cancer-specific death are 5.32, 5.88, and 5.68, respectively. Within European, Asian, and African ancestries, hazard ratios for prostate cancer are: 5.54, 4.49, and 2.54, respectively. PHS risk-stratifies men for any, aggressive, and fatal prostate cancer in a multi-ethnic dataset.
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http://dx.doi.org/10.1038/s41467-021-21287-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7902617PMC
February 2021

Time to Colonoscopy After Abnormal Stool-Based Screening and Risk for Colorectal Cancer Incidence and Mortality.

Gastroenterology 2021 05 2;160(6):1997-2005.e3. Epub 2021 Feb 2.

Division of Gastroenterology, Department of Medicine, Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, California; Vatche and Tamar Manoukian Division of Digestive Diseases and Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, California. Electronic address:

Background And Aims: The optimal time interval for diagnostic colonoscopy completion after an abnormal stool-based colorectal cancer (CRC) screening test is uncertain. We examined the association between time to colonoscopy and CRC outcomes among individuals who underwent diagnostic colonoscopy after abnormal stool-based screening.

Methods: We performed a retrospective cohort study of veterans age 50 to 75 years with an abnormal fecal occult blood test (FOBT) or fecal immunochemical test (FIT) between 1999 and 2010. We used multivariable Cox proportional hazards to generate CRC-specific incidence and mortality hazard ratios (HRs) and 95% confidence intervals (CI) for 3-month colonoscopy intervals, with 1 to 3 months as the reference group. Association of time to colonoscopy with late-stage CRC diagnosis was also examined.

Results: Our cohort included 204,733 patients. Mean age was 61 years (SD 6.9). Compared with patients who received a colonoscopy at 1 to 3 months, there was an increased CRC risk for patients who received a colonoscopy at 13 to 15 months (HR 1.13; 95% CI 1.00-1.27), 16 to 18 months (HR 1.25; 95% CI 1.10-1.43), 19 to 21 months (HR 1.28; 95% CI: 1.11-1.48), and 22 to 24 months (HR 1.26; 95% CI 1.07-1.47). Compared with patients who received a colonoscopy at 1 to 3 months, mortality risk was higher in groups who received a colonoscopy at 19 to 21 months (HR 1.52; 95% CI 1.51-1.99) and 22 to 24 months (HR 1.39; 95% CI 1.03-1.88). Odds for late-stage CRC increased at 16 months.

Conclusions: Increased time to colonoscopy is associated with higher risk of CRC incidence, death, and late-stage CRC after abnormal FIT/FOBT. Interventions to improve CRC outcomes should emphasize diagnostic follow-up within 1 year of an abnormal FIT/FOBT result.
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http://dx.doi.org/10.1053/j.gastro.2021.01.219DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8096663PMC
May 2021

Racial, Ethnic, and Socioeconomic Discrepancies in Opioid Prescriptions Among Older Patients With Cancer.

JCO Oncol Pract 2021 06 3;17(6):e703-e713. Epub 2021 Feb 3.

Department of Radiation Medicine and Applied Sciences, University of California San Diego, La Jolla, CA.

Purpose: Minority race and lower socioeconomic status are associated with lower rates of opioid prescription and undertreatment of pain in multiple noncancer healthcare settings. It is not known whether these differences in opioid prescribing exist among patients undergoing cancer treatment.

Methods And Materials: This observational cohort study involved 33,872 opioid-naive patients of age > 65 years undergoing definitive cancer treatment. We compared rates of new opioid prescriptions by race or ethnicity and socioeconomic status controlling for differences in baseline patient, cancer, and treatment factors. To evaluate downstream impacts of opioid prescribing and pain management, we also compared rates of persistent opioid use and pain-related emergency department (ED) visits.

Results: Compared with non-Hispanic White patients, the covariate-adjusted odds of receiving an opioid prescription were 24.9% (95% CI, 16.0 to 33.9, < .001) lower for non-Hispanic Blacks, 115.0% (84.7 to 150.3, < .001) higher for Asian-Pacific Islanders, and not statistically different for Hispanics (-1.0 to 14.0, = .06). There was no significant association between race or ethnicity and persistent opioid use or pain-related ED visits. Patients living in a high-poverty area had higher odds (53.9% [25.4 to 88.8, < .001]) of developing persistent use and having a pain-related ED visit (39.4% [16.4 to 66.9, < .001]).

Conclusion: For older patients with cancer, rates of opioid prescriptions and pain-related outcomes significantly differed by race and area-level poverty. Non-Hispanic Black patients were associated with a significantly decreased likelihood of receiving an opioid prescription. Patients from high-poverty areas were more likely to develop persistent opioid use and have a pain-related ED visit.
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http://dx.doi.org/10.1200/OP.20.00773DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8258011PMC
June 2021

Breast Cancer Risk Genes - Association Analysis in More than 113,000 Women.

N Engl J Med 2021 02 20;384(5):428-439. Epub 2021 Jan 20.

