Breast Cancer Research : BCR最新文献

{"title":"MRI-based breast cancer radiogenomics using RNA profiling: association with subtypes in a single-center prospective study.","authors":"Ah Young Park, Mi-Ryung Han, Bo Kyoung Seo, Hye-Yeon Ju, Gil Soo Son, Hye Yoon Lee, Young Woo Chang, Jungyoon Choi, Kyu Ran Cho, Sung Eun Song, Ok Hee Woo, Hyun Soo Park","doi":"10.1186/s13058-023-01668-7","DOIUrl":"10.1186/s13058-023-01668-7","url":null,"abstract":"<p><strong>Background: </strong>There are few prospective studies on the correlations between MRI features and whole RNA-sequencing data in breast cancer according to molecular subtypes. The purpose of our study was to explore the association between genetic profiles and MRI phenotypes of breast cancer and to identify imaging markers that influences the prognosis and treatment according to subtypes.</p><p><strong>Methods: </strong>From June 2017 to August 2018, MRIs of 95 women with invasive breast cancer were prospectively analyzed, using the breast imaging-reporting and data system and texture analysis. Whole RNA obtained from surgical specimens was analyzed using next-generation sequencing. The association between MRI features and gene expression profiles was analyzed in the entire tumor and subtypes. Gene networks, enriched functions, and canonical pathways were analyzed using Ingenuity Pathway Analysis. The P value for differential expression was obtained using a parametric F test comparing nested linear models and adjusted for multiple testing by reporting Q value.</p><p><strong>Results: </strong>In 95 participants (mean age, 53 years ± 11 [standard deviation]), mass lesion type was associated with upregulation of CCL3L1 (sevenfold) and irregular mass shape was associated with downregulation of MIR421 (sixfold). In estrogen receptor-positive cancer with mass lesion type, CCL3L1 (21-fold), SNHG12 (11-fold), and MIR206 (sevenfold) were upregulated, and MIR597 (265-fold), MIR126 (12-fold), and SOX17 (fivefold) were downregulated. In triple-negative breast cancer with increased standard deviation of texture analysis on precontrast T1-weighted imaging, CLEC3A (23-fold), SRGN (13-fold), HSPG2 (sevenfold), KMT2D (fivefold), and VMP1 (fivefold) were upregulated, and IGLC2 (73-fold) and PRDX4 (sevenfold) were downregulated (all, P < 0.05 and Q < 0.1). Gene network and functional analysis showed that mass type estrogen receptor-positive cancers were associated with cell growth, anti-estrogen resistance, and poor survival.</p><p><strong>Conclusion: </strong>MRI characteristics are associated with the different expressions of genes related to metastasis, anti-drug resistance, and prognosis, depending on the molecular subtypes of breast cancer.</p>","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 1","pages":"79"},"PeriodicalIF":0.0,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10311893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9745032","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":"Effectiveness of palbociclib with aromatase inhibitors for the treatment of advanced breast cancer in an exposure retrospective cohort study: implications for clinical practice.","authors":"Filipa Alves da Costa, Fábio Cardoso Borges, Adriana Ramos, Alexandra Mayer, Claudia Brito, Catarina Ramos, Catarina Bernardo, Mariane Cossito, Cláudia Furtado, Arlindo R Ferreira, Diogo Martins-Branco, Ana da Costa Miranda, António Lourenço","doi":"10.1186/s13058-023-01678-5","DOIUrl":"10.1186/s13058-023-01678-5","url":null,"abstract":"<p><strong>Background: </strong>New drugs for locally advanced or metastatic breast cancer have led to clinical benefits, aside with increasing costs to healthcare systems. The current financing model for health technology assessment (HTA) privileges real-world data. As part of the ongoing HTA, this study aimed to evaluate the effectiveness of palbociclib with aromatase inhibitors (AI) and compare it with the efficacy reported in PALOMA-2.