PURPOSE:Breast cancer survivors are at elevated risk of multiple new primary cancers compared with the general population. The impact of multicancer screening on late-stage cancer diagnosis is under clinical investigation in average-risk individuals, but it is unclear whether findings will generalize to breast cancer survivors. METHODS:We adapted an existing multicancer natural history model for the average-risk US population to reflect increased risks of second primary cancers and all-cause mortality among female breast cancer survivors. We modeled 16 cancer types other than breast cancer and specified a range of natural history parameters and screening test sensitivities to reflect uncertainty in disease onset, progression, and detectability of target cancers. We evaluated annual multicancer screening over a lifetime horizon in simulated hormone receptor-positive (HR-positive) and hormone receptor-negative (HR-negative) cohorts of survivors age 50-74 years and in age-matched women without prior cancer (average-risk women). Outcomes included absolute and relative reductions in late-stage diagnoses compared with no multicancer screening. RESULTS:Across a range of natural histories and test sensitivities, multicancer screening was projected to reduce 35-99 late-stage diagnoses per 100,000 person-years (PY; 9%-25% reduction) among HR-positive survivors and 39-111 per 100,000 PY (9%-26% reduction) among HR-negative survivors, compared with 30-84 per 100,000 PY (7%-20% reduction) among average-risk women. Lung cancer contributed most to the reduction in late-stage diagnoses (34%-38%), followed by colorectal cancer (14%-16%) in all populations. Ovarian cancer accounted for greater reduction in HR-negative than HR-positive survivors (10%-11% v 6%). CONCLUSION:Model-based projections suggest that multicancer screening may reduce late-stage diagnoses among breast cancer survivors more than among average-risk women. This suggests a potential role in long-term surveillance for second primary cancers in this high-risk population.

BACKGROUND:Bisphosphonates (BPs) are routinely used as an adjuvant therapy for breast cancer to reduce the risk of bone recurrences given their anti-resorptive effects on bones and antitumor characteristics. However, there remains limited evidence regarding their utility across different subtypes. METHODS:In this population-based cohort study, the authors assessed the effects of pre- and post-diagnostic BP use on recurrence, any second breast cancer event, all-cause mortality (ACM), and breast cancer-specific mortality (BCSM) using multivariable-adjusted Cox proportional hazards models among hormone receptor-positive (HR+) and triple-negative breast cancer (TNBC) participants. RESULTS:This study enrolled 2260 HR+ and 1436 TNBC participants. The median age and follow-up time to death was 51 and 52 years old and 168.3 and 147 months in the two subtypes, respectively. Post-diagnostic BP use for at least 1 year was protective for ACM (hazard ratio [HR], 0.67; 95% confidence interval [CI], 0.49-0.93) and BCSM (HR, 0.54; 95% CI, 0.33-0.89) compared to never users in HR+ cases. Among participants who initiated BP after diagnosis only, a lower point estimates on the clinical outcomes were observed across both subtypes, reaching statistical significance for BCSM (HR, 0.62; 95% CI, 0.39-0.98) in HR+ cases. Among TNBC cases who continued BP use post-diagnosis, increased risks of recurrence (HR, 3.43; 95% CI, 1.67-7.07) and BCSM (HR, 2.54; 95% CI, 1.24-5.19) were observed. CONCLUSIONS:Although this study confirmed the protective effects of post-diagnostic BP use on risks of mortality among HR+ cases, further studies are required to prove the effects of post-diagnostic BP use among TNBC participants.

