JNCI Cancer Spectrum最新文献

{"title":"Tumor localization strategies of multi-cancer early detection tests: a quantitative assessment.","authors":"Christopher Tyson, Kevin H Li, Xiting Cao, James M O'Brien, Elliot K Fishman, Elizabeth K O'Donnell, Carlos Duran, Vijay Parthasarathy, Seema P Rego, Omair A Choudhry, Tomasz M Beer","doi":"10.1093/jncics/pkaf011","DOIUrl":"https://doi.org/10.1093/jncics/pkaf011","url":null,"abstract":"<p><strong>Background: </strong>Multi-cancer early detection (MCED) tests may expand cancer screening. Characterizing diagnostic resolution approaches following positive MCED tests is critical. Two trials employed distinct resolution approaches: a molecular signal to predict tissue of origin (TOO) and an imaging-based diagnostic strategy. This modeling study characterizes diagnostic journeys and impact in a hypothetical population of average risk MCED eligible patients.</p><p><strong>Methods: </strong>A mathematical expression for diagnostic burden was derived using positive predictive value (PPV), molecular TOO localization accuracy, and numbers of procedures associated with each diagnostic outcome. Imaging-based and molecular TOO-informed strategies were compared. Excess lifetime cancer risk due to futile radiation exposure was estimated using organ-specific diagnostic imaging radiation doses.</p><p><strong>Results: </strong>Across all PPVs and localization performances, a molecular TOO strategy resulted in a higher diagnostic burden: 3.6 procedures [SD 0.445] vs 2.6 procedures [SD 0.100] for the imaging strategy. Estimated diagnostic burden was higher for molecular TOO in 95.5% of all PPV and TOO accuracy combinations; ≥79% PPV and 90% accuracy would be required for a molecular TOO-informed strategy to be less burdensome than imaging. The maximum rate of excess cancer incidence from radiation exposure for MCED false positive results (individuals aged 50-84) was 64.6/100,000 (annual testing, 99% specificity), 48.5/100,000 (biennial testing, 98.5% specificity), and 64.6/100,000 (biennial testing, 98% specificity).</p><p><strong>Conclusions: </strong>An imaging-based diagnostic strategy is more efficient than a molecular TOO-informed approach across almost all PPV and TOO accuracy combinations. The use of an imaging-based approach for cancer localization can be efficient and low-risk compared to a molecular-informed approach.</p>","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abdominal visceral and subcutaneous adipose tissue associations with postmenopausal breast cancer incidence.","authors":"Jennifer W Bea, Heather M Ochs-Balcom, Celina I Valencia, Zhao Chen, Robert M Blew, Kimberly E Lind, Bette J Caan, Denise J Roe, Thomas E Rohan, Katherine W Reeves, JoAnn E Manson, Tarah Ballinger, Kerryn W Reding, Shawna Follis, Shelby G Ziller, Andrew O Odegaard","doi":"10.1093/jncics/pkaf007","DOIUrl":"https://doi.org/10.1093/jncics/pkaf007","url":null,"abstract":"<p><strong>Background: </strong>Obesity, classified by body mass index (BMI), is associated with higher postmenopausal breast cancer (BCa) risk. Yet, the associations between abdominal visceral (VAT) and subcutaneous adipose tissue (SAT) with BCa are unclear.</p><p><strong>Methods: </strong>We assessed BCa associations with abdominal VAT and SAT in a prospective cohort of postmenopausal women without a history of cancer and with 27 years follow-up (N = 9950), during which all new cancers were adjudicated. Dual-energy X-ray absorptiometry scans assessed adiposity at baseline, year 3, and year 6. Competing risks multivariable sub-hazard ratios (SHR), with adjustments for sociodemographic, behavioral, reproductive, and anthropometric characteristics, were estimated for baseline and time-dependent associations between VAT, SAT, and incident BCa.