Alastair M McKee, Lindsay J Hall, Stephen D Robinson
{"title":"The microbiota, antibiotics and breast cancer.","authors":"Alastair M McKee, Lindsay J Hall, Stephen D Robinson","doi":"10.2217/bmt-2019-0015","DOIUrl":"10.2217/bmt-2019-0015","url":null,"abstract":"","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":"8 3","pages":"BMT29"},"PeriodicalIF":0.7,"publicationDate":"2019-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37475476","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":"A life in breast cancer research: tamoxifen, SERMs and the unique paired-biology of the unfolded protein response and apoptosis","authors":"V. Jordan, B. Abderrahman","doi":"10.2217/BMT-2019-0003","DOIUrl":"https://doi.org/10.2217/BMT-2019-0003","url":null,"abstract":"","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/BMT-2019-0003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45144402","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}
New developments in technology have the potential to change experiences of living with breast cancer (BC). Our project, ‘A Shared Space and a Space for Sharing’, explored people’s experiences of interacting with an online health forum (OHF) provided by the UK-based charity, Breast Cancer Care (BCC). This editorial is based on findings from this study, from research literature, from knowledge gained from working with BCC to develop resources, and by running engagement events for the public and health professionals.
{"title":"Online health forums: the role of online support for people living with breast cancer","authors":"Sarah Hargreaves, P. Bath","doi":"10.2217/BMT-2019-0008","DOIUrl":"https://doi.org/10.2217/BMT-2019-0008","url":null,"abstract":"New developments in technology have the potential to change experiences of living with breast cancer (BC). Our project, ‘A Shared Space and a Space for Sharing’, explored people’s experiences of interacting with an online health forum (OHF) provided by the UK-based charity, Breast Cancer Care (BCC). This editorial is based on findings from this study, from research literature, from knowledge gained from working with BCC to develop resources, and by running engagement events for the public and health professionals.","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/BMT-2019-0008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42000128","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":"Similar 10-year survival in breast cancer patients of Lithuania and Poland with common BRCA1 founder mutations","authors":"P. Elsakov, V. Ostapenko, A. Luksyte, G. Smailytė","doi":"10.2217/BMT-2018-0015","DOIUrl":"https://doi.org/10.2217/BMT-2018-0015","url":null,"abstract":"","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/BMT-2018-0015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46625355","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}
Mohammad Ghanbari, M. Hosseinpourfeizi, R. Safaralizadeh, A. Aghazadeh, V. Montazeri
Aim: This study aimed to demonstrate misregulation of KMT2B gene expression in breast cancer tissue. Materials & methods: Cancerous and marginal tissue samples were collected from 43 female patients. After RNA extraction and cDNA synthesis, quantitative-PCR was used to evaluate the expression level of the KMT2B gene. REST, Sigma plot and SPSS software were used to analyze data. Results: KMT2B gene expression was significantly decreased in tumor tissue compared with marginal tissue (p = 0.02). No significant correlation was found between expression levels of KMT2B and clinical parameters of patients (p > 0.05) Conclusion: Our study demonstrated that downregulation of KMT2B is associated with breast cancer and its misregulation may play an important role in tumorigenesis.
{"title":"Study of KMT2B (MLL2) gene expression changes in patients with breast cancer","authors":"Mohammad Ghanbari, M. Hosseinpourfeizi, R. Safaralizadeh, A. Aghazadeh, V. Montazeri","doi":"10.2217/BMT-2018-0016","DOIUrl":"https://doi.org/10.2217/BMT-2018-0016","url":null,"abstract":"Aim: This study aimed to demonstrate misregulation of KMT2B gene expression in breast cancer tissue. Materials & methods: Cancerous and marginal tissue samples were collected from 43 female patients. After RNA extraction and cDNA synthesis, quantitative-PCR was used to evaluate the expression level of the KMT2B gene. REST, Sigma plot and SPSS software were used to analyze data. Results: KMT2B gene expression was significantly decreased in tumor tissue compared with marginal tissue (p = 0.02). No significant correlation was found between expression levels of KMT2B and clinical parameters of patients (p > 0.05) Conclusion: Our study demonstrated that downregulation of KMT2B is associated with breast cancer and its misregulation may play an important role in tumorigenesis.","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/BMT-2018-0016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47102846","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":"Therapeutic potential of estradiol in treating breast cancer","authors":"Avijit Mallick, Shane Taylor","doi":"10.2217/BMT-2019-0013","DOIUrl":"https://doi.org/10.2217/BMT-2019-0013","url":null,"abstract":"","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/BMT-2019-0013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49519750","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}
T. Sanft, A. Berkowitz, B. Schroeder, C. Hatzis, C. Schnabel, A. Brufsky, G. Gustavsen, L. Pusztai, G. J. Londen
Aim: To prospectively assess the impact of gene expression-based assay Breast Cancer Index (BCI) on extended endocrine therapy (EET) decision-making. Patients & methods: The BCI-tested samples from primary tumors (Stage I–III, hormone receptor positive breast cancer, >3.5 year endocrine therapy). Patients and physicians completed questionnaires on EET preferences and decision conflict. Using these data, a fact-based economic model was developed to project the cost impact of BCI. Results: The BCI results affected treatment recommendations for 42/141 patients (overall mean, 62 year; 83% postmenopausal; 63% Stage I). Patient decision conflict decreased pre- to post-test. The BCI-related projected net savings (US$5190/patient) was robust under sensitivity analysis. Conclusion: Incorporating BCI into clinical practice meaningfully impacted physician EET recommendations and decreased patient decision conflict, with projected cost savings.