Survivors of breast cancer face a substantially increased risk of developing contralateral breast cancer (CBC). We assessed whether risk prediction models for CBC are improved by integrating mammographic density (MD) and polygenic risk scores (PRS). We analyzed data from 399 European-ancestry breast cancer survivors in the WECARE Study, an international, population-based case-control study. Cases were women who developed CBC, and controls were women with unilateral breast cancer (UBC). All participants had genome-wide genotyping and MD measurements at three intensity levels (Cumulus, Altocumulus, and Cirrocumulus) using the CUMULUS software. A weighted PRS was constructed comprised of 64 previously identified genome-wide significant single nucleotide polymorphisms (SNPs) associated with MD (PRS_MD). Linear and logistic regression models were used to assess the associations between PRS_MD, MD measurements, and CBC risk, adjusting for potential confounders. PRS_MD was significantly associated with Cumulus and Altocumulus densities, but not Cirrocumulus. In multivariable-adjusted predictive models, the inclusion of PRS_MD improved adjusted R-squared values for Cumulus (from 20.6% to 22.8%) and Altocumulus (22.7% to 24.7%). However, for Cirrocumulus the PRS_MD was not a significant predictor of CBC risk, with an effect estimate of 0.27 (95% CI: -0.9,1.4; P = 0.69). PRS_MD was not independently associated with CBC risk and adding it to MD models resulted in only small, non‑significant gains in AUC. Exploratory interaction analyses did not indicate that PRS_MD modified the association between MD and CBC risk. MD remains a robust independent predictor of CBC risk. Although PRS_MD captures inherited predisposition to MD, the current PRS explains only a small fraction of MD variance and does not enhance CBC risk prediction beyond measured MD. Further research is needed to elucidate the genetic underpinnings of MD and their relevance to CBC susceptibility.

PURPOSE:Women treated with radiation therapy (RT) for breast cancer have an increased risk of developing radiation-associated contralateral breast cancer (CBC). Predicting CBC events is challenging because of the complex interplay of genomic, treatment, personal, and clinical factors. This study investigated computational methods that integrate genome-wide single-nucleotide polymorphisms and nongenomic data to develop a risk stratification model for developing CBC in women treated with RT for their first primary breast cancer. METHODS AND MATERIALS:This study used a subset of the population-based Women's Environmental Cancer and Radiation Epidemiology study that included 633 CBC cases and 1253 individually matched unilateral breast cancer controls who were treated with RT and had single-nucleotide polymorphism data available from a genome-wide association study. The study population was split into training, validation, and test sets for rigorous modeling and validation. Three data integration methods were compared in terms of their ability to stratify CBC risk: (1) naive integration; (2) sequential integration; and (3) sequential iterative integration. A biological analysis of the final model was performed using gene set enrichment analysis and protein-protein interaction analysis with gene annotation information informed by the model. RESULTS:The best-performing integration method was the sequential iterative integration equipped with the mixed-effect random forest algorithm. This approach achieved an area under the curve of 0.64 to stratify CBC risk in the test set, representing moderate predictive power. Calibration analysis showed good agreement between the lowest and highest risk bins stratified using sorted predicted values in the test set, resulting in an odds ratio of 3.27 for both predicted and observed CBC occurrence. Gene set enrichment analysis and protein-protein interaction analysis revealed that genes with high importance scores were associated with pathways relevant to lipid and fatty acid metabolism as well as breast cancer sensitivity to tamoxifen. CONCLUSIONS:The mixed-effect random forest approach demonstrated the potential for integrating high-dimensional genomic and low-dimensional nongenomic data to stratify CBC risk.

Women with estrogen receptor negative (ER-) contralateral breast cancer (CBC) are 50% more likely to die of CBC compared to women with estrogen receptor positive (ER+) CBC. We comprehensively investigated risk factors for ER subtype-specific CBC using the Women's Environmental Cancer and Radiation Epidemiology Study, a population-based, case-control study of 1521 CBC cases under age 55 years and 2212 individually matched unilateral breast cancer controls. Information about breast cancer risk factors and ER status was obtained by interview and medical record abstraction and common genetic variants with GWAS. Multivariable rate ratios and 95% confidence intervals were estimated using conditional logistic regression models, adjusting for known and suspected risk factors. Among 2800 women where the matched case had known ER CBC status, chemotherapy, hormone therapy, and increasing number of full-term pregnancies were associated with decreased ER+ CBC risk. Drinking, smoking, first breast cancer lobular histology, first-degree breast cancer family history, a polygenic risk score (PRS) of 313 common variants, and an ER+ subtype-specific PRS were associated with increased ER+ CBC risk. More than 2 years of breastfeeding was associated with decreased ER- CBC risk. While none of the PRSs were associated with ER- CBC risk, first- and second-degree family history of breast cancer and second-degree family history of ovarian cancer were associated with increased ER- CBC risk. We identified differential risk factors for ER subtype-specific CBC which can inform individualized risk prediction models for future clinical impact. There remains an unexplained genetic component of ER- CBC.

