Does age matter?-the significance of age in breast cancer.
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ABSTRACT:
SUBMITTER: Diaz Roldan J
PROVIDER: S-EPMC9403945 | biostudies-literature | 2022 Aug
REPOSITORIES: biostudies-literature
Publications
Does age matter?-the significance of age in breast cancer.
Annals of translational medicine 20220801 15
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Project description:PURPOSE:The aims of this study were to investigate outcomes corresponding to age at diagnosis as categorized into 5-year intervals and to explore whether endocrine-responsive tumors display clinical benefits from endocrine therapy after chemotherapy among young breast cancer patients. METHODS:A total of 1,171 patients who were under 40 years old at diagnosis between 1985 and 2007 were divided into 3 subgroups: ?30 years (Group I, 13.3%), 31-35 years (Group II, 30.5%), and 36-40 years (Control group, 56.2%). Clinicopathological factors and outcomes were compared using a chi-square test, the Kaplan-Meier method, and Cox's hazards models. RESULTS:There were no significant differences in the characteristics and treatment patterns between the 3 groups, except for the grade, hormone receptors expression, and use of endocrine therap. Group I showed the worst survival and subsequently Group II presented worse outcomes than the Control group, mainly among hormone receptors-positive patients. Groups I and II showed increased risks of recurrence and death in multivariate analyses. Among 529 hormone receptors-positive patients who received chemotherapy, favorable outcomes for patients who were treated with endocrine agents were demonstrated, mainly in patients aged 35 years or less. However, interaction tests between the use of endocrine therapy and age at diagnosis were not significant. CONCLUSION:Age at diagnosis is an independent prognostic factor and the age of 35 years is a rational cut-off among young patients. Our subgroup analysis suggests that endocrine therapy may provide additional benefits even in young breast cancers. Therefore, further researches should be directed towards improving outcomes for this population.
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Project description:Ethnic or racial differences in breast cancer (BC) survival outcomes have been reported, but current data are largely restricted to comparisons between African Americans and non-Hispanic whites. Most analyses have traditionally been based on self-reported race which may not always be accurate, or are oversimplified in their classification. With increasing globalization, quantification of the genetic ancestry from genomic data may offer a solution to infer the complex makeup from admixture of races. Focusing on the larger and the latest studies, we will discuss recent findings on the differing host and tumor biology that may be driving these disparities, in addition to the extrinsic environmental or lifestyle factors. Socioeconomic disparities with lower cancer literacy may lead to late presentation, poorer adherence to treatment, and other lifestyle factors such as unhealthy diet, obesity, and inadequate physical activity. These hardships may also result in greater allostatic load, which is in turn associated with aggressive BC features in disadvantaged populations. Epigenetic reprogramming may mediate the effects of the environment or lifestyle factors on gene expression, with ensuing differences in BC characteristics and outcome. There is increasing evidence that germline genetics can influence somatic gene alterations or expression, as well as modulate the tumor or immune microenvironment. Although the precise mechanisms remain elusive, this may account for the varying distribution of different BC subtypes across ethnicities. These gaps in our knowledge highlight the need to interrogate the multiomics landscape of BC in diverse populations, ideally in large-scale collaborative settings with standardized methodology for the comparisons to be statistically robust. Together with improving BC awareness and access to good quality health care, a holistic approach with insights of the biological underpinnings is much needed to eradicate ethnic disparities in BC outcomes.
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Project description:Secreted protein acidic and cysteine-rich like 1 (SPARCL1; also known as MAST9) exhibits low expression levels in several malignant tumors and is positively associated with tumor growth and poor prognosis. Furthermore, there may be an association between SPARCL1 and breast cancer; however, further comprehensive research is necessary. The present study assessed the relationship between SPARCL1 expression and breast cancer using RNA sequencing and clinical data from The Cancer Genome Atlas database (including tumor mutations, immune infiltration and prognosis data), cell experiments and clinical samples. The findings indicated that SPARCL1 expression was significantly lower in breast cancer tissues compared with other malignant tumors, with its downregulation negatively associated with the overall survival rate of patients. Moreover, analysis of receiver operator characteristic curve analysis, and univariate and multivariate Cox regression models suggested that SPARCL1 has potential as a diagnostic biomarker for breast cancer detection. Additionally, low expression of SPARCL1 was demonstrated to be associated with the degree of immune infiltration, whilst functional enrichment analysis revealed its involvement in key areas such as cell cycle regulation, protein/ATP binding processes, cellular aging mechanisms, oocyte meiosis pathways and DNA replication processes. Overall, the results of the present study highlight how big data mining combined with experimental verification can provide insights into the role of SPARCL1 in breast cancer pathogenesis and its potential as a biomarker for the disease. However, further investigations are warranted to validate these findings and provide a more comprehensive understanding of the implications of SPARCL1 therapy in patients with breast cancer.