{"title":"A prospective decision-impact study incorporating Breast Cancer Index into extended endocrine therapy decision-making","authors":"T. Sanft, A. Berkowitz, B. Schroeder, C. Hatzis, C. Schnabel, A. Brufsky, G. Gustavsen, L. Pusztai, G. J. Londen","doi":"10.2217/BMT-2019-0001","DOIUrl":"https://doi.org/10.2217/BMT-2019-0001","url":null,"abstract":"Aim: To prospectively assess the impact of gene expression-based assay Breast Cancer Index (BCI) on extended endocrine therapy (EET) decision-making. Patients & methods: The BCI-tested samples from primary tumors (Stage I–III, hormone receptor positive breast cancer, >3.5 year endocrine therapy). Patients and physicians completed questionnaires on EET preferences and decision conflict. Using these data, a fact-based economic model was developed to project the cost impact of BCI. Results: The BCI results affected treatment recommendations for 42/141 patients (overall mean, 62 year; 83% postmenopausal; 63% Stage I). Patient decision conflict decreased pre- to post-test. The BCI-related projected net savings (US$5190/patient) was robust under sensitivity analysis. Conclusion: Incorporating BCI into clinical practice meaningfully impacted physician EET recommendations and decreased patient decision conflict, with projected cost savings.","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/BMT-2019-0001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43693606","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}
Metastasis is a complex, multistep process involving the spread of cancer cells from a primary tumor to distal sites throughout the body via the circulatory or lymphatic systems [1]. Breast cancers typically arise from a host of genetic aberrations [2,3] that influence both disease progression and the therapeutic approaches utilized by physicians to combat the disease [4]. With the exceptions of estrogen receptor (ER), HER2, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha, PIK3CA, and AKT1, validated oncogenic drivers of breast cancer remain elusive. Directly targeting metastasis is essential with regards to therapeutic interventions and could have major medical and societal implications, as mounting scientific evidence shows that metastasis accounts for 90% of the cancer-related deaths [5]. Although targeting metastasis itself may seem a daunting task scientifically and logistically, progressive improvements in our knowledge of the disease is providing novel and innovative approaches. Many chemokines and cytokines (mainly interleukins) play critical roles in the metastatic process, from influencing epithelial to mesenchymal transition (EMT) [6] and facilitating the detachment of tumor cells from the primary tumor mass, to regulating cell migration [7], promoting seeding by circulating tumor cells (CTCs) [8] and stimulating proliferation [9]. Recent studies have demonstrated that interleukins cooperatively regulate aspects of metastasis. For instance, IL-6 and IL-8 co-regulate tumor cell proliferation and migration and the seeding of CTCs [10–13]. Since tumor cells rely on coordinated interactions with different cell populations within the microenvironment (both malignant and stromal cells) for fitness and survival during tumorigenesis [14], it is logical that they would also rely on the synergistic interplay of secreted proteins, particularly employing interleukins to successfully metastasize. Tumor cells autonomously produce IL-6 and IL-8 which synergistically attracts CTCs and promotes the selfseeding of breast, colon and melanoma tumors [13]. Furthermore, these cytokines enhance tumor cell migration through cell-autonomous paracrine mechanisms driven in part by the increase in local cell density [10,11]. Interestingly, this signaling is unique to tumorigenic metastatic cells but not normal or non-metastatic cancer cells. IL-6 and IL-8 promote cell migration within collagen rich extracellular matrices through downstream signaling via WASF3 and Arp2/3 complex and increases the formation of dendritic protrusions. Furthermore, pharmacological inhibition of the binding of these interleukins to their cognate receptors using tocilizumab (a humanized monoclonal antibody that targets the IL-6 receptor) and reparixin (a small molecule that targets the IL-8 receptor) decreases effective metastasis to the lungs, liver and lymph nodes in preclinical breast cancer models [10]. Breast cancers, particularly triple negative breast cance
{"title":"Targeting metastasis through the inhibition of interleukin 6 and 8","authors":"Hasini Jayatilaka, J. Phillip","doi":"10.2217/BMT-2019-0002","DOIUrl":"https://doi.org/10.2217/BMT-2019-0002","url":null,"abstract":"Metastasis is a complex, multistep process involving the spread of cancer cells from a primary tumor to distal sites throughout the body via the circulatory or lymphatic systems [1]. Breast cancers typically arise from a host of genetic aberrations [2,3] that influence both disease progression and the therapeutic approaches utilized by physicians to combat the disease [4]. With the exceptions of estrogen receptor (ER), HER2, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha, PIK3CA, and AKT1, validated oncogenic drivers of breast cancer remain elusive. Directly targeting metastasis is essential with regards to therapeutic interventions and could have major medical and societal