As breast cancer survival has increased with advances in treatment, there is an increasing number of women at risk of developing a second primary cancer. Smoking is a modifiable behavior associated with increased risk of multiple cancers, however the impact of smoking on the risk of second primary cancers has not yet been explored for breast cancer survivors. Here we evaluated the associations between smoking and risk of the four most common second primary cancers in a population-based case-cohort study. We identified a total of 2630 breast cancer survivors from the Seattle-Puget Sound region including 1930 cases who developed a second primary cancer (602 breast, 621 lung, 300 colorectal, and 307 endometrial) and 800 non-cases who did not develop a second primary cancer. Smoking exposure was assessed by interview at first breast cancer diagnosis and at second cancer diagnosis. Associations between smoking and second primary cancer risk were assessed using multivariable Cox proportional hazards models adjusting for age, year of diagnosis, histology, estrogen receptor status, stage, and confounders that changed estimates by 10%. Smoking at initial breast cancer diagnosis was associated with a second breast cancer, hazard ratio (HR) 2.07 (95% Confidence interval (CI) 1.39 - 3.06); this association did not appear clearly dose dependent. Smoking was associated with subsequent lung cancer, HR 32.69 (21.29 - 50.20). This association was dose-dependent and remained significant after adjusting for radiation treatment for breast cancer HR 1.79 (1.02 - 3.14) for <10 pack-years, HR 10.41 (6.30 - 16.94) for 10-25 pack-years, HR 20.52 (11.75 - 35.83) for 25-40 pack-years, and HR 47.34 (28.37 - 78.99) for 40+ pack-years. Smoking was associated with subsequent colorectal cancer, HR 2.54 (1.42 - 4.54); this association appears to be dose-dependent but did not reach statistical significance due to limited size when dividing by pack-year groups. Smoking appeared to reduce the risk of subsequent endometrial cancer diagnosis, but did not reach statistical significance, HR 0.47 (0.21 - 1.03); this association appears dose-dependent but again did not reach statistical significance with limited subgroup size. These findings suggest that smoking remains an important modifiable risk factor for secondary cancer in breast cancer survivors and have important implications on risk assessment for tailored surveillance and preventative strategies for breast cancer survivors, an estimated 4 million women in the U.S. Asra N. Shaik, David R. Doody, Kathleen E. Malone, Christopher I. Li. Smoking and subsequent primary cancer in breast cancer survivors: A case-cohort study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_2):Abstract nr LB328.

BACKGROUND:Cardiovascular disease is a leading cause of death for long-term breast cancer survivors. We evaluated whether a polygenic risk score for coronary artery disease (CAD-PRS) was associated with the risk of incident CAD for survivors of unilateral or contralateral breast cancer. METHODS:The study included 1307 women with breast cancer first diagnosed at younger than 55 years of age who participated in the Women's Environmental Cancer and Radiation Epidemiology Follow-up Study. The CAD-PRS was based on a PRS developed and validated in a separate population. We modeled the association between incident CAD and the CAD-PRS, adjusting for age, CAD risk factors, first (and second) breast cancer treatment, study recruitment phase, and genetic population stratification. We also explored whether the risk of CAD depended on interactions between the CAD-PRS and cardiotoxic cancer treatment. RESULTS:There were 66 incident CAD diagnoses reported at a median of 16 years after breast cancer diagnosis. Participants with CAD-PRS at or above the median had a 2.48-times increased risk of CAD (95% confidence interval [CI] = 1.44 to 4.29) relative to participants with CAD-PRS below the median. Anthracycline-based chemotherapy was associated with increased CAD risk (hazard ratio [HR] = 2.04, 95% CI = 1.04 to 3.98), and the association was not modified by the CAD-PRS. The association between incident CAD and left-sided radiation therapy (RT) was increased for those with CAD-PRS at or above the median (HR = 2.90, 95% CI = 1.26 to 6.68) but not for those with CAD-PRS below the median (HR = 0.96, 95% CI = 0.32 to 2.88). There was evidence of super-additive interaction between the CAD-PRS and left-sided RT (relative excess risk due to interaction = 2.06, 95% CI = 0.05 to 4.06). CONCLUSION:A genome-wide CAD-PRS was associated with nonfatal CAD risk for long-term breast cancer survivors, providing potential utility for personalized cardiovascular care, particularly after RT.

