The Role of Stromal Myofibroblast and Extracellular Matrix in Tumor Angiogenesis

Vong, Sylvia; Kalluri, Raghu

doi:10.1177/1947601911423940

Cited by 107 publications

(90 citation statements)

References 92 publications

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“…The stroma includes cancer-associated fibroblasts (CAFs), inflammatory cells and endothelial cells, which facilitate EMT induction and drive metastatic progression through interaction with cancer cells (Vong & Kalluri 2012). Arnold et al (2002) observed that secretions from normal endometrial fibroblast cells can inhibit proliferation of Ishikawa cells.…”

Section: Role Of Tumor Microenvironmentmentioning

confidence: 99%

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Makker

Goel

2015

Endocrine-Related Cancer

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Endometrioid endometrial carcinoma (EEC), also known as type 1 endometrial cancer (EC), accounts for over 70-80% of all cases that are usually associated with estrogen stimulation and often develops in a background of atypical endometrial hyperplasia. The increased incidence of EC is mainly confined to this type of cancer. Most EEC patients present at an early stage and generally have a favorable prognosis; however, up to 30% of EEC present as high risk tumors, which have invaded deep into the myometrium at diagnosis and progressively lead to local or extra pelvic metastasis. The poor survival of advanced EC is related to the lack of effective therapies, which can be attributed to poor understanding of the molecular mechanisms underlying the progression of disease toward invasion and metastasis. Multiple lines of evidence illustrate that epithelial-mesenchymal transition (EMT)-like events are central to tumor progression and malignant transformation, endowing the incipient cancer cell with invasive and metastatic properties. The aim of this review is to summarize the current knowledge on molecular events associated with EMT in progression, invasion, and metastasis of EEC. Further, the role of epigenetic modifications and microRNA regulation, tumor microenvironment, and microcystic elongated and fragmented glands like invasion pattern have been discussed. We believe this article may perhaps stimulate further research in this field that may aid in identifying high risk patients within this clinically challenging patient group and also lead to the recognition of novel targets for the prevention of metastasis -the most fatal consequence of endometrial carcinogenesis.

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Section: Role Of Tumor Microenvironmentmentioning

confidence: 99%

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Makker

Goel

2015

Endocrine-Related Cancer

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“…58,111,112 It has been estimated that a tumour cannot grow beyond a volume of 2 mm 3 without the development of new vessels to provide the proliferating cells with oxygen and nutrients. 58 Angiogenesis is thus a pivotal step in tumour development, and is one of the so-called 'hallmarks of cancer'.…”

Section: Vasculature/endotheliummentioning

confidence: 99%

“…For more detail the reader is referred to the review by Vong and Kalluri. 58 During tumour progression, matrix remodelling leads to the release of matrixassociated growth factors which may function to suppress or induce tumour growth.…”

Section: Extracellular Matrixmentioning

confidence: 99%

Is carcinoma a mesenchymal disease? The role of the stromal microenvironment in carcinogenesis

Hemmings

2013

Pathology

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“…A Study have showed that TGF-β1 expressing exosomes can initiate the development of fibroblasts to myofibroblasts [56]. Myofibroblasts release considerable matrix remodeling proteins within the tumor microenvironment and contribute to tumor angiogenesis [57]. Cancer exosome-induced stimulation of fibroblasts could favor tumor angiogenesis.…”

Section: Mini Reviewmentioning

confidence: 99%

Prostate Cancer Cells Produce Exosomes Modulating Metastasis to the Bones

Famuyiwa¹

2017

JCPCR

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Prostate cancer metastasis to the bone is a frightening cause of death world-wide. Patients do not live a functional and active life before they eventually die. The major reason for prostate cancer metastasis is the use of poor bio markers such as Prostatespecific antigen (PSA) and histopathological grading to diagnose prostate cancer incorrectly, indicating that a patient who has a stage four prostate has a benign tumor. New and effective markers for prostate cancer are urgently needed. The goal of this review is to examine modulation of prostate cancer (PCa) exosome interaction with prostate cancer micro-environment as a major support system to prevent incurable bone cancer. Conventional prostate cancer therapy is weakened by exchange of growth factors between cancer cells and it surroundings, leading to increase tumor growth and metastasis to other parts of the body. The surrounding of tumor includes prostate cancer exosomes, which can be release under suitable condition. Basically, the interactions between prostate cancer exosomes, growth factors and cell microenvironment support uncontrollable metastasis of prostate cancer to the bone. PCa exosome modification may be the solution to the increasing patient death caused by prostate cancer metastasis to the bone. PCa exosome is in the fore-front of research as a biomarker for early prostate cancer detection.

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The Role of Stromal Myofibroblast and Extracellular Matrix in Tumor Angiogenesis

Cited by 107 publications

References 92 publications

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Is carcinoma a mesenchymal disease? The role of the stromal microenvironment in carcinogenesis

Prostate Cancer Cells Produce Exosomes Modulating Metastasis to the Bones

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