The authors' affiliations are as follows: the Centre for Cancer Genetic Epidemiology, Departments of Public Health and Primary Care (L.D., S. Carvalho, J.A., K.A.P., Q.W., M.K.B., J.D., B.D., N. Mavaddat, K. Michailidou, A.C.A., P.D.P.P., D.F.E.) and Oncology (C.L., P.A.H., C. Baynes, D.M.C., L.F., V.R., M. Shah, P.D.P.P., A.M.D., D.F.E.), University of Cambridge, Cambridge, the Centre for Genomic and Experimental Medicine, MRC Institute of Genetics and Molecular Medicine (A. Campbell, D.J.P.), and the Centre for Cognitive Ageing and Cognitive Epidemiology, Department of Psychology (D.J.P.), University of Edinburgh, the Cancer Research UK Edinburgh Centre (D.A.C., J.F.), and the Usher Institute of Population Health Sciences and Informatics, University of Edinburgh Medical School (A. Campbell, J.F.), Edinburgh, the Divisions of Informatics, Imaging, and Data Sciences (E.F.H.), Cancer Sciences (A. Howell), Population Health, Health Services Research, and Primary Care (A. Lophatananon, K. Muir), and Evolution and Genomic Sciences, School of Biological Sciences (W.G.N., E.M.V., D.G.E.), University of Manchester, the NIHR Manchester Biomedical Research Unit (E.F.H.) and the Nightingale Breast Screening Centre, Wythenshawe Hospital (E.F.H., H.I.), Academic Health Science Centre and North West Genomics Laboratory Hub, and the Manchester Centre for Genomic Medicine, St. Mary's Hospital, Manchester University NHS Foundation Trust (W.G.N., E.M.V., D.G.E.), Manchester, the School of Cancer and Pharmaceutical Sciences, Comprehensive Cancer Centre, Guy's Campus, King's College London, London (E.J.S.), the Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham (I.T.), and the Wellcome Trust Centre for Human Genetics and Oxford NIHR Biomedical Research Centre, University of Oxford, Oxford (I.T.) - all in the United Kingdom; the Human Genotyping-CEGEN Unit, Human Cancer Genetic Program (A.G.-N., M.R.A., N.Á., B.H., R.N.-T.), and the Human Genetics Group (V.F., A.O., J.B.), Spanish National Cancer Research Center, Centro de Investigación en Red de Enfermedades Raras (A.O., J.B.), Servicio de Oncología Médica, Hospital Universitario La Paz (M.P.Z.), and Molecular Oncology Laboratory, Hospital Clinico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (M. de la Hoya), Madrid, the Genomic Medicine Group, Galician Foundation of Genomic Medicine, Instituto de Investigación Sanitaria de Santiago de Compostela, Complejo Hospitalario Universitario de Santiago (A. Carracedo, M.G.-D.), and Centro de Investigación en Red de Enfermedades Raras y Centro Nacional de Genotipado, Universidad de Santiago de Compostela (A. Carracedo), Santiago de Compostela, the Oncology and Genetics Unit, Instituto de Investigacion Sanitaria Galicia Sur, Xerencia de Xestion Integrada de Vigo-Servizo Galeo de Saúde, Vigo (J.E.C.), and Servicio de Cirugía General y Especialidades, Hospital Monte Naranco, Oviedo (J.I.A.P.) - all in Spain; the Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund (C. Wahlström, J.V., M.L., T. Törngren, Å.B., A.K.), the Department of Oncology, Örebro University Hospital, Örebro (C. Blomqvist), and the Departments of Medical Epidemiology and Biostatistics (K.C., M.E., M.G., P. Hall, W.H., K.H.), Oncology, Södersjukhuset (P. Hall, S. Margolin), Molecular Medicine and Surgery (A. Lindblom), and Clinical Science and Education, Södersjukhuset (S. Margolin, C. Wendt), Karolinska Institutet, and the Department of Clinical Genetics, Karolinska University Hospital (A. Lindblom), Stockholm - all in Sweden; the Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD (M.T.P., C.F., G.C.-T., A.B.S.), the Cancer Epidemiology Division, Cancer Council Victoria (G.G.G., R.J.M., R.L.M.), the Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health (G.G.G., R.J.M., R.L.M.), and the Department of Clinical Pathology (M.C.S.), University of Melbourne, Anatomical Pathology, Alfred Hospital (C.M.), and the Cancer Epidemiology Division, Cancer Council Victoria (M.C.S.), Melbourne, VIC, and Precision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, VIC (G.G.G., M.C.S., R.L.M.) - all in Australia; the Division of Molecular Pathology (R.K., S. Cornelissen, M.K.S.), Family Cancer Clinic (F.B.L.H., L.E.K.), Department of Epidemiology (M.A.R.), and Division of Psychosocial Research and Epidemiology (M.K.S.), the Netherlands Cancer Institute-Antoni van Leeuwenhoek Hospital, Amsterdam, Division Laboratories, Pharmacy and Biomedical Genetics, Department of Genetics, University Medical Center, Utrecht (M.G.E.M.A.), the Department of Clinical Genetics, Erasmus University Medical Center (J.M.C., A.M.W.O.), and the Department of Medical Oncology, Family Cancer Clinic, Erasmus MC Cancer Institute (B.A.M.H.-G., A. Hollestelle, M.J.H.), Rotterdam, the Department of Clinical Genetics, Maastricht University Medical Center, Maastricht (E.B.G.G.), the Departments of Human Genetics (I.M.M.L., M.P.G.V., P.D.), Clinical Genetics (C.J.A.), and Pathology (P.D.), Leiden University Medical Center, Leiden, the Department of Human Genetics, Radboud University Medical Center, Nijmegen (A.R.M.), and the Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen (J.C.O.) - all in the Netherlands; the Cancer Genetics and Comparative Genomics Branch, National Human Genome Research Institute (B.D.), and the Division of Cancer Epidemiology and Genetics, National Cancer Institute (T.A., S.J.C., X.R.Y., M.G.-C.), National Institutes of Health, Bethesda, MD; the Department of Pathology, Brigham and Women's Hospital, Harvard Medical School (B.D.), and the Department of Nutrition, Harvard T.H. Chan School of Public Health (R.M.V.D.), Boston; the Departments of Clinical Genetics (K.A.), Oncology (C. Blomqvist), and Obstetrics and Gynecology (H.N., M. Suvanto), Helsinki University Hospital, University of Helsinki, Helsinki, and the Unit of Clinical Oncology, Kuopio University Hospital (P. Auvinen), the Institute of Clinical Medicine, Oncology (P. Auvinen), the Translational Cancer Research Area (J.M.H., V.-M.K., A. Mannermaa), and the Institute of Clinical Medicine, Pathology, and Forensic Medicine (J.M.H., V.-M.K., A. Mannermaa), University of Eastern Finland, and the Biobank of Eastern Finland, Kuopio University Hospital (V.-M.K., A. Mannermaa), Kuopio - both in Finland; the N.N. Alexandrov Research Institute of Oncology and Medical Radiology, Minsk, Belarus (N.N.A., N.V.B.); the Department of Gynecology and Obstetrics and Institute of Clinical Molecular Biology, University Hospital of Schleswig-Holstein, Campus Kiel, Christian-Albrechts University Kiel, Kiel (N.A.), the Institute of Medical Biometry and Epidemiology (H. Becher) and Cancer Epidemiology Group (T.M., J.C.-C.), University Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, the Department of Gynecology and Obstetrics (M.W.B., P.A.F., L.H.) and Institute of Human Genetics (A.B.E.), University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Comprehensive Cancer Center Erlangen-European Metropolitan Region of Nuremberg, Erlangen, the Division of Cancer Epidemiology (S.B., A. Jung, P.M.K., J.C.