Supplementary Table 2 presents results for breast cancer recurrence associated with metabolic syndrome and its components by molecular subtype of breast cancer and stratified by age at diagnosis.

Supplementary Table 1 presents the distribution of patient characteristics among those with and without extended follow-up for recurrence.

e22562 Background: With continued advances in treatment, there are an increasing number of breast cancer survivors at risk of developing a second primary cancer. Not much is known about modifiable behaviors such as alcohol use on the risk of second primary cancers in breast cancer survivors. Here we evaluated the associations between alcohol use and risk of the four most common second primary cancers in a population-based case-cohort study. Methods: We identified a total of 2630 breast cancer survivors from the Seattle-Puget Sound region including 1930 cases who developed a second primary cancer (602 breast, 621 lung, 300 colorectal, and 307 endometrial) and 800 non-cases who did not develop a second primary cancer. Alcohol exposure was assessed by interview at first breast cancer diagnosis as never, former or current. Alcohol dose was further classified as heavy use (4 or more drinks a week) or moderate use (< 4 drinks a week). Associations between alcohol use and second primary cancer risk were assessed using multivariable Cox proportional hazards models adjusting for age, year of diagnosis, histology, estrogen receptor status, stage, and confounders that changed estimates by 10%. Results: Ongoing alcohol use at initial breast cancer diagnosis was associated with a more than 2.5-fold increased risk of developing lung cancer [hazard ratio (HR): 2.57, 95% confidence interval (CI): 1.52-4.34]. Former alcohol use also appeared to increase lung cancer risk but did not reach statistical significance (HR: 1.95, 95% CI: 0.97-3.92). The association between ongoing alcohol use and developing lung cancer was not observed to be dose dependent. Ongoing alcohol was associated with a reduced risk of developing endometrial cancer, but the risk estimate was within the limits of chance (HR: 0.69, 95% CI: 0.44-1.06). Former alcohol use was not associated with developing endometrial cancer (HR: 0.96, 95% CI: 0.32-2.90). The protective association between ongoing alcohol use and developing endometrial cancer appeared to be dose dependent (HR for moderate use: 0.92, 95% CI: 0.55-1.55 vs. HR for heavy use: 0.39, 95% CI: CI 0.22- 0.70). Ongoing or former alcohol use at initial breast cancer diagnosis was not associated with risk of developing either a second breast cancer or a subsequent colorectal cancer. Conclusions: These findings suggest that alcohol remains an important modifiable risk factor for specific secondary cancers in breast cancer survivors and have important implications on risk assessment for tailored surveillance and preventative strategies for breast cancer survivors.

Background: We evaluated the association between metabolic syndrome (MetS; obesity plus two metabolic risk factors) and breast cancer outcomes according to molecular subtype.Methods: This population-based prospective cohort consisted of 3,267 women ages 20 to 69 years diagnosed with a first primary invasive breast cancer from 2004 to 2015 in the Seattle-Puget Sound region. Breast cancer was categorized into three subtypes based on estrogen receptor (ER), progesterone receptor, and HER2 expression: luminal (ER+), triple-negative (ER-/progesterone receptor negative/HER2-), and HER2-overexpressing (H2E; ER-/HER2+) subtypes. We used time-varying Cox models to assess the association of prevalent and incident MetS with risks of recurrence, breast cancer-specific mortality (BCSM), and all-cause mortality (ACM).Results: MetS was associated with a greater risk of recurrence [HR, 3.24; 95% confidence interval (CI), 1.13-9.33] and BCSM (HR, 5.34; 95% CI, 2.32-12.31) only for the H2E subtype and greater risks of ACM for luminal (HR, 1.92; 95% CI, 1.37-2.68), H2E (HR, 5.09; 95% CI, 2.51-10.32), and all cases combined (HR, 1.90; 95% CI, 1.42-2.53). We also observed heterogeneity in recurrence and mortality outcomes across specific components of MetS and molecular subtypes.Conclusions: MetS is associated with ACM among women with breast cancer and with BCSM among women with the H2E subtype.Impact: These results highlight the importance of managing comorbidities to decrease the risk for adverse outcomes among breast cancer survivors.

