Current Landscape: The Mechanism and Therapeutic Impact of Obesity for Breast Cancer

Obesity is defined as a chronic disease induced by an imbalance of energy homeostasis. Obesity is a widespread health problem with increasing prevalence worldwide. Breast cancer (BC) has already been the most common cancer and one of the leading causes of cancer death in women worldwide. Nowadays, the impact of the rising prevalence of obesity has been recognized as a nonnegligible issue for BC development, outcome, and management. Adipokines, insulin and insulin-like growth factor, sex hormone and the chronic inflammation state play critical roles in the vicious crosstalk between obesity and BC. Furthermore, obesity can affect the efficacy and side effects of multiple therapies such as surgery, radiotherapy, chemotherapy, endocrine therapy, immunotherapy and weight management of BC. In this review, we focus on the current landscape of the mechanisms of obesity in fueling BC and the impact of obesity on diverse therapeutic interventions. An in-depth exploration of the underlying mechanisms linking obesity and BC will improve the efficiency of the existing treatments and even provide novel treatment strategies for BC treatment.

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Missing links — epigenetic regulators of the pancreatic cancer–associated inflammation

Clinical Science ◽

10.1042/cs20210181 ◽

2021 ◽

Vol 135 (10) ◽

pp. 1289-1293

Author(s):

Gregor Werba ◽

Tamas A. Gonda

Keyword(s):

Pancreatic Cancer ◽

Noncoding Rna ◽

Current Knowledge ◽

Treatment Strategies ◽

Therapeutic Interventions ◽

Ductal Adenocarcinoma ◽

Gastrointestinal Cancers ◽

Novel Treatment ◽

Epigenetic Regulator ◽

Novel Treatment Strategies

Abstract Pancreatic ductal adenocarcinoma (PDAC) features a hostile tumor microenvironment (TME) that renders it remarkably resistant to most therapeutic interventions. Consequently, survival remains among the poorest compared with other gastrointestinal cancers. Concerted efforts are underway to decipher the complex PDAC TME, break down barriers to efficacious therapies and identify novel treatment strategies. In the recent Clinical Science, Li and colleagues identify the long noncoding RNA KLHDC7B-DT as a crucial epigenetic regulator of IL-6 transcription in PDAC and illustrate its potent influences on the pancreatic TME. In this commentary, we introduce epigenetics in pancreatic cancer and put the findings by Li et al. in context with current knowledge.

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Therapy after cyclin‐dependent kinase inhibition in metastatic hormone receptor‐positive breast cancer: Resistance mechanisms and novel treatment strategies

Cancer ◽

10.1002/cncr.32931 ◽

2020 ◽

Vol 126 (15) ◽

pp. 3400-3416 ◽

Cited By ~ 2

Author(s):

Marina N. Sharifi ◽

Apoorva Anandan ◽

Patrick Grogan ◽

Ruth M. O’Regan

Keyword(s):

Breast Cancer ◽

Hormone Receptor ◽

Treatment Strategies ◽

Resistance Mechanisms ◽

Cyclin Dependent Kinase ◽

Cancer Resistance ◽

Hormone Receptor Positive ◽

Novel Treatment ◽

Novel Treatment Strategies ◽

Positive Breast Cancer

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Provasopressin expression by breast cancer cells: implications for growth and novel treatment strategies

Breast Cancer Research and Treatment ◽

10.1007/s10549-005-9024-8 ◽

2005 ◽

Vol 95 (3) ◽

pp. 265-277 ◽

Cited By ~ 29

Author(s):

Brendan P. Keegan ◽

Bonnie L. Akerman ◽

Christel Péqueux ◽

William G. North

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Treatment Strategies ◽

Novel Treatment ◽

Novel Treatment Strategies

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Novel treatment strategies for patients with relapsed classical Hodgkin lymphoma

Hematology ◽

10.1182/asheducation-2009.1.507 ◽

2009 ◽

Vol 2009 (1) ◽

pp. 507-519 ◽

Cited By ~ 37

Author(s):