implications, as mounting scientific evidence shows that metastasis accounts for 90% of the cancer-related deaths [5]. Although targeting metastasis itself may seem a daunting task scientifically and logistically, progressive improvements in our knowledge of the disease is providing novel and innovative approaches. Many chemokines and cytokines (mainly interleukins) play critical roles in the metastatic process, from influencing epithelial to mesenchymal transition (EMT) [6] and facilitating the detachment of tumor cells from the primary tumor mass, to regulating cell migration [7], promoting seeding by circulating tumor cells (CTCs) [8] and stimulating proliferation [9]. Recent studies have demonstrated that interleukins cooperatively regulate aspects of metastasis. For instance, IL-6 and IL-8 co-regulate tumor cell proliferation and migration and the seeding of CTCs [10–13]. Since tumor cells rely on coordinated interactions with different cell populations within the microenvironment (both malignant and stromal cells) for fitness and survival during tumorigenesis [14], it is logical that they would also rely on the synergistic interplay of secreted proteins, particularly employing interleukins to successfully metastasize. Tumor cells autonomously produce IL-6 and IL-8 which synergistically attracts CTCs and promotes the selfseeding of breast, colon and melanoma tumors [13]. Furthermore, these cytokines enhance tumor cell migration through cell-autonomous paracrine mechanisms driven in part by the increase in local cell density [10,11]. Interestingly, this signaling is unique to tumorigenic metastatic cells but not normal or non-metastatic cancer cells. IL-6 and IL-8 promote cell migration within collagen rich extracellular matrices through downstream signaling via WASF3 and Arp2/3 complex and increases the formation of dendritic protrusions. Furthermore, pharmacological inhibition of the binding of these interleukins to their cognate receptors using tocilizumab (a humanized monoclonal antibody that targets the IL-6 receptor) and reparixin (a small molecule that targets the IL-8 receptor) decreases effective metastasis to the lungs, liver and lymph nodes in preclinical breast cancer models [10]. Breast cancers, particularly triple negative breast cance","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":"1 1","pages":""},"PeriodicalIF":0.7,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/BMT-2019-0002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41454220","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}
Cynthia Wan, K. Boileau, Danielle D'Amico, V. Huang, A. Fiocco, R. Clément, C. Bielajew
Aim: In this study, we examined whether Chinese and White women with and without a history of breast cancer exhibit differences in physiological and psychological stress profiles. Methods: Diurnal and reactive salivary cortisol profiles and psychological stress patterns of 41 breast cancer survivors and 58 healthy women were assessed. Results: Breast cancer survivors displayed a blunted acute cortisol response but there was no main effect of ethnocultural membership. Subjective appraisals of stress during the acute stressor revealed a significant interaction between ethnocultural group, health status and time (p = 0.032). Conclusion: Our results support the existing literature though suggest group differences in the appraisal of stress; thus, underscoring the importance of cultural sensitivity and awareness among clinicians and existing programs.
{"title":"A cross-cultural analysis of salivary cortisol patterns in breast cancer survivors","authors":"Cynthia Wan, K. Boileau, Danielle D'Amico, V. Huang, A. Fiocco, R. Clément, C. Bielajew","doi":"10.2217/BMT-2019-0004","DOIUrl":"https://doi.org/10.2217/BMT-2019-0004","url":null,"abstract":"Aim: In this study, we examined whether Chinese and White women with and without a history of breast cancer exhibit differences in physiological and psychological stress profiles. Methods: Diurnal and reactive salivary cortisol profiles and psychological stress patterns of 41 breast cancer survivors and 58 healthy women were assessed. Results: Breast cancer survivors displayed a blunted acute cortisol response but there was no main effect of ethnocultural membership. Subjective appraisals of stress during the acute stressor revealed a significant interaction between ethnocultural group, health status and time (p = 0.032). Conclusion: Our results support the existing literature though suggest group differences in the appraisal of stress; thus, underscoring the importance of cultural sensitivity and awareness among clinicians and existing programs.","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/BMT-2019-0004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44898352","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":"Welcome to Volume 8 of Breast Cancer Management","authors":"Jennifer Straiton","doi":"10.2217/BMT-2018-0019","DOIUrl":"https://doi.org/10.2217/BMT-2018-0019","url":null,"abstract":"","PeriodicalId":43086,"journal":{"name":"Breast Cancer Management","volume":" ","pages":""},"PeriodicalIF":0.7,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/BMT-2018-0019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49196556","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}
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