The association between statin use and cancer survival has been investigated in previous studies with conflicting findings. This study aimed to assess the association between statin use following cancer diagnosis and survival in six common cancers using the Surveillance, Epidemiology, and End Results (SEER)-Medicare database. Individuals aged ≥ 66 years diagnosed with prostate cancer, colorectal cancer, lung cancer, bladder cancer, pancreatic cancer, or non-Hodgkin lymphoma (NHL) from 2008 through 2017 were identified. Statin use was defined as two or more statin prescription fills after cancer diagnosis. Time-dependent Cox proportional hazard regression models were used to estimate the association between statin use and cancer-specific mortality for each cancer. This study included 34,618 patients with prostate cancer (median follow-up 4.0 years), 20,579 with colorectal cancer (2.9 years), 20,133 with lung cancer (1.7 years), 6,163 with bladder cancer (2.1 years), 4,538 with pancreatic cancer (0.8 years), and 3,270 with NHL (2.9 years). Statin use post-diagnosis was associated with a reduced risk of cancer-specific mortality in lung cancer (hazard ratio [HR], 0.81; 95

AbstractBackground: This study evaluates the relationship between smoking, alcohol, and breast cancer outcomes according to molecular subtype. Methods: This population-based prospective cohort consisted of 3,876 women ages 20 to 69 diagnosed with a first primary invasive breast cancer from 2004 to 2015 in the Seattle–Puget Sound region. Breast cancer was categorized into three subtypes based on estrogen receptor (ER), progesterone receptor (PR), and HER2 expressions: luminal (ER+), triple-negative (TN; ER−/PR−/HER2−), and HER2-overexpressing (H2E; ER−/HER2+). We fit Cox proportional hazards models to assess the association between alcohol consumption and smoking status at diagnosis and risks of recurrence, breast cancer–specific mortality, and all-cause mortality. Results: Histories of ever smoking [HR, 1.33; 95% confidence interval (CI), 1.01–1.74] and current smoking (HR, 1.59; 95% CI, 1.07–2.35) were associated with greater risk of breast cancer recurrence among TN cases. Smoking was also associated with greater risk of recurrence to bone among all cases and among luminal cases. Elevated risks of breast cancer–specific and all-cause mortality were observed among current smokers across all subtypes. Alcohol use was not positively associated with risk of recurrence or mortality overall; however, TN patients who drank four or more drinks per week had a decreased risk of recurrence (HR, 0.71; 95% CI, 0.51–0.98) and breast cancer–specific mortality (HR, 0.73; 95% CI, 0.55–0.97) compared with non-current drinkers. Conclusions: Patients with breast cancer with a history of smoking at diagnosis have elevated risks of recurrence and mortality. Impact: These findings underscore the need to prioritize smoking cessation among women diagnosed with breast cancer.

ImportanceHeterogeneity in development of estrogen receptor (ER)-specific first primary breast cancer exists due to deleterious germline variants in moderate- to high-penetrance breast cancer susceptibility genes, but it is unknown if these associations occur in ER-specific CBC.ObjectiveTo determine the association of deleterious germline variants in breast cancer susceptibility genes with ER-specific CBC development and whether ER status of the first primary breast cancer modifies these associations.Design, Setting, and ParticipantsThis case-control study included CBC cases and matched unilateral breast cancer controls from The Women’s Environment, Cancer, and Radiation Epidemiology (WECARE) Study, a population-based case-control study. Eligible women were diagnosed between 1985 and 2000 with data and biospecimens collected from 2001 to 2004. Eligible participants were women younger than 55 years at first invasive breast cancer diagnosis. Participants were matched on age, diagnosis year, cancer registry region, and race and ethnicity, and countermatched on radiation treatment. For cases, CBC occurred 1 year or more following first breast cancer diagnosis. Analyses were performed from May to October 2024.ExposuresCHEK2 1100delC and deleterious variants in ATM, BRCA1, and BRCA2.Main Outcome and MeasureDevelopment of CBC, measured as a rate ratio (RR).ResultsA total of 1290 women were included in analysis (median [IQR] age at first diagnosis, 47 [42-51] years). The ER-positive CBC rate for women with deleterious ATM variants was 4 times higher than for women without deleterious ATM variants (RR, 4.84; 95% CI, 1.11-21.08; P = .04); no women with ER-negative CBC carried deleterious ATM variants. The ER-positive CBC rates for women with deleterious variants in BRCA2 or CHEK2 1100delC were 5 to 6 times higher than for women without deleterious variants in BRCA2 or CHEK2 1100delC, respectively (BRCA2: RR, 5.88; 95% CI, 2.61-13.26, P < .001; CHEK2 1100delC: RR, 6.06; 95% CI, 1.26-29.04; P = .02). The ER-negative CBC rate for women with deleterious BRCA1 variants was 26 times higher than for women without deleterious BRCA1 variants (RR, 26.16; 95% CI, 8.01-85.44; P < .001). First primary breast cancer ER status did not modify associations between deleterious variants and ER-specific CBC development.Conclusions and RelevanceIn this case-control study of CBC, deleterious variants in breast cancer susceptibility genes were differentially associated with ER-specific CBC development. Germline variation profile may inform estimates of outcomes for ER-specific CBC subtypes.