-C.), Molecular Epidemiology Group, C080 (B. Burwinkel, H.S.), Division of Pediatric Neurooncology (A.F.), and Molecular Genetics of Breast Cancer (U.H., M.M., M.U.R., D.T.), German Cancer Research Center, Molecular Biology of Breast Cancer, University Women's Clinic Heidelberg, University of Heidelberg (B. Burwinkel, A.S., H.S.), Hopp Children's Cancer Center (A.F.), Faculty of Medicine, University of Heidelberg (P.M.K.), and National Center for Tumor Diseases, University Hospital and German Cancer Research Center (A.S., C.S.), Heidelberg, the Department of Radiation Oncology (N.V.B., M. Bremer, H.C.) and the Gynecology Research Unit (N.V.B., T.D., P. Hillemanns, T.-W.P.-S., P.S.), Hannover Medical School, Hannover, the Institute of Human Genetics, University of Münster, Münster (N.B.-M.), Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart (H. Brauch, W.-Y.L.), iFIT-Cluster of Excellence, University of Tübingen, and the German Cancer Consortium, German Cancer Research Center, Partner Site Tübingen (H. Brauch), and the University of Tübingen (W.-Y.L.), Tübingen, Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum, Bochum (T.B.), Institute for Medical Informatics, Statistics, and Epidemiology, University of Leipzig, Leipzig (C.E.), Center for Hereditary Breast and Ovarian Cancer (E.H., R.K.S.) and Center for Integrated Oncology (E.H., R.K.S.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, the Department of Internal Medicine, Evangelische Kliniken Bonn, Johanniter Krankenhaus, Bonn (Y.-D.K.), the Department of Gynecology and Obstetrics, University of Munich, Campus Großhadern, Munich (A. Meindl), and the Institute of Pathology, Städtisches Klinikum Karlsruhe, Karlsruhe (T.R.) - all in Germany; the Gynecological Cancer Registry, Centre Georges-François Leclerc, Dijon (P. Arveux), and the Center for Research in Epidemiology and Population Health, Team Exposome and Heredity, INSERM, University Paris-Saclay, Villejuif (E.C.-D., P.G., T. Truong) - both in France; the Institute of Biochemistry and Genetics, Ufa Federal Research Center of the Russian Academy of Sciences (M. Bermisheva, E.K.), the Department of Genetics and Fundamental Medicine, Bashkir State University (E.K., D.P., Y.V.), and the Ufa Research Institute of Occupational Health and Human Ecology (Y.V.), Ufa, Russia; the Department of Genetics and Pathology (K.B., A. Jakubowska, J. Lubiński, K.P.) and the Independent Laboratory of Molecular Biology and Genetic Diagnostics (A. Jakubowska), Pomeranian Medical University, Szczecin, Poland; the Copenhagen General Population Study, the Department of Clinical Biochemistry (S.E.B., B.G.N.), and the Department of Breast Surgery (H.F.), Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, and the Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen (S.E.B., B.G.N.) - both in Denmark; the Division of Cancer Prevention and Genetics, European Institute of Oncology Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) (B. Bonanni), the Unit of Medical Genetics, Department of Medical Oncology and Hematology, Fondazione IRCCS Istituto Nazionale dei Tumori di Milano (S. Manoukian), the Genome Diagnostics Program, FIRC Institute of Molecular Oncology (P.P.), and the Unit of Molecular Bases of Genetic Risk and Genetic Testing, Department of Research, Fondazione IRCCS Istituto Nazionale dei Tumori (P.R.), Milan; the Department of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital-Radiumhospitalet (A.-L.B.-D., G.I.G.A., V.N.K.), and the Institute of Clinical Medicine, Faculty of Medicine, University of Oslo (A.-L.B.-D., V.N.K.), Oslo; Medical Faculty, Universidad de La Sabana (I.B.), and the Clinical Epidemiology and Biostatistics Department (F.G.) and Institute of Human Genetics (D.T.), Pontificia Universidad Javeriana, Bogota, Colombia; the Department of Internal Medicine and Huntsman Cancer Institute, University of Utah (N.J.C., M.J.M., J.A.W.), and the Intermountain Healthcare Biorepository and Department of Pathology, Intermountain Healthcare (M.H.C.), Salt Lake City; the David Geffen School of Medicine, Department of Medicine Division of Hematology and Oncology, University of California, Los Angeles (P.A.F.), and Moores Cancer Center (M.G.-D., M.E.M.) and the Department of Family Medicine and Public Health (M.E.M.), University of California San Diego, La Jolla; the Departments of Medical Oncology (V.G., D.M.) and Pathology (M.T.), University Hospital of Heraklion, Heraklion, and the Department of Oncology, University Hospital of Larissa, Larissa (E.S.) - both in Greece; the Fred A. Litwin Center for Cancer Genetics, Lunenfeld-Tanenbaum Research Institute of Mount Sinai Hospital (G.G., I.L.A.), the Departments of Laboratory Medicine and Pathobiology (A.M.M.) and Molecular Genetics (I.L.A.), University of Toronto, and the Laboratory Medicine Program, University Health Network (A.M.M.), Toronto, and the Genomics Center, Centre Hospitalier Universitaire de Québec-Université Laval Research Center, Québec City, QC (J.S.) - both in Canada; the Department of Electron Microscopy and Molecular Pathology (A. Hadjisavvas, K.K., M.A.L.), the Cyprus School of Molecular Medicine (A. Hadjisavvas, K.K., M.A.L., K. Michailidou), and the Biostatistics Unit (K. Michailidou), Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus; the Saw Swee Hock School of Public Health (M. Hartman, R.M.V.D.) and the Department of Medicine, Yong Loo Lin School of Medicine (R.M.V.D.), National University of Singapore, the Department of Surgery, National University Health System (M. Hartman, J. Li), and the Human Genetics Division, Genome Institute of Singapore (J. Li), Singapore; the Department of Mathematical Sciences, Faculty of Science and Engineering, University of Nottingham Malaysia (W.K.H.), and the Breast Cancer Research Programme, Cancer Research Malaysia (W.K.H., P.S.N., S.-Y.Y., S.H.T.), Selangor, and the Breast Cancer Research Unit, Cancer Research Institute (N.A.M.T.), and the Department of Surgery, Faculty of Medicine (N.A.M.T., P.S.N., S.H.T.), University Malaya, Kuala Lumpur - both in Malaysia; Surgery, School of Medicine, National University of Ireland, Galway (M.J.K., N. Miller); the Department of Surgery, Daerim Saint Mary's Hospital (S.-W.K.), the Department of Surgery, Ulsan University College of Medicine and Asan Medical Center (J.W.L.), the Department of Surgery, Soonchunhyang University College of Medicine and Soonchunhyang University Hospital (M.H.L.), Integrated Major in Innovative Medical Science, Seoul National University College of Medicine (S.K.P.), and the Cancer Research Institute, Seoul National University (S.K.P.), Seoul, South Korea; the Department of Basic Sciences, Shaukat Khanum Memorial Cancer Hospital and Research Center, Lahore, Pakistan (M.U.R.); and the National Cancer Institute, Ministry of Public Health, Nonthaburi, Thailand (S.T.).