</p><p><strong>Results: </strong>Participants averaged 63.3 ± 7.4 years of age and a BMI of 28.20 ± 5.72 kg/m2 at baseline. The models included 738 incident BCa cases (N = 593 invasive; N = 145 in situ). Baseline VAT and SAT area were associated with significantly increased BCa risk, by 36% and 19% respectively. Increasing VAT/SAT ratio was associated with an 8% increase in incident BCa. Time-dependent models produced similar results. VAT and VAT/SAT associated BCa risk was highest for African American/Black women, though not significantly different from other groups. Quartiles (Q) of VAT/SAT were also explored; the SHR for Q4 compared to Q1 was 1.49 (95% CI: 1.18, 1.87).</p><p><strong>Conclusion: </strong>Higher abdominal VAT and SAT are associated with an increased risk of postmenopausal BCa, and VAT/SAT may provide a distinctive risk estimate. Potential racial and ethnic differences require replication in a larger sample.(NCT00000611).</p>","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Outpatient Palliative Care and End-of-Life Care Intensity: Linking Massachusetts Cancer Registry with All-Payer Claims.","authors":"Nancy L Keating, Joel S Weissman, Alexi A Wright, Robert Wolf, Susan Gershman, Richard Knowlton, John Z Ayanian","doi":"10.1093/jncics/pkaf010","DOIUrl":"https://doi.org/10.1093/jncics/pkaf010","url":null,"abstract":"<p><strong>Background: </strong>Early palliative care is associated with better outcomes for patients with advanced-stage cancers. Using a novel data linkage, we assessed outpatient palliative care use before death and its association with end-of-life care intensity and variation across eight provider networks.</p><p><strong>Methods: </strong>We linked Massachusetts Cancer Registry and the All-Payer Claims Database for individuals with commercial insurance, Medicaid or Medicare Advantage diagnosed with colorectal, lung, prostate, and breast cancers from 2010 through 2013 who died by December 31, 2014. We characterized outpatient palliative care visits in the 6 months before death and identified end-of-life hospitalizations, emergency department visits, intensive care unit admissions, chemotherapy, no/late hospice enrollment, and in-hospital deaths. We used logistic regression to assess factors associated with outpatient palliative care and ordinal logistic regression with provider network fixed effects to assess the association of palliative care with a composite measure summing individual end-of-life intensity measures.</p><p><strong>Results: </strong>Among 6,279 decedents, 11.3% had at least one outpatient palliative care visit. Palliative care use varied across provider networks from 6.0% to 19.3%. In adjusted analyses, younger age, longer duration from diagnosis to death, death in 2012-2014 vs. 2010, and provider network were associated with palliative care visits (all P < 0.05). End-of-life care intensity varied across provider networks. Patients with palliative care visits had lower adjusted odds of receiving intensive end-of-life care (adjusted odds ratio (OR) 0.62 per additional measure of end-of-life intensity, 95%CI 0.53, 0.72).</p><p><strong>Conclusions: </strong>Outpatient palliative care use varied substantially among regional provider networks and was associated with less intensive end-of-life care.</p>","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parental loss at age 0-21 and daughters' breast cancer and tumor characteristics.","authors":"Corinna Keeler, Nickilou Y Krigbaum, Barbara Cohn, Piera Cirillo","doi":"10.1093/jncics/pkaf004","DOIUrl":"https://doi.org/10.1093/jncics/pkaf004","url":null,"abstract":"<p><strong>Background: </strong>Adverse events in childhood are linked to cancer risk across the life course, but evidence is lacking regarding parental death during childhood and breast cancer (BrCa) characteristics. We investigated whether parental loss in childhood defines women at higher risk of BrCa incidence and aggressive disease.