scholarly journals Tumor-Associated Macrophages as Multifaceted Regulators of Breast Tumor Growth

2021 ◽  
Vol 22 (12) ◽  
pp. 6526
Author(s):  
Maliha Tabassum Munir ◽  
Matthew K. Kay ◽  
Min H. Kang ◽  
Md Mizanur Rahman ◽  
Ahmed Al-Harrasi ◽  
...  

Breast cancer is the most commonly occurring cancer in women of Western countries and is the leading cause of cancer-related mortality. The breast tumor microenvironment contains immune cells, fibroblasts, adipocytes, mesenchymal stem cells, and extracellular matrix. Among these cells, macrophages or tumor-associated macrophages (TAMs) are the major components of the breast cancer microenvironment. TAMs facilitate metastasis of the breast tumor and are responsible for poor clinical outcomes. High TAM density was also found liable for the poor prognosis of breast cancer. These observations make altering TAM function a potential therapeutic target to treat breast cancer. The present review summarizes the origin of TAMs, mechanisms of macrophage recruitment and polarization in the tumor, and the contributions of TAMs in tumor progression. We have also discussed our current knowledge about TAM-targeted therapies and the roles of miRNAs and exosomes in re-educating TAM function.

2017 ◽  
Vol 11 (1) ◽  
pp. 15-27 ◽  
Author(s):  
S. Pasquereau ◽  
F. Al Moussawi ◽  
W. Karam ◽  
M. Diab Assaf ◽  
A. Kumar ◽  
...  

The human cytomegalovirus (HCMV) is a betaherpesvirus that is highly host specific, infects among others epithelial cells and macrophages, and has been recently mentioned as having oncomodulatory properties. HCMV is detected in the breast tumor tissue where macrophages, especially tumor associated macrophages, are associated with a poor prognosis. In this review, we will discuss the potential implication of HCMV in breast cancer with emphasis on the role played by macrophages.


2004 ◽  
Vol 22 (14_suppl) ◽  
pp. 9510-9510 ◽  
Author(s):  
L. A. Carey ◽  
C. M. Perou ◽  
L. G. Dressler ◽  
C. A. Livasy ◽  
J. Geradts ◽  
...  

2004 ◽  
Vol 22 (14_suppl) ◽  
pp. 9510-9510 ◽  
Author(s):  
L. A. Carey ◽  
C. M. Perou ◽  
L. G. Dressler ◽  
C. A. Livasy ◽  
J. Geradts ◽  
...  

2020 ◽  
Vol 8 (1) ◽  
pp. 333-341 ◽  
Author(s):  
Roberto Molinaro ◽  
Jonathan O. Martinez ◽  
Assaf Zinger ◽  
Alessandro De Vita ◽  
Gianluca Storci ◽  
...  

Biomimetic nanovesicles deriving from leukocytes membrane proteins, called leukosomes, exhibit increased targeting of cancer vasculature and stroma by exploiting the inflammatory pathway responsible for recruiting immune cells to the cancer lesion.


Pteridines ◽  
2015 ◽  
Vol 26 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Marie Bartouskova ◽  
Bohuslav Melichar ◽  
Beatrice Mohelnikova-Duchonova

AbstractOvarian cancer is the most frequent cause of gynecological cancer-related death. Unfortunately, many patients are diagnosed at an advanced stage and have a poor prognosis. The standard treatment for advanced disease involves maximal cytoreductive surgery and chemotherapy based on platinum compounds and taxanes. Patients presenting at an advanced stage have a higher risk of recurrence. The development of drug resistance currently represents a major obstacle in the systematic treatment and, therefore, the discovery of new anticancer agents and approaches should improve the poor prognosis of these patients. Folate receptor α is overexpressed in epithelial ovarian cancer (EOC), but has limited expression in nonmalignant human tissues. The degree of folate receptor expression corresponds with the stage and grade of the disease. Because of this, folate receptor α seems to be a potential therapeutic target for the treatment of ovarian cancer. Currently, several approaches have been studied to target this protein in ovarian cancer treatment. This review summarizes current knowledge about the potential usage of folate receptors as prognostic and predictive biomarkers as well as their role in the management and targeted therapy of ovarian cancer.