Background: Genetic testing for breast cancer susceptibility is widely used, but for many genes, evidence of an association with breast cancer is weak, underlying risk estimates are imprecise, and reliable subtype-specific risk estimates are lacking.

Methods: We used a panel of 34 putative susceptibility genes to perform sequencing on samples from 60,466 women with breast cancer and 53,461 controls. In separate analyses for protein-truncating variants and rare missense variants in these genes, we estimated odds ratios for breast cancer overall and tumor subtypes. We evaluated missense-variant associations according to domain and classification of pathogenicity.

Results: Protein-truncating variants in 5 genes (, , , , and ) were associated with a risk of breast cancer overall with a P value of less than 0.0001. Protein-truncating variants in 4 other genes (, , , and ) were associated with a risk of breast cancer overall with a P value of less than 0.05 and a Bayesian false-discovery probability of less than 0.05. For protein-truncating variants in 19 of the remaining 25 genes, the upper limit of the 95% confidence interval of the odds ratio for breast cancer overall was less than 2.0. For protein-truncating variants in and , odds ratios were higher for estrogen receptor (ER)-positive disease than for ER-negative disease; for protein-truncating variants in , , , , , and , odds ratios were higher for ER-negative disease than for ER-positive disease. Rare missense variants (in aggregate) in , , and were associated with a risk of breast cancer overall with a P value of less than 0.001. For , , and , missense variants (in aggregate) that would be classified as pathogenic according to standard criteria were associated with a risk of breast cancer overall, with the risk being similar to that of protein-truncating variants.

Conclusions: The results of this study define the genes that are most clinically useful for inclusion on panels for the prediction of breast cancer risk, as well as provide estimates of the risks associated with protein-truncating variants, to guide genetic counseling. (Funded by European Union Horizon 2020 programs and others.).
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http://dx.doi.org/10.1056/NEJMoa1913948DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7611105PMC
February 2021

Young-onset colorectal cancer risk among individuals with iron-deficiency anaemia and haematochezia.

Gut 2020 Dec 18. Epub 2020 Dec 18.

Department of Medicine, Division of Gastroenterology, University of California San Diego, La Jolla, California, USA

Objective: Young-onset colorectal cancer (YCRC) incidence is rising. Scant data exist on YCRC risk after presentation with concerning symptoms such as iron-deficiency anaemia (IDA) or haematochezia. We examined the association between IDA and YCRC, and haematochezia and YCRC.

Design: Cohort study of US Veterans aged 18-49 years receiving Veterans Health Administration (VHA) care 1999-2016. IDA analytic cohort was created matching individuals without incident IDA to those with IDA 4:1 based on sex, birth year and first VHA visit date (n=239 000). We used this approach to also create a distinct haematochezia analytic cohort (n=653 740). Incident YCRC was ascertained via linkage to cancer registry and/or cause-specific mortality data. We computed cumulative incidence, risk difference (RD) and HRs using Cox models in each cohort.

Results: Five-year YCRC cumulative incidence was 0.45% among individuals with IDA versus 0.05% without IDA (RD: 0.39%, 95% CI: 0.33%-0.46%), corresponding to an HR of 10.81 (95% CI: 8.15-14.33). Comparing IDA versus no IDA, RD was 0.78% for men (95% CI: 0.64%-0.92%) and 0.08% for women (95% CI: 0.03%-0.13%), and RD increased by age from 0.14% for <30 years to 0.53% for 40-49 years. YCRC cumulative incidence was 0.33% among individuals with haematochezia versus 0.03% without haematochezia (RD: 0.30%, 95% CI: 0.26%-0.33%), corresponding to an HR of 10.66 (95% CI: 8.76-12.97). Comparing haematochezia versus no haematochezia, RD increased by age from 0.04% for <30 years to 0.43% for 40-49 years.

Conclusion: Colonoscopy should be strongly considered in adults aged <50 years with IDA or haematochezia without a clinically confirmed alternate source.
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http://dx.doi.org/10.1136/gutjnl-2020-321849DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8284839PMC
December 2020

The dual pandemic of COVID-19 and systemic inequities in US Latino communities.