</p><p><strong>Methods: </strong>A population-based retrospective exposure cohort study was conducted including all patients initiating treatment in Portugal with palbociclib under early access use and registered in the National Oncology Registry. The primary outcome was progression free survival (PFS). Secondary outcomes considered included time to palbociclib failure (TPF), overall survival (OS), time to next treatment (TTNT), and proportion of patients discontinuing treatment due to  adverse events (AEs). The Kaplan-Meier method was used and median, 1- and 2-year survival rates were computed, with two-sided 95% confidence intervals (95%CI). STrengthening the Reporting of OBservational studies in Epidemiology (STROBE) guidelines for reporting observational studies were used.</p><p><strong>Results: </strong>There were 131 patients included. Median follow-up was 28.3 months (IQR: 22.7-35.2) and median duration of treatment was 17.5 months (IQR: 7.8-29.1). Median PFS was 19.5 months (95%CI 14.2-24.2), corresponding to a 1-year PFS rate of 67.9% (95%CI 59.2-75.2) and a 2-year PFS rate of 42.0% (95%CI 33.5-50.3). Sensitivity analysis showed median PFS would increase slightly when excluding those not initiating treatment with the recommended dose, raising to 19.8 months (95%CI 14.4-28.9). By considering only patients meeting PALOMA-2 criteria, we could observe a major difference in treatment outcomes, with a mean PFS of 28.8 months (95%CI 19.4-36.0). TPF was 19.8 months (95%CI 14.2-24.9). Median OS was not reached. Median TTNT was 22.5 months (95%CI 18.0-29.8). A total of 14 patients discontinued palbociclib because of AEs (10.7%).</p><p><strong>Conclusions: </strong>Data suggest palbociclib with AI to have an effectiveness of 28.8 months, when used in patients with overlapping characteristics to those used in PALOMA-2. However, when used outside of these eligibility criteria, namely in patients with less favorable prognosis (e.g., presence of visceral disease), the benefits are inferior, even though still favorable.</p>","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 1","pages":"78"},"PeriodicalIF":0.0,"publicationDate":"2023-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10308630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9735459","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":"Noninvasive imaging signatures of HER2 and HR using ADC in invasive breast cancer: repeatability, reproducibility, and association with pathological complete response to neoadjuvant chemotherapy.","authors":"Xinzhi Teng,&nbsp;Jiang Zhang,&nbsp;Xinyu Zhang,&nbsp;Xinyu Fan,&nbsp;Ta Zhou,&nbsp;Yu-Hua Huang,&nbsp;Lu Wang,&nbsp;Elaine Yuen Phin Lee,&nbsp;Ruijie Yang,&nbsp;Jing Cai","doi":"10.1186/s13058-023-01674-9","DOIUrl":"https://doi.org/10.1186/s13058-023-01674-9","url":null,"abstract":"<p><strong>Background: </strong>The immunohistochemical test (IHC) of HER2 and HR can provide prognostic information and treatment guidance for invasive breast cancer patients. We aimed to develop noninvasive image signatures IS_HER2 and IS_HR of HER2 and HR, respectively. We independently evaluate their repeatability, reproducibility, and association with pathological complete response (pCR) to neoadjuvant chemotherapy.</p><p><strong>Methods: </strong>Pre-treatment DWI, IHC receptor status HER2/HR, and pCR to neoadjuvant chemotherapy of 222 patients from the multi-institutional ACRIN 6698 trial were retrospectively collected. They were pre-separated for development, independent validation, and test-retest. 1316 image features were extracted from DWI-derived ADC maps within manual tumor segmentations. IS_HER2 and IS_HR were developed by RIDGE logistic regression using non-redundant and test-retest reproducible features relevant to IHC receptor status. We evaluated their association with pCR using area under receiver operating curve (AUC) and odds ratio (OR) after binarization. Their reproducibility was further evaluated using the test-retest set with intra-class coefficient of correlation (ICC).