Background Contralateral breast cancer (CBC) is the most common second primary cancer diagnosed in breast cancer survivors, yet the understanding of the genetic susceptibility of CBC, particularly with respect to common variants, remains incomplete. This study aimed to investigate the genetic basis of CBC to better understand this malignancy. Findings We performed a genome-wide association analysis in the Women’s Environmental Cancer and Radiation Epidemiology (WECARE) Study of women with first breast cancer diagnosed at age < 55 years including 1161 with CBC who served as cases and 1668 with unilateral breast cancer (UBC) who served as controls. We observed two loci (rs59657211, 9q32, SLC31A2 / FAM225A and rs3815096, 6p22.1, TRIM31 ) with suggestive genome-wide significant associations ( P < 1 × 10 –6 ). We also found an increased risk of CBC associated with a breast cancer-specific polygenic risk score (PRS) comprised of 239 known breast cancer susceptibility single nucleotide polymorphisms (SNPs) (rate ratio per 1-SD change: 1.25; 95% confidence interval 1.14–1.36, P < 0.0001). The protective effect of chemotherapy on CBC risk was statistically significant only among patients with an elevated PRS ( P heterogeneity = 0.04). The AUC that included the PRS and known breast cancer risk factors was significantly elevated. Conclusions The present GWAS identified two previously unreported loci with suggestive genome-wide significance. We also confirm that an elevated risk of CBC is associated with a comprehensive breast cancer susceptibility PRS that is independent of known breast cancer risk factors. These findings advance our understanding of genetic risk factors involved in CBC etiology.

Supplementary Table 2 presents the risk of locoregional and distant breast cancer recurrence and risk of recurrence to bone, lung, and liver associated with smoking status at diagnosis, for luminal, triple-negative (TN), and overall breast cancer

BackgroundPreclinical evidence suggests improved breast cancer survival associated with statin use, but findings from observational studies are conflicting and remain inconclusive. The objective of this study was to assess the association between statin use after cancer diagnosis and cancer outcomes among breast cancer patients.MethodsIn this retrospective cohort study, 38,858 women aged >= 66 years who were diagnosed with localized and regional stage breast cancer from 2008 through 2017 were identified from the linked Surveillance, Epidemiology, and End Results Medicare database. Statin use was ascertained from Medicare Part D pharmacy claims data. Multivariable Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between post-diagnosis statin use and risks of breast cancer recurrence and breast cancer-specific mortality.ResultsOver a median follow-up of 2.9 years for recurrence and 3.7 years for mortality, 1446 women experienced a recurrence, and 2215 died from breast cancer. The mean duration of post-diagnosis statin use was 2.2 years. Statin use post-diagnosis was not associated with recurrence risk (HR, 1.05; 95% CI, 0.91-1.21), but was associated with a reduced risk of cancer-specific mortality (HR, 0.85; 95% CI, 0.75-0.96). The reduction was more pronounced in women with hormone receptor-positive/human epidermal growth factor receptor 2-negative breast cancer (HR, 0.71; 95% CI, 0.57-0.88).ConclusionsThese findings suggest that post-diagnosis statin use is associated with improved cancer-specific survival in women with breast cancer and should be confirmed in randomized trials of statin therapy in breast cancer patients. Statin use after cancer diagnosis is associated with improved cancer survival in a large cohort of elderly women with breast cancer, highlighting the potential of statins as anticancer agents in improving breast cancer outcomes.