Cancer 2021 05 6;127(10):1548-1550. Epub 2021 Jan 6.

Department of Biochemistry and Molecular Medicine, School of Medicine, University of California Davis, Sacramento, California.

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http://dx.doi.org/10.1002/cncr.33401DOI Listing
May 2021

Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction.

Nat Genet 2021 01 4;53(1):65-75. Epub 2021 Jan 4.

Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria, Australia.

Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction.
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http://dx.doi.org/10.1038/s41588-020-00748-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8148035PMC
January 2021

Author Correction: Neutrophil to lymphocyte ratio and breast cancer risk: analysis by subtype and potential interactions.

Sci Rep 2020 Nov 20;10(1):20641. Epub 2020 Nov 20.

Oncology and Genetics Unit, Instituto de Investigación Sanitaria Galicia Sur, Vigo, Spain.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.
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http://dx.doi.org/10.1038/s41598-020-75458-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680152PMC
November 2020

Association Between African American Race and Clinical Outcomes in Men Treated for Low-Risk Prostate Cancer With Active Surveillance.

JAMA 2020 11;324(17):1747-1754

VHA San Diego Health Care System, La Jolla, California.

Importance: There is concern that African American men with low-risk prostate cancer may harbor more aggressive disease than non-Hispanic White men. Therefore, it is unclear whether active surveillance is a safe option for African American men.

Objective: To compare clinical outcomes of African American and non-Hispanic White men with low-risk prostate cancer managed with active surveillance.

Design, Setting, And Participants: Retrospective cohort study in the US Veterans Health Administration Health Care System of African American and non-Hispanic White men diagnosed with low-risk prostate cancer between January 1, 2001, and December 31, 2015, and managed with active surveillance. The date of final follow-up was March 31, 2020.

Exposures: Active surveillance was defined as no definitive treatment within the first year of diagnosis and at least 1 additional surveillance biopsy.

Main Outcomes And Measures: Progression to at least intermediate-risk, definitive treatment, metastasis, prostate cancer-specific mortality, and all-cause mortality.

Results: The cohort included 8726 men, including 2280 African American men (26.1%) (median age, 63.2 years) and 6446 non-Hispanic White men (73.9%) (median age, 65.5 years), and the median follow-up was 7.6 years (interquartile range, 5.7-9.9; range, 0.2-19.2). Among African American men and non-Hispanic White men, respectively, the 10-year cumulative incidence of disease progression was 59.9% vs 48.3% (difference, 11.6% [95% CI, 9.2% to 13.9%); P < .001); of receipt of definitive treatment, 54.8% vs 41.4% (difference, 13.4% [95% CI, 11.0% to 15.7%]; P < .001); of metastasis, 1.5% vs 1.4% (difference, 0.1% [95% CI, -0.4% to 0.6%]; P = .49); of prostate cancer-specific mortality, 1.1% vs 1.0% (difference, 0.1% [95% CI, -0.4% to 0.6%]; P = .82); and of all-cause mortality, 22.4% vs 23.5% (difference, 1.1% [95% CI, -0.9% to 3.1%]; P = 0.09).

Conclusions And Relevance: In this retrospective cohort study of men with low-risk prostate cancer followed up for a median of 7.6 years, African American men, compared with non-Hispanic White men, had a statistically significant increased 10-year cumulative incidence of disease progression and definitive treatment, but not metastasis or prostate cancer-specific mortality. Longer-term follow-up is needed to better assess the mortality risk.
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http://dx.doi.org/10.1001/jama.2020.17020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7610194PMC
November 2020

The Intrinsic Activity of Thyroxine Is Critical for Survival and Growth and Regulates Gene Expression in Neonatal Liver.

Thyroid 2021 03 16;31(3):528-541. Epub 2020 Sep 16.

Maine Medical Center Research Institute, MaineHealth, Scarborough, Maine, USA.

Thyroxine (T4) is generally considered to be a prohormone that requires conversion to triiodothyronine (T3) to exert biological activity. Although evidence suggests that T4 has intrinsic activity, it is questionable if this activity has any physiological relevance. To answer this question, triple knockout (KO) mice (Triples) that cannot express the types 1 (D1) and 2 (D2) deiodinase and the genes were generated. Thus, they lack a thyroid and cannot convert T4 to T3. Triples were injected on alternate days with either vehicle or physiological doses of T4, T3, or T3+T4 from postnatal days 2-14. They were euthanized at P15, and RNA-seq was employed to profile gene expression in the liver. In another experiment, KO mice were injected with T3, T4, or T4+T3, and growth rate and survival to P84 were determined. The growth retardation of Triples was not improved by either T3 or T4 alone but was significantly improved by T4+T3. In the liver, T4 significantly regulated the expression of genes that were also regulated by T3, but the proportion of genes that were negatively regulated was higher in mice treated with T4 than in mice treated with T3. Treatment with T4+T3 identified genes that were regulated synergistically by T3 and T4, and genes that were regulated only by T4+T3. Analysis of these genes revealed enrichment in mechanisms related to cell proliferation and cholesterol physiology, suggesting a unique contribution of T4 to these biological functions. KO mice all survived to P84 when injected with T4 or T4+T3. However, survival rate with T3 was only 50% and 10% at 3.5 and 12 weeks of life, respectively. T4 has intrinsic activity and is critical for survival and growth. At a physiological level, T4 can upregulate or downregulate many T3 target genes in the neonatal liver. While most of these genes are also regulated by T3, subsets respond exclusively to T4 or demonstrate enhanced or normalized expression only in the presence of both hormones. These studies demonstrate for the first time a complex dependency on both T4 and T3 for normal mammalian growth and development.
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http://dx.doi.org/10.1089/thy.2020.0508DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7994419PMC
March 2021

The COVID-19 Pandemic: Identifying Adaptive Solutions for Colorectal Cancer Screening in Underserved Communities.

