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2 edition of Mechanisms of epithelial tumor growth and metastasis: a role for transforming growth factor gbs. found in the catalog.

Mechanisms of epithelial tumor growth and metastasis: a role for transforming growth factor gbs.

Dan Theodorescu

Mechanisms of epithelial tumor growth and metastasis: a role for transforming growth factor gbs.

by Dan Theodorescu

  • 338 Want to read
  • 23 Currently reading

Published .
Written in English


The Physical Object
Pagination202 leaves.
Number of Pages202
ID Numbers
Open LibraryOL14723768M

Inhibition of tumor suppressive signaling is linked to cancer progression, metastasis and epithelial–mesenchymal transition (EMT). Transforming growth factor-β1 (TGF-β)/Smad signaling plays an important role in tumor suppression. Kruppel-like-factor 17 (KLF17) is a negative regulator of metastasis and EMT. However, underlying mechanisms leading to tumor suppressive and anti-metastatic. Transforming growth factor {beta}1 (TGF{beta}) is a tumor suppressor during the initial stage of tumorigenesis, but it can switch to a tumor promoter during neoplastic progression. Ionizing radiation (IR), both a carcinogen and a therapeutic agent, induces TGF{beta}, activation in vivo.

  Epidermal Growth Factor (EGF) and Transforming Growth Factor α (TGF-α) • • • • • • • These two factors belong to the EGF family and share a common receptor (EGFR). EGF is mitogenic for a variety of epithelial cells, hepatocytes and fibroblasts, Widely distributed in tissue secretions and fluids.   Metastasis to distant organs and particularly the brain still represents the most serious obstacle in melanoma therapies. Melanoma cells acquire a phenotype to metastasize to the brain and successfully grow there through complex mechanisms determined by microenvironmental than rather genetic cues. There do appear to be some prerequisites, including the presence of oncogenic BRAF Cited by: 6.

Abstract. Transforming growth factor beta (TGF-β) plays a significant role in the regulation of the tumor microenvironment. To explore the role of TGF-β in oral cancer-induced bone destruction, we investigated the immunohistochemical localization of TGF-β and phosphorylated Smad2 (p-Smad2) in 12 surgical specimens of oral squamous cell carcinoma (OSCC). Transforming growth factor-beta signaling in epithelial-mesenchymal transition and progression of cancer. and plays an important role in the induction of -beta inhibitors prevent invasion and metastasis of advanced cancer through multiple mechanisms, TGF-beta-induced EMT but not TGF-beta-induced growth arrest may be an ideal.


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Mechanisms of epithelial tumor growth and metastasis: a role for transforming growth factor gbs by Dan Theodorescu Download PDF EPUB FB2

Transforming growth factor-beta signaling during epithelial-mesenchymal transformation: implications for embryogenesis and tumor metastasis.

Nawshad A(1), Lagamba D, Polad A, Hay ED. Author information: (1)Department of Oral Biology, College of Dentistry, University of Nebraska Medical Center, Lincoln, NEUSA.

[email protected] by:   Transforming growth factor β generally has a positive role in cancer dissemination and metastasis due to the shift of the TGFβ response from growth arrest to invasion and metastatic Cited by:   The process of epithelial to mesenchymal transition (EMT), first noted during embryogenesis, has also been reported in tumor formation and leads to the development of metastatic growth.

It is a naturally occurring process that drives the transformation of adhesive, non-mobile epithelial like cells into mobile cells with a mesenchymal phenotype Cited by: All of these mechanisms have been found to play a role in transforming growth factor‐α, angiogenin ‐cadherin has been found to be associated with cancer progression.

27 Transfection of the E‐cadherin cDNA into highly metastatic epithelial tumor lines results in decreased invasiveness of cells in vitro and more. In Breast Cancer: Cellular and Molecular Biology [Kluwer Academic Pub lishers, ], we tried to present an introduction to the emerging basic studies on steroid receptors, oncogenes, and growth factors in the regulation of normal and malignant mammary epithelium.

The response to this volume was superb, indicating a tremendous interest in basic growth regulatory mechanisms governing breast.

The invasion of bone tissue by tumor cells indeed affects the balance between bone resorption and bone formation. This deregulation induces the release of cytokines or growth factors initially trapped in the bone matrix, such as transforming growth factor-β (TGF-β), which in turn promote tumor by:   Transforming growth factor-β is one factor which can promote the growth and motility of Walker cells, a rat cell line with a propensity to metastasize spontaneously to bone.