</p><p><strong>Methods: </strong>The Child Health and Development Studies (CHDS) comprises over 15,000 families who enrolled during mothers' pregnancies between 1959-1967; family members were followed for cancer incidence and cause-specific mortality. We constructed an analytical cohort of all live-born CHDS daughters (N = 9,169), linked to their parents' cause and date of death. We estimated adjusted hazard ratios of incident BrCa, stage at diagnosis, and tumor hormone receptor expression for parental loss in Cox models adjusted for race, maternal BrCa, and paternal age. Generalized linear models estimated associations between breast density and parental loss among a subsample CHDS daughters (N = 610) with available mammography.</p><p><strong>Results: </strong>137 CHDS daughters were diagnosed with BrCa by age 52, and 654 daughters lost one or both parents at age ≤21. Loss of both parents was associated with BrCa incidence [aHR(95%CI)=4.69(1.68,13.04)], late-stage at diagnosis [aHR(95%CI)=9.47(1.38,64.84)], and HER2-positive, PR-negative, and ER-negative tumors. Loss of mother or father was associated with HER2-positive tumors. Breast density in the premenopause window was associated with loss of mother or both parents.</p><p><strong>Conclusion: </strong>Death of one or both parents during childhood was strongly associated with BrCa and aggressive disease. Parental death during childhood could be added to medical histories to indicate counseling regarding prevention and early detection of BrCa.</p>","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Head and Neck Paraganglioma in Pacak-Zhuang Syndrome.","authors":"Jared S Rosenblum, Yasemin Cole, Danielle Dang, Pashayar P Lookian, Hussam Alkaissi, Mayank Patel, Anthony J Cappadona, Abhishek Jha, Nancy Edwards, Danielle R Donahue, Jeeva Munasinghe, Herui Wang, Russell H Knutsen, Alberto S Pappo, Ronald M Lechan, Beth A Kozel, James G Smirniotopoulos, H Jeffrey Kim, Alexander Vortmeyer, Markku Miettinen, John D Heiss, Zhengping Zhuang, Karel Pacak","doi":"10.1093/jncics/pkaf001","DOIUrl":"https://doi.org/10.1093/jncics/pkaf001","url":null,"abstract":"<p><p>Head and neck paragangliomas (HNPGLs) are typically slow-growing, hormonally inactive tumors of parasympathetic paraganglia. Inactivation of prolyl-hydroxylase domain-containing 2 protein causing indirect gain-of-function of hypoxia-inducible factor-2α (HIF-2α), encoded by EPAS1, was recently shown to cause carotid body hyperplasia. We previously described a syndrome with multiple sympathetic paragangliomas caused by direct gain-of-function variants in EPAS1 (Pacak-Zhuang syndrome, PZS) and developed a corresponding mouse model. We evaluated a cohort of patients with PZS (n = 9) for HNPGL by positron emission tomography, magnetic resonance imaging, and computed tomography and measured carotid body size compared to literature reference values. Three patients had imaging consistent with HNPGL, one of which warranted resection and was confirmed on histology. Three additional patients had carotid body enlargement (Z-score > 2.0), and three had carotid artery malformations. Using high resolution ex vivo imaging and histology, we found that nine of ten adult mutant mice had carotid body tumors and six of eight had a paraganglioma on the cranio-caval vein, the murine homologue of the superior vena cava; these were also found in four of five mutant mice at post-natal day 8. These tumors and the one resected from a patient were positive for tyrosine hydroxylase, synaptophysin, and chromogranin A. Brown fat in a resected patient tumor carried the EPAS1 pathogenic variant. These findings 1) suggest HNPGL as a feature of PZS and 2) show that these pathogenic variants are sufficient to cause the development of these tumors, which we believe represents a continuous spectrum of disease starting from hyperplasia.