J Natl Cancer Inst 2021 08;113(8):962-968

Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.

The 2019 novel coronavirus disease (COVID-19) pandemic has dramatically impacted numerous health and economic fronts. Because of the stay-at-home mandate and practice of physical distancing, nearly all preventive care measures have been halted, including colorectal cancer (CRC) screening. The health consequences of this temporary suspension are of great concern, particularly for underserved populations, who experience substantial CRC-related disparities. In this commentary, we describe challenges and opportunities to deliver COVID-19-adapted CRC screening to medically underserved populations receiving care in community health centers (CHC). This perspective is based on key informant interviews with CHC medical directors, teleconference discussions, and strategic planning assessments. To address the unprecedented challenges created by the COVID-19 pandemic, we identify 2 broad calls to action: invest in CHCs now and support equitable and adaptable telehealth solutions now and in the future. We also recommend 4 CRC-specific calls to action: establish COVID-19-adapted best practices to implement mailed fecal immunochemical test programs, implement grassroots advocacy to identify community gastroenterologists who commit to performing colonoscopies for CHC patients, assess cancer prevention priorities among individuals in underserved communities, and assess regional CRC screening and follow-up barriers and solutions. The COVID-19 pandemic may further exacerbate existing CRC screening disparities in underserved individuals. This will likely lead to delayed diagnosis, a shift to later-stage disease, and increased CRC deaths. To prevent this from happening, we call for timely action and a commitment to address the current extraordinary CRC screening challenges for vulnerable populations.
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http://dx.doi.org/10.1093/jnci/djaa117DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7454700PMC
August 2021

Population-Based Analysis of Differences in Gastric Cancer Incidence Among Races and Ethnicities in Individuals Age 50 Years and Older.

Gastroenterology 2020 11 6;159(5):1705-1714.e2. Epub 2020 Aug 6.

Greater Bay Area Cancer Registry, University of California San Francisco, San Francisco, California; Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, California.

Background & Aims: There are racial and ethnic differences in the incidence of gastric adenocarcinoma worldwide and in the US. Based on a decision analysis, screening for noncardia gastric adenocarcinoma might be cost-effective for non-White individuals 50 years or older. However, a lack of precise, contemporary information on gastric adenocarcinoma incidence in specific anatomic sites for this age group has impeded prevention and early detection programs in the US. We aimed to estimate the differences in gastric adenocarcinoma incidence in specific anatomic sites among races and ethnicities in individuals 50 years or older.

Methods: We analyzed California Cancer Registry data from 2011 through 2015 to estimate incidences of gastric adenocarcinoma in specific anatomic sites for non-Hispanic White (NHW), non-Hispanic Black, Hispanic, and the 7 largest Asian American populations. We calculated the differential incidence between non-White groups and NHW using incidence rate ratios and 95% confidence intervals (CIs).

Results: Compared with NHW subjects, all non-White groups had significantly higher incidences of noncardia gastric adenocarcinoma; the incidence was highest among Korean American men 50 years and older (70 cases per 100,000). Compared with NHW subjects 50 years and older, the risk of noncardia gastric adenocarcinoma was 1.8-fold (95% CI, 1.37-2.31) to 7.3-fold (95% CI, 5.73-9.19) higher in most non-White groups and 12.0-fold (95% CI, 9.96-14.6) to 14.5-fold (95% CI, 12.5-16.9) higher among Korean American men and women 50 years and older, respectively. Compared with NHW men 50 years and older, all non-White men, except Japanese and Korean American men, had a significantly lower risk of cardia gastric adenocarcinoma.

Conclusions: We identified several-fold differences in incidences of gastric adenocarcinoma in specific anatomic sites among racial and ethnic groups, with significant age and sex differences. These findings can be used to develop targeted risk reduction programs for gastric adenocarcinoma.
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http://dx.doi.org/10.1053/j.gastro.2020.07.049DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680373PMC
November 2020

Neutrophil to lymphocyte ratio and breast cancer risk: analysis by subtype and potential interactions.

Sci Rep 2020 08 6;10(1):13203. Epub 2020 Aug 6.

Oncology and Genetics Unit, Instituto de Investigación Sanitaria Galicia Sur, Vigo, Spain.

Multiple studies have found the neutrophil to lymphocyte ratio (NLR) to be associated with adverse breast cancer (BC) prognosis and survival. Very limited data exist on the role of NLR and risk of BC. The BREOGAN study is a population-based case-control study conducted in Galicia, Spain. We examined the WBC- and NLR-BC relationships. The risk of BC increased with increasing levels of neutrophils percentage (NE%) (multivariable OR for the highest category (95% CI) = 2.14 (1.39-3.32), P-trend < 0.001) and of the NLR (multivariable OR for the highest category (95% CI) = 1.93 (1.26-2.97), P-trend < 0.001). Lymphocytes absolute (L#) and percentage (L%) were associated with a decreased risk of BC (multivariable OR for the highest category (95% CI) = 0.54 (0.35-0.83), and 0.51 (0.33-0.79), P-trend = 0.001 and < 0.001, respectively). The NLR-BC association was more pronounced among Luminal A BC (multivariable OR for the highest category (95% CI) = 2.00 (1.17-3.45), P-trend < 0.001), HER2-negative BC (multivariable OR for the highest category (95% CI) = 1.87 (1.16-3.02), P-trend < 0.001), and those with high total cholesterol and low HO levels.
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http://dx.doi.org/10.1038/s41598-020-70077-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7413522PMC
August 2020

Mental Health Outcomes in Adolescent and Young Adult Female Cancer Survivors of a Sexual Minority.

J Adolesc Young Adult Oncol 2021 04 27;10(2):148-155. Epub 2020 Jul 27.

Department of Obstetrics, Gynecology, & Reproductive Science and Moores Cancer Center, University of California, San Diego, La Jolla, California, USA.