The metastasis of cancer to bone is a frequent outcome of common malignancies and is often associated with significant morbidity due to by:   Transforming growth factor-beta (TGF-β) is a multifunctional regulatory polypeptide that is the prototypical member of a large family of cytokines that controls many aspects of cellular function, including cellular proliferation, differentiation, migration, apoptosis, adhesion, angiogenesis, immune surveillance, and by: 1.

There is also in vitro evidence that exposure of rat alveolar epithelial cells to transforming growth factor (TGF)-β1 can induce fibroblast-like function and morphology (Willis et al. It is possible that anticancer drug-induced pulmonary fibrosis develops in part as a consequence of epithelial injuries caused by the cytotoxic drugs.

EMT is the transformation of epithelial cells to a mesenchymal phenotype exacerbating motility and invasiveness of various epithelial cell types. In this review we focus on EMT in hepatic fibrosis, HCC and CCC that is governed by the transforming growth factor (TGF)-β signaling.

Lung cancer metastasis involves specific molecular pathways that confer the cancer cells abilities to survive in circulation, be motile, and form new tumors.

Recent evidences have widened the understanding of cancer disseminating basis and emphasized the role of genetic and epigenetic imperfections, epithelial to mesenchymal transition, and Cited by: 4.

Transforming Growth Factor-ß in Cancer Therapy, Volumes 1 and 2, provides a compendium of findings about the role of transforming growth factor-ß (TGF-ß) in cancer treatment and therapy. The second volume, Cancer Treatment and Therapy, is divided into three parts.

Part I examines transforming growth factor-ß in developing and advanced cancers. This specificity seems to be mediated by soluble signal molecules such as chemokines and transforming growth factor beta. The body resists metastasis by a variety of mechanisms through the actions of a class of proteins known as metastasis suppressors, of which about a dozen are ciation: Metastasis /mᵻˈtastəsɪs/ metastases.

For example, transforming growth factor beta (TGFβ) promotes metastasis of breast cancer to the lungs but it is dispensable to bone metastasis, which is mediated Cited by: TGF-β supresses tumor growth in the early phase of neoplasia, while promotes tumor progression and metastasis in later phases.

Thus, many malignant cells produce large amounts of TGF-β, but are resistant to its growth inhibitory by: 6. Accelerated bone resorption, in turn, promotes the release of bone-derived growth factors such as transforming growth factor-beta (TGF-β), the insulin-like growth factor (IGF)-1, and raised extracellular calcium concentration to further support the growth of cancer cells [9,10].

However, the mechanism of action of bone metastases development Cited by: 2. Graphical Abstract Mechanisms of integrin-mediated transforming growth factor beta (TGFβ) activation and its effect on stromal processes.

1 Matrix-bound latent LAP-TGFβ1 binds αv integrins. Cancer metastasis is a multistep process that involves tumor cell migration and invasion through tumor stroma, intravasation into and extravasation out of the blood vessels, and accumulation at a distant organ site.

These events arise from concomitant alterations in the genetic, chemical, and physical state of tumor cells and its by: 1. Experimental oncogene induced prostate cancer --Regulation of differentiation and growth of normal adult and neoplastic epithelia by inductive mesenchyme --Reciprocal mesenchymal-epithelial interaction affecting prostate tumour growth and hormonal responsiveness --Polypeptide modulators of prostatic growth and development.

INTRODUCTION. Epithelial-mesenchymal transition (EMT) is a fundamental mechanism of development (Hay, ) that is responsible for initiating pathological conditions in the adult organism, such as tumor metastasis (Thiery, ) and organ fibrosis (Zeisberg and Kalluri, ).This cellular transformation results in loss of cell adhesion and apical-basal polarity, followed by a shift in.

Epidermal growth factor receptor (EGFR) is overexpressed in several epithelial malignancies, including head and neck squamous cell carcinoma (HNSCC), which exhibits EGFR overexpression in up to 90% of tumors.

EGFR ligands such as transforming growth factor alpha are also overexpressed in HNSCC. EGFR plays a critical role in HNSCC growth, invasion, metastasis and angiogenesis. However, Cited by: Transforming Growth Factor- ss in Cancer Therapy, Vols. 1 and 2, provides a compendium of findings about the role of transforming growth factor- ss (TGF- ss) in cancer treatment and therapy.

The second volume, Cancer Treatment in Therapy, is divided into three parts. The companion volume details the role of TGF- ss on basic and clinical biology. Metastases account for 90% of all cancer-related deaths, becoming a therapeutic problem.

Approximately 50% of all uveal melanoma (UM) patients will develop metastases, mainly in the liver. Post-mortem analyses of livers from metastatic UM patients showed two different metastatic growth patterns: infiltrative and nodular.

The infiltrative pattern exhibits tumor infiltration directly to the Cited by: 3.