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Project description:BACKGROUND/AIM:In 2016, in the United States, more than 50% of breast cancer (BC) cases were diagnosed in patients older than 60 years of age. Our study aimed to estimate the risk of locoregional recurrence (LR) in patients who underwent breast-conservative treatment (BCT), according to age. PATIENTS AND METHODS:This retrospective monocentric study analyzed 613 cases of patients who underwent BCT between 2003 and 2014. Patients were divided into groups according to age: Under70 (under 70 years old) and Over70 (above 70 years old). Margins width, histology results, prognostic and predictive factors were compared. Subgroup analysis was performed for patients who experienced LR. RESULTS:LR Incidence among Under70 and Over70 was 5.4% and 1.7%, respectively (p<0.01). Group Over70 is characterized by larger tumors and a lower Ki67 index (p<0.01). CONCLUSION:Operation time reduction, better aesthetic results and reduced LR risk support BCT. The Over70 group exhibited better outcomes in terms of LR despite larger tumor dimensions.
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Project description:High metabolic activity, reflected in increased glucose uptake, is one of the hallmarks of many cancers including breast cancer. However, not all cancers avidly take up glucose, suggesting heterogeneity in their metabolic demand. Thus, we aim to generate a genomic signature of glucose hypermetabolism in breast cancer and examine its clinical relevance. To identify genes significantly associated with glucose uptake, gene expression data were analyzed together with the standardized uptake values (SUVmax) of 18F-fluorodeoxy-glucose on positron emission tomography (PET) for 11 breast cancers. The resulting PET signature was evaluated for prognostic significance in four large independent patient cohorts (n = 5417). Potential upstream regulators accountable for the high glucose uptake were identified by gene network analysis. A PET signature of 242 genes was significantly correlated with SUVmax in breast cancer. In all four cohorts, high PET signature was significantly associated with poorer prognosis. The prognostic value of this PET signature was further supported by Cox regression analyses (hazard ratio 1.7, confidential interval 1.48-2.02; P < 0.001). The PET signature was also strongly correlated with previously established prognostic genomic signatures such as PAM50, Oncotype DX, and NKI. Gene network analyses suggested that MYC and TBX2 were the most significant upstream transcription factors in the breast cancers with high glucose uptake. A PET signature reflecting high glucose uptake is a novel independent prognostic factor in breast cancer. MYC and TBX2 are potential regulators of glucose uptake.
| S-EPMC8356554 | biostudies-literature
Project description:Currently, when determining treatment regimens, there is an emphasis on the quality of life (QOL), in addition to treatment efficacy. Especially in hormone receptor-positive breast cancer with distant metastases, unless death is imminent, a common first-line treatment is endocrine therapy, which has fewer side effects. In the present study, the differences in QOL were evaluated based on the age and prognostic indicators of 46 patients with hormone receptor-positive breast cancer with distant metastases (stage IV), who received first-line endocrine therapy at the Osaka City University Hospital (Osaka, Japan) between November 2007 and November 2016. QOL score before and after endocrine therapy was retrospectively analyzed, using the Quality of Life Questionnaire for Cancer Patients Treated with Anti-Cancer Drugs-Breast (QOL-ACD-B). There was no significant association between age and any of the clinicopathological features investigated. However, the QOL score of the elderly patient group was significantly higher compared with that of the younger group in the 'Satisfaction with treatment and coping with disease' subcategory (P=0.008). The QOL score of the younger age group in the same subcategory was significantly improved by the treatment (P=0.013). The patients that had an increased overall QOL score 3 months after treatment initiation had a significant extension of progression-free survival (PFS) rate compared to the patients with decreased or no change in QOL (P=0.032). In conclusion, psychological stress was more prominent in younger patients with stage IV breast cancer treated with hormonal therapy compared with elderly patients. Importantly, improving QOL within the 3 months after treatment initiation could lead to longer PFS rate.
| S-EPMC7471707 | biostudies-literature
Project description:This study aimed to evaluate the significance of chemotherapy (CT) among metaplastic breast cancer (MpBC), and to compare the survival outcomes between triple negative MpBC (MpBC-TNBC) and triple negative invasive ductal carcinoma (IDC-TNBC). SEER database was indexed to identify female unilateral primary MpBC diagnosed from 2010 to 2017. Patients were classified into neoadjuvant chemotherapy (NAC) with response (NAC-response), NAC-no response, adjuvant chemotherapy, and no CT. Breast cancer-specific survival (BCSS) and overall survival (OS) was estimated using the Kaplan-Meier method and compared by log-rank test. Cox regression was used to evaluate the independent prognostic factors. A 1:4 propensity score matching method was adopted to balance baseline differences. Altogether 1186 MpBC patients were enrolled, among them 181 received NAC, 647 received adjuvant CT and 358 did not receive any CT. Chemotherapy was an independent favorable prognostic factor. NAC-response and adjuvant CT had a significant or an obvious trend of survival improvement compared with NAC-no response or no CT. MpBC-TNBC was an independent unfavorable prognostic factor compared with IDC-TNBC. Among them, there was significant or trend of survival improvement among all TNBCs receiving NAC or adjuvant CT compared with no CT. Chemotherapy was of important significance to MpBC prognosis and should be integrated in comprehensive treatment for MpBC.