Sexual minority (SM) individuals experience higher rates of anxiety and depression. Previous research on mental health disparities for SM cancer survivors has largely focused on adult survivors; however, studies are limited in the adolescent and young adult (AYA) population. This study's objective is to compare depression and anxiety symptoms between AYA, female cancer survivors who identify as an SM and those who identify as heterosexual. A cross-sectional analysis of 1025 AYA survivors aged 18-40 years (2015-2017) was performed. Patients self-reported SM identification and depression and anxiety symptoms, as measured by the Patient Health Questionnaire (PHQ8) and Generalized Anxiety Disorder Scale (GAD7), respectively. Multivariable logistic regression tested associations between SM identification and depression and anxiety. Sixty-four participants (6%) identified as an SM. In adjusted analyses, SM participants had 1.88 higher odds of anxiety (odds ratio [OR] 1.88, confidence interval [95% CI] 1.05-3.35,  = 0.033) compared with heterosexual participants. SM participants did not have significantly higher odds of depression (OR 1.36, CI 0.75-2.47,  = 0.31). More social support was significantly associated with lower odds of depression (OR 0.91, CI 0.89-0.93,  < 0.001) and anxiety (OR 0.93, CI 0.91-0.94,  < 0.001). AYA cancer survivors identifying as an SM had nearly twice the odds of anxiety, with social support that is protective for both anxiety and depression. While mental health screening is recommended throughout the cancer care continuum, these data support the need for reliable screening, clinician awareness of increased vulnerability in the AYA, SM survivor population, and clinician training on culturally competent care and generation of evidence-based interventions.
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http://dx.doi.org/10.1089/jayao.2020.0082DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8064930PMC
April 2021

Genome-wide association study identifies 32 novel breast cancer susceptibility loci from overall and subtype-specific analyses.

Nat Genet 2020 06 18;52(6):572-581. Epub 2020 May 18.

Molecular Medicine Unit, Fundación Pública Galega de Medicina Xenómica, Santiago de Compostela, Spain.

Breast cancer susceptibility variants frequently show heterogeneity in associations by tumor subtype. To identify novel loci, we performed a genome-wide association study including 133,384 breast cancer cases and 113,789 controls, plus 18,908 BRCA1 mutation carriers (9,414 with breast cancer) of European ancestry, using both standard and novel methodologies that account for underlying tumor heterogeneity by estrogen receptor, progesterone receptor and human epidermal growth factor receptor 2 status and tumor grade. We identified 32 novel susceptibility loci (P < 5.0 × 10), 15 of which showed evidence for associations with at least one tumor feature (false discovery rate < 0.05). Five loci showed associations (P < 0.05) in opposite directions between luminal and non-luminal subtypes. In silico analyses showed that these five loci contained cell-specific enhancers that differed between normal luminal and basal mammary cells. The genetic correlations between five intrinsic-like subtypes ranged from 0.35 to 0.80. The proportion of genome-wide chip heritability explained by all known susceptibility loci was 54.2% for luminal A-like disease and 37.6% for triple-negative disease. The odds ratios of polygenic risk scores, which included 330 variants, for the highest 1% of quantiles compared with middle quantiles were 5.63 and 3.02 for luminal A-like and triple-negative disease, respectively. These findings provide an improved understanding of genetic predisposition to breast cancer subtypes and will inform the development of subtype-specific polygenic risk scores.
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http://dx.doi.org/10.1038/s41588-020-0609-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7808397PMC
June 2020

Sugar-Sweetened Beverage Intake and Cardiovascular Disease Risk in the California Teachers Study.

J Am Heart Assoc 2020 05 13;9(10):e014883. Epub 2020 May 13.

Department of Family Medicine and Public Health School of Medicine University of California San Diego La Jolla CA.

Background Sugar-sweetened beverage (SSB) consumption has been associated with cardiometabolic risk. However, the association between total and type of SSB intake and incident cardiovascular disease (CVD) end points such as myocardial infarction, stroke, and revascularization is limited. Methods and Results We examined the prospective association of baseline SSB consumption with incident CVD in 106 178 women free from CVD and diabetes mellitus in the CTS (California Teachers Study), a cohort of female teachers and administrators, followed since 1995. SSBs were defined as caloric soft drinks, sweetened bottled waters or teas, and fruit drinks, and derived from a self-administered food frequency questionnaire. CVD end points were based on annual linkage with statewide inpatient hospitalization records. Cox proportional hazards models were used to assess the association between SSB consumption and incident CVD. A total of 8848 CVD incident cases were documented over 20 years of follow-up. After adjusting for potential confounders, we observed higher hazard ratios (HRs) for CVD (HR, 1.19; 95% CI, 1.06-1.34), revascularization (HR, 1.26; 95% CI, 1.04-1.54]), and stroke (HR, 1.21; 95% CI, 1.04-1.41) in women who consumed ≥1 serving per day of SSBs compared with rare/never consumers. We also observed a higher risk of CVD in women who consumed ≥1 serving per day of fruit drinks (HR, 1.42; 95% CI, 1.00-2.01 [ trend=0.021]) and caloric soft drinks (HR, 1.23; 95% CI, 1.05-1.44 [ trend=0.0002]), compared with rare/never consumers. Conclusions Consuming ≥1 serving per day of SSB was associated with CVD, revascularization, and stroke. SSB intake might be a modifiable dietary target to reduce risk of CVD among women.
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http://dx.doi.org/10.1161/JAHA.119.014883DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7660873PMC
May 2020

The COronavirus Pandemic Epidemiology (COPE) Consortium: A Call to Action.

Cancer Epidemiol Biomarkers Prev 2020 07 5;29(7):1283-1289. Epub 2020 May 5.

Social & Scientific Systems, Durham, North Carolina.