</p><p><strong>Results: </strong>A 5-feature IS_HER2 targeting HER2 was developed (AUC = 0.70, 95% CI 0.59 to 0.82) and validated (AUC = 0.72, 95% CI 0.58 to 0.86) with high perturbation repeatability (ICC = 0.92) and test-retest reproducibility (ICC = 0.83). IS_HR was developed using 5 features with higher association with HR during development (AUC = 0.75, 95% CI 0.66 to 0.84) and validation (AUC = 0.74, 95% CI 0.61 to 0.86) and similar repeatability (ICC = 0.91) and reproducibility (ICC = 0.82). Both image signatures showed significant associations with pCR with AUC of 0.65 (95% CI 0.50 to 0.80) for IS_HER2 and 0.64 (95% CI 0.50 to 0.78) for IS_HER2 in the validation cohort. Patients with high IS_HER2 were more likely to achieve pCR to neoadjuvant chemotherapy with validation OR of 4.73 (95% CI 1.64 to 13.65, P value = 0.006). Low IS_HR patients had higher pCR with OR = 0.29 (95% CI 0.10 to 0.81, P value = 0.021). Molecular subtypes derived from the image signatures showed comparable pCR prediction values to IHC-based molecular subtypes (P value > 0.05).</p><p><strong>Conclusion: </strong>Robust ADC-based image signatures were developed and validated for noninvasive evaluation of IHC receptors HER2 and HR. We also confirmed their value in predicting treatment response to neoadjuvant chemotherapy. Further evaluations in treatment guidance are warranted to fully validate their potential as IHC surrogates.</p>","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 1","pages":"77"},"PeriodicalIF":0.0,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10308682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9835349","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":"Targeting the oncogenic transcription factor FOXM1 to improve outcomes in all subtypes of breast cancer.","authors":"Benita S Katzenellenbogen,&nbsp;Valeria Sanabria Guillen,&nbsp;John A Katzenellenbogen","doi":"10.1186/s13058-023-01675-8","DOIUrl":"https://doi.org/10.1186/s13058-023-01675-8","url":null,"abstract":"<p><p>FOXM1 (Forkhead box M1) is an oncogenic transcription factor that is greatly upregulated in breast cancer and many other cancers where it promotes tumorigenesis, and cancer growth and progression. It is expressed in all subtypes of breast cancer and is the factor most associated with risk of poor patient survival, especially so in triple negative breast cancer (TNBC). Thus, new approaches to inhibiting FOXM1 and its activities, and combination therapies utilizing FOXM1 inhibitors in conjunction with known cancer drugs that work together synergistically, could improve cancer treatment outcomes. Targeting FOXM1 might prove especially beneficial in TNBC where few targeted therapies currently exist, and also in suppressing recurrent advanced estrogen receptor (ER)-positive and HER2-positive breast cancers for which treatments with ER or HER2 targeted therapies that were effective initially are no longer beneficial. We present these perspectives and future directions in the context of what is known about FOXM1, its regulation, and its key roles in promoting cancer aggressiveness and metastasis, while being absent or very low in most normal non-regenerating adult tissues. We discuss new inhibitors of FOXM1 and highlight FOXM1 as an attractive target for controlling drug-resistant and difficult-to-suppress breast cancers, and how blocking FOXM1 might improve outcomes for patients with all subtypes of breast cancer.</p>","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 1","pages":"76"},"PeriodicalIF":0.0,"publicationDate":"2023-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10304361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10211541","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":"Transcriptionally regulated miR-26a-5p may act as BRCAness in Triple-Negative Breast Cancer.","authors":"Yue Zhang,&nbsp;Lianqiu Lv,&nbsp;Renjing Zheng,&nbsp;Rong Xie,&nbsp;Yuanhang Yu,&nbsp;Han Liao,&nbsp;Jianying Chen,&nbsp;Bo Zhang","doi":"10.1186/s13058-023-01663-y","DOIUrl":"https://doi.org/10.1186/s13058-023-01663-y","url":null,"abstract":"<p><strong>Background: </strong>DNA damage and DNA damage repair (DDR) are important therapeutic targets for triple-negative breast cancer (TNBC), a subtype with limited chemotherapy efficiency and poor outcome. However, the role of microRNAs in the therapy is emerging. In this study, we explored whether miR-26a-5p could act as BRCAness and enhance chemotherapy sensitivity in TNBC.