Anas Younes

Keyword(s):

Stem Cell ◽

Stem Cell Transplantation ◽

Hodgkin Lymphoma ◽

Cell Transplantation ◽

Treatment Strategies ◽

Treatment Modalities ◽

Classical Hodgkin Lymphoma ◽

Novel Treatment ◽

Novel Treatment Strategies ◽

The Impact

AbstractAlthough classical Hodgkin lymphoma (HL) is considered one of the most curable human cancers, the treatment of patients with relapsed and refractory disease, especially those who relapse after autologous stem cell transplantation, remains challenging. Furthermore, because the median age of the patients is in the mid-30s, the impact of early mortality on the number of years lost from productive life is remarkable. Patients with HL whose disease relapses after stem cell transplantation are rarely cured with current treatment modalities. New drugs and novel treatment strategies that are based on our understanding of the disease biology and signaling pathways are needed to improve treatment outcome for these patients. This review will focus on emerging new treatment modalities that are currently under investigation for patients with relapsed classical HL.

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Novel treatment strategies in triple-negative breast cancer: specific role of poly(adenosine diphosphate-ribose) polymerase inhibition

Pharmacogenomics and Personalized Medicine ◽

10.2147/pgpm.s39765 ◽

2014 ◽

pp. 307 ◽

Cited By ~ 8

Author(s):

William Audeh

Keyword(s):

Breast Cancer ◽

Triple Negative Breast Cancer ◽

Triple Negative ◽

Treatment Strategies ◽

Adenosine Diphosphate ◽

Specific Role ◽

Novel Treatment ◽

Novel Treatment Strategies

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Breast Cancer Stem Cell-Derived ANXA6-Containing Exosomes Sustain Paclitaxel Resistance and Cancer Aggressiveness in Breast Cancer

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.718721 ◽

2021 ◽

Vol 9 ◽

Author(s):

Zihe Guo ◽

Ayao Guo ◽

Chuang Zhou

Keyword(s):

Breast Cancer ◽

Cancer Progression ◽

Molecular Mechanisms ◽

Hippo Pathway ◽

Treatment Strategies ◽

Dependent Manner ◽

Promote Cell Migration ◽

Cancer Aggressiveness ◽

Novel Treatment Strategies ◽

Underlying Mechanisms

Continuous chemotherapy pressure-elicited annexin-A6 (ANXA6)-containing exosome (ANXA6-exo) secretion contributes to paclitaxel (PTX) resistance in breast cancer (BC), but the molecular mechanisms are not fully elucidated. The present study managed to investigate this issue and found that ANXA6-exo promoted PTX resistance and cancer progression in BC cells in a Yes-associated protein 1 (YAP1)-dependent manner. Specifically, the parental PTX-sensitive BC (PS-BC) cells were exposed to continuous low-dose PTX to generate PTX-resistant BC (PR-BC) cells, and we found that BC stem cells tended to be enriched in the descendent PR-BC cells in contrast with the PS-BC cells. In addition, PR-BC cell-derived exosomes were featured with highly expressed ANXA6, and ANXA6-exo delivered ANXA6 to promote cell migration, growth, autophagy, and stemness in PS-BC cells. Interestingly, ANXA6-exo increased PTX resistance in PS-BC cells via inducing autophagy, and the effects of ANXA6-exo on PTX resistance in PS-BC cells were abrogated by co-treating cells with the autophagy inhibitor 3-methyladenine. Moreover, the underlying mechanisms were uncovered, and we evidenced that ANXA6-exo up-regulated YAP1 to promote Hippo pathway dysregulation, and the promoting effects of ANXA6-exo on PTX resistance and cancer aggressiveness in BC cells were abrogated by silencing YAP1. Taken together, this study firstly elucidated the underlying mechanisms by which BCSC-derived ANXA6-exo facilitated BC progression and PTX resistance, which might help to develop novel treatment strategies for BC in clinic.

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