The rapid pace of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; COVID-19) pandemic presents challenges to the real-time collection of population-scale data to inform near-term public health needs as well as future investigations. We established the COronavirus Pandemic Epidemiology (COPE) consortium to address this unprecedented crisis on behalf of the epidemiology research community. As a central component of this initiative, we have developed a COVID Symptom Study (previously known as the COVID Symptom Tracker) mobile application as a common data collection tool for epidemiologic cohort studies with active study participants. This mobile application collects information on risk factors, daily symptoms, and outcomes through a user-friendly interface that minimizes participant burden. Combined with our efforts within the general population, data collected from nearly 3 million participants in the United States and United Kingdom are being used to address critical needs in the emergency response, including identifying potential hot spots of disease and clinically actionable risk factors. The linkage of symptom data collected in the app with information and biospecimens already collected in epidemiology cohorts will position us to address key questions related to diet, lifestyle, environmental, and socioeconomic factors on susceptibility to COVID-19, clinical outcomes related to infection, and long-term physical, mental health, and financial sequalae. We call upon additional epidemiology cohorts to join this collective effort to strengthen our impact on the current health crisis and generate a new model for a collaborative and nimble research infrastructure that will lead to more rapid translation of our work for the betterment of public health.
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http://dx.doi.org/10.1158/1055-9965.EPI-20-0606DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7357669PMC
July 2020

Combined Associations of a Polygenic Risk Score and Classical Risk Factors With Breast Cancer Risk.

J Natl Cancer Inst 2021 03;113(3):329-337

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

We evaluated the joint associations between a new 313-variant PRS (PRS313) and questionnaire-based breast cancer risk factors for women of European ancestry, using 72 284 cases and 80 354 controls from the Breast Cancer Association Consortium. Interactions were evaluated using standard logistic regression and a newly developed case-only method for breast cancer risk overall and by estrogen receptor status. After accounting for multiple testing, we did not find evidence that per-standard deviation PRS313 odds ratio differed across strata defined by individual risk factors. Goodness-of-fit tests did not reject the assumption of a multiplicative model between PRS313 and each risk factor. Variation in projected absolute lifetime risk of breast cancer associated with classical risk factors was greater for women with higher genetic risk (PRS313 and family history) and, on average, 17.5% higher in the highest vs lowest deciles of genetic risk. These findings have implications for risk prevention for women at increased risk of breast cancer.
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http://dx.doi.org/10.1093/jnci/djaa056DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7936056PMC
March 2021

Potential impact of family history-based screening guidelines on the detection of early-onset colorectal cancer.

Cancer 2020 07 20;126(13):3013-3020. Epub 2020 Apr 20.

Moores Cancer Center, University of California at San Diego, La Jolla, California.

Background: Initiating screening at an earlier age based on cancer family history is one of the primary recommended strategies for the prevention and detection of early-onset colorectal cancer (EOCRC), but data supporting the effectiveness of this approach are limited. The authors assessed the performance of family history-based guidelines for identifying individuals with EOCRC.

Methods: The authors conducted a population-based, case-control study of individuals aged 40 to 49 years with (2473 individuals) and without (772 individuals) incident CRC in the Colon Cancer Family Registry from 1998 through 2007. They estimated the sensitivity and specificity of family history-based criteria jointly recommended by the American Cancer Society, the US Multi-Society Task Force on CRC, and the American College of Radiology in 2008 for early screening, and the age at which each participant could have been recommended screening initiation if these criteria had been applied.

Results: Family history-based early screening criteria were met by approximately 25% of cases (614 of 2473 cases) and 10% of controls (74 of 772 controls), with a sensitivity of 25% and a specificity of 90% for identifying EOCRC cases aged 40 to 49 years. Among 614 individuals meeting early screening criteria, 98.4% could have been recommended screening initiation at an age younger than the observed age of diagnosis.

Conclusions: Of CRC cases aged 40 to 49 years, 1 in 4 met family history-based early screening criteria, and nearly all cases who met these criteria could have had CRC diagnosed earlier (or possibly even prevented) if earlier screening had been implemented as per family history-based guidelines. Additional strategies are needed to improve the detection and prevention of EOCRC for individuals not meeting family history criteria for early screening.
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http://dx.doi.org/10.1002/cncr.32851DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7702222PMC
July 2020

Age-related differences in breast cancer mortality according to race/ethnicity, insurance, and socioeconomic status.

BMC Cancer 2020 Mar 17;20(1):228. Epub 2020 Mar 17.

Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.

Background: We assessed breast cancer mortality in older versus younger women according to race/ethnicity, neighborhood socioeconomic status (nSES), and health insurance status.

Methods: The study included female breast cancer cases 18 years of age and older, diagnosed between 2005 and 2015 in the California Cancer Registry. Multivariable Cox proportional hazards modeling was used to generate hazard ratios (HR) of breast cancer specific deaths and 95% confidence intervals (CI) for older (60+ years) versus younger (< 60 years) patients separately by race/ethnicity, nSES, and health insurance status.

Results: Risk of dying from breast cancer was higher in older than younger patients after multivariable adjustment, which varied in magnitude by race/ethnicity (P-interaction< 0.0001). Comparing older to younger patients, higher mortality differences were shown for non-Hispanic White (HR = 1.43; 95% CI, 1.36-1.51) and Hispanic women (HR = 1.37; 95% CI, 1.26-1.50) and lower differences for non-Hispanic Blacks (HR = 1.17; 95% CI, 1.04-1.31) and Asians/Pacific Islanders (HR = 1.15; 95% CI, 1.02-1.31). HRs comparing older to younger patients varied by insurance status (P-interaction< 0.0001), with largest mortality differences observed for privately insured women (HR = 1.51; 95% CI, 1.43-1.59) and lowest in Medicaid/military/other public insurance (HR = 1.18; 95% CI, 1.10-1.26). No age differences were shown for uninsured women. HRs comparing older to younger patients were similar across nSES strata.

Conclusion: Our results provide evidence for the continued disparity in Black-White breast cancer mortality, which is magnified in younger women. Moreover, insurance status continues to play a role in breast cancer mortality, with uninsured women having the highest risk for breast cancer death, regardless of age.
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http://dx.doi.org/10.1186/s12885-020-6696-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7076958PMC
March 2020
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