</p><p><strong>Methods: </strong>Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-26a-5p in breast cancer tissues and cell lines. CCK-8 was used to measure drug sensitivity in concentration gradient and time gradient. Comet assay was used to detect DNA damage. Flow cytometry was performed to examine apoptosis. Moreover, we used western blot and immunofluorescence to detect biomarkers. Luciferase reporter assay was performed to verify the combination of miR-26a-5p and 3'UTR of target gene. Hormone deprivation and stimulation assay were used to validate the effect of hormone receptors on the expression of miR-26a-5p. Chromatin immunoprecipitation (ChIP) assays were used to verify the binding sites of ER-a or PR with the promoter of miR-26a-5p. Animal experiments were performed to the effect of miR-26a-5p on Cisplatin treatment.</p><p><strong>Results: </strong>The expression of miR-26a-5p was significantly downregulated in TNBC. Overexpressing miR-26a-5p enhanced the Cisplatin-induced DNA damage and following apoptosis. Interestingly, miR-26a-5p promoted the expression of Fas without Cisplatin stimulating. It suggested that miR-26a-5p provided a hypersensitivity state of death receptor apoptosis and promoted the Cisplatin sensitivity of TNBC cells in vitro and in vivo. Besides, miR-26a-5p negatively regulated the expression of BARD1 and NABP1 and resulted in homologous recombination repair defect (HRD). Notably, overexpressing miR-26a-5p not only facilitated the Olaparib sensitivity of TNBC cells but also the combination of Cisplatin and Olaparib. Furthermore, hormone receptors functioned as transcription factors in the expression of miR-26a-5p, which explained the reasons that miR-26a-5p expressed lowest in TNBC.</p><p><strong>Conclusions: </strong>Taken together, we reveal the important role of miR-26a-5p in Cisplatin sensitivity and highlight its new mechanism in DNA damage and synthetic lethal.</p>","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 1","pages":"75"},"PeriodicalIF":0.0,"publicationDate":"2023-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10294332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9717536","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":"RHAMM regulates MMTV-PyMT-induced lung metastasis by connecting STING-dependent DNA damage sensing to interferon/STAT1 pro-apoptosis signaling.","authors":"Cornelia Tolg, Maja Milojevic, Freda W Qi, Hailie A Pavanel, M Elizabeth O Locke, Jenny Ma, Mathew Price, Andrew C Nelson, James B McCarthy, Kathleen A Hill, Eva A Turley","doi":"10.1186/s13058-023-01652-1","DOIUrl":"10.1186/s13058-023-01652-1","url":null,"abstract":"<p><strong>Background: </strong>RHAMM is a multifunctional protein that is upregulated in breast tumors, and the presence of strongly RHAMM^+ve cancer cell subsets associates with elevated risk of peripheral metastasis. Experimentally, RHAMM impacts cell cycle progression and cell migration. However, the RHAMM functions that contribute to breast cancer metastasis are poorly understood.</p><p><strong>Methods: </strong>We interrogated the metastatic functions of RHAMM using a loss-of-function approach by crossing the MMTV-PyMT mouse model of breast cancer susceptibility with Rhamm^-/- mice. In vitro analyses of known RHAMM functions were performed using primary tumor cell cultures and MMTV-PyMT cell lines. Somatic mutations were identified using a mouse genotyping array. RNA-seq was performed to identify transcriptome changes resulting from Rhamm-loss, and SiRNA and CRISPR/Cas9 gene editing was used to establish cause and effect of survival mechanisms in vitro.</p><p><strong>Results: </strong>Rhamm-loss does not alter initiation or growth of MMTV-PyMT-induced primary tumors but unexpectedly increases lung metastasis. Increased metastatic propensity with Rhamm-loss is not associated with obvious alterations in proliferation, epithelial plasticity, migration, invasion or genomic stability. SNV analyses identify positive selection of Rhamm^-/- primary tumor clones that are enriched in lung metastases. Rhamm^-/- tumor clones are characterized by an increased ability to survive with ROS-mediated DNA damage, which associates with blunted expression of interferon pathway and target genes, particularly those implicated in DNA damage-resistance. Mechanistic analyses show that ablating RHAMM expression in breast tumor cells by siRNA knockdown or CRISPR-Cas9 gene editing blunts interferon signaling activation by STING agonists and reduces STING agonist-induced apoptosis. The metastasis-specific effect of RHAMM expression-loss is linked to microenvironmental factors unique to tumor-bearing lung tissue, notably high ROS and TGFB levels. These factors promote STING-induced apoptosis of RHAMM^+ve tumor cells to a significantly greater extent than RHAMM^-ve comparators. As predicted by these results, colony size of Wildtype lung metastases is inversely related to RHAMM expression.