</p>","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rethinking the rise of early onset gastrointestinal cancers: a call to action.","authors":"Benjamin A Weinberg, Caitlin C Murphy, David R Freyer, K Leigh Greathouse, Jan K Blancato, Elena M Stoffel, Julia L Drewes, Anne Blaes, John M Salsman, Y Nancy You, Hannah Arem, Reetu Mukherji, Priyanka Kanth, Xin Hu, Anne Fabrizio, Marion L Hartley, Marios Giannakis, John L Marshall","doi":"10.1093/jncics/pkaf002","DOIUrl":"https://doi.org/10.1093/jncics/pkaf002","url":null,"abstract":"<p><p>Since the early 1990s, there has been a dramatic rise in gastrointestinal cancers diagnosed in patients under age 50 for reasons that remain poorly understood. The most significant change has been the increase in incidence rates of early-onset colorectal cancer, especially rates of left-sided colon and rectal cancers. Increases in gastric, pancreatic, and other gastrointestinal cancer diagnoses have further contributed to this trend. We formed a multidisciplinary Think Tank to develop a strategic, coordinated approach to studying early-onset gastrointestinal cancers. This area of research is challenging given multifactorial etiologies. We focused on epidemiology and the environment, the microbiome, and survivorship as key pillars to structure a research framework. We advocate a comprehensive strategy to 1) utilize existing biospecimens, especially those collected longitudinally, with correlation to exposures (\"the exposome\"), 2) standardize microbiome specimen collection and analyses of blood, tissue, and stool specimens to minimize contamination and biases, 3) prioritize mechanistic studies to evaluate findings from biomarker studies, and 4) explore the unique survivorship needs of this young population. These recommendations build upon prior efforts with the goal of streamlining research into this important field of study while minimizing redundant efforts. We hope that our findings serve as a clarion call to motivate others to discover why young individuals are being diagnosed with gastrointestinal cancers at such an alarming rate and how to best support those who have been diagnosed.</p>","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex Differences in Melanoma Survival-a GEM study.","authors":"Tharani Murali, Matthew Schwartz, Adam Z Reynolds, Li Luo, Grace Ridgeway, Klaus J Busam, Anne E Cust, Hoda Anton-Culver, Richard P Gallagher, Roberto Zanetti, Stefano Rosso, Lidia Sacchetto, Colin B Begg, Irene Orlow, Nancy E Thomas, Marianne Berwick","doi":"10.1093/jncics/pkaf005","DOIUrl":"https://doi.org/10.1093/jncics/pkaf005","url":null,"abstract":"<p><p>Sex differences in melanoma are prominent, with females having a significant survival advantage. However, it is unclear why we see this survival advantage. Here we investigate the relationship between sex, clinicopathologic variables, and melanoma specific survival in 1,753 single primary melanomas from patients in the GEM study. Using Cox proportional hazard models and formal mediation analysis, the effect of sex on survival is explained largely by differences in the clinicopathologic features of tumors at diagnosis. Specifically, we find evidence that 86.5% of the effect of sex on melanoma survival is mediated by differences in age at diagnosis, Breslow thickness, ulceration, mitoses and site (HR 1.85, P < .001). This analysis indicates that the female survival advantage in melanoma is not due primarily to a direct effect of sex (HR 1.19, P = .42) but is largely a result of an indirect effect of sex mediated by clinicopathologic features.</p>","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Menopausal hormone therapy: assessing associations with breast and colorectal cancers by familial risk.","authors":"Robert J MacInnis, Mark A Jenkins, Roger L Milne, Esther M John, Mary B Daly, Irene L Andrulis, Sarah V Colonna, Kelly-Anne Phillips, Loic Le Marchand, Polly A Newcomb, Amanda I Phipps, Stephanie L Schmit, Finlay A Macrae, Daniel D Buchanan, Steven Gallinger, Rish K Pai, Niloy J Samadder, Graham G Giles, Melissa C Southey, John L Hopper, Mary Beth Terry","doi":"10.1093/jncics/pkae121","DOIUrl":"10.1093/jncics/pkae121","url":null,"abstract":"<p><p>Menopausal users of hormone replacement therapy (HRT) are at increased breast cancer risk and decreased colorectal cancer (CRC) risk compared with individuals who have never used HRT, but these opposing associations may differ by familial risk of breast cancer and CRC. We harmonized data