2020 ◽  
Author(s):  
Ai Amioka ◽  
Takayuki Kadoya ◽  
Satoshi Sueoka ◽  
Yoshie Kobayashi ◽  
Shinsuke Sasada ◽  
...  

Abstract BackgroundIt was previously reported by us that Wnt5a-positive breast cancer can be classified as estrogen receptor (ER)-positive breast cancer and its prognosis is worse than that of Wnt5a-negative breast cancer. Herein, the molecular mechanisms underlying the poor prognosis of Wnt5a-positive breast cancer patients were examined. MethodsA total of 151 consecutive ER-positive breast cancer patients who underwent resection between January 2011 and February 2014 were enrolled. DNA microarray and pathway analyses were performed conducted using MCF-7 cells stably expressing Wnt5a (MCF-7/Wnt5a(+)). Based on the results, cell viability and drug sensitivity assays as well as mutation analysis , were performed using culture cells and breast cancer tissue. The relationship between Wnt5a and the PI3K–AKT–mTOR signaling pathway was examined.ResultsThe relapse-free survival rate in patients with Wnt5a-positive breast cancer was significantly lower than that in patients with Wnt5a-negative breast cancer ( P = 0.047). DNA microarray data indicated that only the cytochrome P450 (CYP) pathway was significantly upregulated in MCF-7/Wnt5a(+) cells ( P = 0.0440). MCF-7/Wnt5a(+) cells showed reduced sensitivity to the metabolic substrates of CYP, tamoxifen ( P < 0.001), and paclitaxel ( P < 0.001). PIK3CA mutations were unrelated to Wnt5a expression in breast cancer tissue and culture cells.ConclusionsIn ER-positive breast cancer, Wnt5a upregulated the CYP metabolic pathway; additionally, it inhibited the sensitivity to tamoxifen and paclitaxel, which constitute the standard treatment options for ER-positive breast cancer. Wnt5a could be involved in the poor prognosis of ER-positive breast cancer independently of the PI3K–AKT–mTOR signaling pathway.


Author(s):  
Mengyao Xu ◽  
Shan Huang ◽  
Xiaoli Dong ◽  
Yanan Chen ◽  
Miao Li ◽  
...  

Abstract Metastases are the main cause of cancer-related mortality in breast cancer. Although significant progress has been made in the field of tumor metastasis, the exact molecular mechanisms involved in tumor metastasis are still unclear. Here, we report that ATOH8-V1, a novel isoform of ATOH8, is highly expressed in breast cancer and is a negative prognostic indicator of survival for patients. Forced expression of ATOH8-V1 dramatically enhances, while silencing of ATOH8-V1 decreases the metastasis of breast cancer cell lines. Moreover, ATOH8-V1 directly binds to the RhoC promoter and stimulates the expression of RhoC, which in turn enhances the metastasis of breast cancer. Altogether, our data demonstrate that ATOH8-V1 is a novel pro-metastatic factor that enhances cancer metastasis, suggesting that ATOH8-V1 is a potential therapeutic target for treatment of metastatic cancers.


Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2479
Author(s):  
Xiaoping Wang ◽  
Takashi Semba ◽  
Lan Thi Hanh Phi ◽  
Sudpreeda Chainitikun ◽  
Toshiaki Iwase ◽  
...  

Inflammatory breast cancer (IBC), although rare, is the most aggressive type of breast cancer. Only 2–4% of breast cancer cases are classified as IBC, but—owing to its high rate of metastasis and poor prognosis—8% to 10% of breast cancer-related mortality occur in patients with IBC. Currently, IBC-specific targeted therapies are not available, and there is a critical need for novel therapies derived via understanding novel targets. In this review, we summarize the biological functions of critical signaling pathways in the progression of IBC and the preclinical and clinical studies of targeting these pathways in IBC. We also discuss studies of crosstalk between several signaling pathways and the IBC tumor microenvironment.


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