</p><p><strong>Conclusion: </strong>RHAMM expression-loss blunts STING-IFN signaling, which offers growth advantages under specific microenvironmental conditions of lung tissue. These results provide mechanistic insight into factors controlling clonal survival/expansion of metastatic colonies and has translational potential for RHAMM expression as a marker of sensitivity to interferon therapy.</p>","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 1","pages":"74"},"PeriodicalIF":0.0,"publicationDate":"2023-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10286489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10089084","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":"Meeting Abstracts from the British Society of Breast Radiology Annual Scientific Meeting 2022.","authors":"","doi":"10.1186/s13058-023-01659-8","DOIUrl":"https://doi.org/10.1186/s13058-023-01659-8","url":null,"abstract":"","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 Suppl 1","pages":"73"},"PeriodicalIF":0.0,"publicationDate":"2023-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10283171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9709943","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":"Associations of height, body mass index, and weight gain with breast cancer risk in carriers of a pathogenic variant in BRCA1 or BRCA2: the BRCA1 and BRCA2 Cohort Consortium.","authors":"Karin Kast, Esther M John, John L Hopper, Nadine Andrieu, Catherine Noguès, Emmanuelle Mouret-Fourme, Christine Lasset, Jean-Pierre Fricker, Pascaline Berthet, Véronique Mari, Lucie Salle, Marjanka K Schmidt, Margreet G E M Ausems, Encarnacion B Gomez Garcia, Irma van de Beek, Marijke R Wevers, D Gareth Evans, Marc Tischkowitz, Fiona Lalloo, Jackie Cook, Louise Izatt, Vishakha Tripathi, Katie Snape, Hannah Musgrave, Saba Sharif, Jennie Murray, Sarah V Colonna, Irene L Andrulis, Mary B Daly, Melissa C Southey, Miguel de la Hoya, Ana Osorio, Lenka Foretova, Dita Berkova, Anne-Marie Gerdes, Edith Olah, Anna Jakubowska, Christian F Singer, Yen Tan, Annelie Augustinsson, Johanna Rantala, Jacques Simard, Rita K Schmutzler, Roger L Milne, Kelly-Anne Phillips, Mary Beth Terry, David Goldgar, Flora E van Leeuwen, Thea M Mooij, Antonis C Antoniou, Douglas F Easton, Matti A Rookus, Christoph Engel","doi":"10.1186/s13058-023-01673-w","DOIUrl":"10.1186/s13058-023-01673-w","url":null,"abstract":"<p><strong>Introduction: </strong>Height, body mass index (BMI), and weight gain are associated with breast cancer risk in the general population. It is unclear whether these associations also exist for carriers of pathogenic variants in the BRCA1 or BRCA2 genes.</p><p><strong>Patients and methods: </strong>An international pooled cohort of 8091 BRCA1/2 variant carriers was used for retrospective and prospective analyses separately for premenopausal and postmenopausal women. Cox regression was used to estimate breast cancer risk associations with height, BMI, and weight change.</p><p><strong>Results: </strong>In the retrospective analysis, taller height was associated with risk of premenopausal breast cancer for BRCA2 variant carriers (HR 1.20 per 10 cm increase, 95% CI 1.04-1.38). Higher young-adult BMI was associated with lower premenopausal breast cancer risk for both BRCA1 (HR 0.75 per 5 kg/m², 95% CI 0.66-0.84) and BRCA2 (HR 0.76, 95% CI 0.65-0.89) variant carriers in the retrospective analysis, with consistent, though not statistically significant, findings from the prospective analysis. In the prospective analysis, higher BMI and adult weight gain were associated with higher postmenopausal breast cancer risk for BRCA1 carriers (HR 1.20 per 5 kg/m², 95% CI 1.02-1.42; and HR 1.10 per 5 kg weight gain, 95% CI 1.01-1.19, respectively).