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Project description:BackgroundDicer, an RNase III-type endonuclease, is the key enzyme involved in RNA interference and microRNA pathways. Aberrant expression of Dicer is reported in several human cancers. Our aim was to assess the prognostic role of Dicer in breast cancer.MethodsThe entire series comprised 666 invasive breast cancers (IBCs), 480 DCIS cases (397 associated with IBC and 83 pure DCIS) and 305 lymph node metastases. Cytoplasmic Dicer expression by immunohistochemistry was scored as negative (no staining) and positive (weak, moderate or strong staining).ResultsDicer staining was assessable in 446 IBC, 128 DCIS and 101 lymph node metastases. Expression of Dicer was observed in 33% (145/446) of IBCs, 34% (44/128) of DCIS and 57% (58/101) of lymph node metastases. Dicer expression was increased in nodal metastases compared to primary tumours (p<0.001); and was associated with ER negativity (p<0.001), HER2 positivity (p<0.001), high Ki67 labeling index (p<0.001) and expression of basal-like biomarkers (p = 0.002). Dicer positivity was more frequent in the HER2 overexpressing (p<0.001) and basal-like (p = 0.002) subtypes compared to luminal A subtype. Dicer expression was associated with reduced overall survival (OS) on univariate analysis (p = 0.058) and remained an independent predictor of OS on multivariate analysis (HR 2.84, 95% CI 1.43-5.62, p = 0.003), with nodal status (HR 2.61, 95% CI 1.18-5.80, p = 0.018) and PR (HR 0.28, 95% CI 0.13-0.59, p = 0.001). Further, moderate or strong expression of Dicer was associated with improved disease-free survival in the HER2-overexpressing subtype compared to negative or weak expression (p = 0.038).ConclusionDeregulated Dicer expression is associated with aggressive tumour characteristics and is an independent prognostic factor for OS. Our findings suggest that Dicer is an important prognostic marker in breast cancer and that its prognostic role may be subtype specific.
| S-EPMC3875475 | biostudies-literature
Project description:Breast cancer is a heterogeneous disease associated with diverse clinical, biological and molecular features, presenting huge challenges for prognosis and treatment. Here we found that perilipin-1 (PLIN1) mRNA expression is significantly downregulated in human breast cancer. Kaplan-Meier analysis indicated that patients presenting with reduced PLIN1 expression exhibited poorer overall metastatic relapse-free survival (p = 0.03). Further Cox proportional hazard models analysis revealed that the reduced expression of PLIN1 is an independent predictor of overall survival in estrogen receptor positive (p < 0.0001, HR = 0.87, 95% CI = 0.81-0.92, N = 3,600) and luminal A-subtype (p = 0.02, HR = 0.88, 95% CI = 0.78-0.98, N = 1,469) breast cancer patients. We also demonstrated that the exogenous expression of PLIN1 in human breast cancer MCF-7 and MDA-MB-231 cells significantly inhibits cell proliferation, migration, invasion and in vivo tumorigenesis in mice. Together, these data provide novel insights into a prognostic significance of PLIN1 in human breast cancer and reveal a potentially new gene therapy target for breast cancer.
| S-EPMC5342357 | biostudies-literature
Project description:Breast cancer metastasis is a major clinical problem. The molecular basis of breast cancer progression to metastasis remains poorly understood. PELP1 is an estrogen receptor (ER) coregulator that has been implicated as a proto-oncogene whose expression is deregulated in metastatic breast tumors and whose expression is retained in ER-negative tumors. We examined the mechanism and significance of PELP1-mediated signaling in ER-negative breast cancer progression using two ER-negative model cells (MDA-MB-231 and 4T1 cells) that stably express PELP1-shRNA. These model cells had reduced PELP1 expression (75% of endogenous levels) and exhibited less propensity to proliferate in growth assays in vitro. PELP1 downregulation substantially affected migration of ER-negative cells in Boyden chamber and invasion assays. Using mechanistic studies, we found that PELP1 modulated expression of several genes involved in the epithelial mesenchymal transition (EMT), including MMPs, SNAIL, TWIST, and ZEB. In addition, PELP1 knockdown reduced the in vivo metastatic potential of ER-negative breast cancer cells and significantly reduced lung metastatic nodules in a xenograft assay. These results implicate PELP1 as having a role in ER-negative breast cancer metastasis, reveal novel mechanism of coregulator regulation of metastasis via promoting cell motility/EMT by modulating expression of genes, and suggest PELP1 may be a potential therapeutic target for metastatic ER-negative breast cancer.
| S-EPMC3262052 | biostudies-literature