from 3 cohorts and generated separate breast cancer and CRC familial risk scores based on cancer family history. We defined moderate or strong family history as a risk score of 0.4 or higher, where 0.4 was equivalent to a 50-year-old woman with 1 parent diagnosed with either breast cancer or CRC at 55 years of age. Of 24 486 women assessed, 1243 and 405 were diagnosed with incident breast cancer and CRC, respectively. For breast cancer, menopausal HRT ever use versus never use hazard ratios were 1.27 (95% CI = 1.11 to 1.45) for a breast cancer familial risk score below 0.4 and 1.01 (95% CI = 0.82 to 1.25) for a breast cancer familial risk score of 0.4 or higher (Pdifference = .08). For CRC, menopausal HRT hazard ratios were 0.63 (95% CI = 0.50 to 0.78) for a CRC familial risk score below 0.4 and 1.21 (95% CI = 0.73 to 2.00) for a CRC familial risk score of 0.4 or higher (Pdifference = .03). Associations with menopausal HRT use that apply to the general population may not hold for women at moderate or strong familial risk of these cancers.</p>","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of undifferentiated carcinomas of the pancreas with and without osteoclast-like giant cells.","authors":"Jamie N Mills, Valerie Gunchick, Jake McGue, Zhaoping Qin, Chandan Kumar-Sinha, Filip Bednar, Noah Brown, Jiaqi Shi, Aaron M Udager, Timothy Frankel, Mark M Zalupski, Vaibhav Sahai","doi":"10.1093/jncics/pkae097","DOIUrl":"10.1093/jncics/pkae097","url":null,"abstract":"<p><strong>Background: </strong>Undifferentiated carcinoma (UC) is a rare subtype of pancreatic cancer distinguished from UC with osteoclast-like giant cells (UC-OGC) in 2019, affecting interpretation of literature that does not distinguish these subtypes. We sought to identify translationally relevant differences between these 2 variants and compared with pancreatic ductal adenocarcinoma.</p><p><strong>Methods: </strong>We characterized clinical and multiomic differences between UC (n = 32) and UC-OGC (n = 15) using DNA sequencing, RNA sequencing, and multiplex immunofluorescence and compared these findings with pancreatic ductal adenocarcinoma.</p><p><strong>Results: </strong>Characteristics at diagnosis were similar between UC and UC-OGC, though the latter was more resectable (P = .009). Across all stages, median overall survival was shorter for UC than for UC-OGC (0.4 years vs 10.8 years, respectively; P = .003). This shorter survival was retained after stratification by resection, albeit without statistical significance (1.8 years vs 11.9 years, respectively; P = .08). In a subset of patients with available tissue, the genomic landscape was similar among UC (n = 9), UC-OGC (n = 5), and pancreatic ductal adenocarcinoma (n = 159). Bulk RNA sequencing was deconvoluted and, along with multiplex immunofluorescence in UC (n = 13), UC-OGC (n = 5), and pancreatic ductal adenocarcinoma (n = 16), demonstrated statistically significantly increased antigen-presenting cells, including M2 macrophages and natural killer cells, and decreased cytotoxic and regulatory T cells in UC and UC-OGC vs pancreatic ductal adenocarcinoma. Findings were similar between UC and UC-OGC , except for decreased regulatory T cells in UC-OGC (P = .04).</p><p><strong>Conclusions: </strong>In this series, UC was more aggressive than UC-OGC, with these variants having more antigen-presenting cells and fewer regulatory T cells than pancreatic ductal adenocarcinoma, suggesting potential for immune-modulating therapies in the treatment of these pancreatic cancer subtypes.</p>","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RE: \"Narrative review of lifestyle interventions in breast cancer survivors: current evidence and future directions\".","authors":"Alain Braillon","doi":"10.1093/jncics/pkae125","DOIUrl":"10.1093/jncics/pkae125","url":null,"abstract":"","PeriodicalId":14681,"journal":{"name":"JNCI Cancer Spectrum","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142869322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}