</p><p><strong>Conclusion: </strong>Anthropometric measures are associated with breast cancer risk for BRCA1 and BRCA2 variant carriers, with relative risk estimates that are generally consistent with those for women from the general population.</p>","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 1","pages":"72"},"PeriodicalIF":0.0,"publicationDate":"2023-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10280955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9763512","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":"BluePrint molecular subtypes predict response to neoadjuvant pertuzumab in HER2-positive breast cancer.","authors":"M C Liefaard,&nbsp;A van der Voort,&nbsp;M S van Ramshorst,&nbsp;J Sanders,&nbsp;S Vonk,&nbsp;H M Horlings,&nbsp;S Siesling,&nbsp;L de Munck,&nbsp;A E van Leeuwen,&nbsp;M Kleijn,&nbsp;L Mittempergher,&nbsp;M M Kuilman,&nbsp;A M Glas,&nbsp;J Wesseling,&nbsp;E H Lips,&nbsp;G S Sonke","doi":"10.1186/s13058-023-01664-x","DOIUrl":"https://doi.org/10.1186/s13058-023-01664-x","url":null,"abstract":"<p><strong>Background: </strong>The introduction of pertuzumab has greatly improved pathological complete response (pCR) rates in HER2-positive breast cancer, yet effects on long-term survival have been limited and it is uncertain which patients derive most benefit. In this study, we determine the prognostic value of BluePrint subtyping in HER2-positive breast cancer. Additionally, we evaluate its use as a biomarker for predicting response to trastuzumab-containing neoadjuvant chemotherapy with or without pertuzumab.</p><p><strong>Methods: </strong>From a cohort of patients with stage II-III HER2-positive breast cancer who were treated with neoadjuvant chemotherapy and trastuzumab with or without pertuzumab, 836 patients were selected for microarray gene expression analysis, followed by readout of BluePrint standard (HER2, Basal and Luminal) and dual subtypes (HER2-single, Basal-single, Luminal-single, HER2-Basal, Luminal-HER2, Luminal-HER2-Basal). The associations between subtypes and pathological complete response (pCR), overall survival (OS) and breast cancer-specific survival (BCSS) were assessed, and pertuzumab benefit was evaluated within the BluePrint subgroups.</p><p><strong>Results: </strong>BluePrint results were available for 719 patients. In patients with HER2-type tumors, the pCR rate was 71.9% in patients who received pertuzumab versus 43.5% in patients who did not (adjusted Odds Ratio 3.43, 95% CI 2.36-4.96). Additionally, a significantly decreased hazard was observed for both OS (adjusted hazard ratio [aHR] 0.45, 95% CI 0.25-0.80) and BCSS (aHR 0.46, 95% CI 0.24-0.86) with pertuzumab treatment. Findings were similar in the HER2-single subgroup. No significant benefit of pertuzumab was seen in other subtypes.</p><p><strong>Conclusions: </strong>In patients with HER2-type or HER2-single-type tumors, pertuzumab significantly improved the pCR rate and decreased the risk of breast cancer mortality, which was not observed in other subtypes. BluePrint subtyping may be valuable in future studies to identify patients that are likely to be highly sensitive to HER2-targeting agents.</p>","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 1","pages":"71"},"PeriodicalIF":0.0,"publicationDate":"2023-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10280902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9708126","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":"Correction to: National and subnational burden of female and male breast cancer and risk factors in Iran from 1990 to 2019: results from the Global Burden of Disease study 2019.","authors":"Armin Aryannejad,&nbsp;Sahar Saeedi Moghaddam,&nbsp;Baharnaz Mashinchi,&nbsp;Mohammadreza Tabary,&nbsp;Negar Rezaei,&nbsp;Sarvenaz Shahin,&nbsp;Nazila Rezaei,&nbsp;Mohsen Naghavi,&nbsp;Bagher Larijani,&nbsp;Farshad Farzadfar","doi":"10.1186/s13058-023-01666-9","DOIUrl":"https://doi.org/10.1186/s13058-023-01666-9","url":null,"abstract":"","PeriodicalId":9283,"journal":{"name":"Breast Cancer Research : BCR","volume":"25 1","pages":"70"},"PeriodicalIF":0.0,"publicationDate":"2023-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10273695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10010973","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}