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Mechanisms of Acquired Resistance to Tyrosine Kinase Inhibitors in Clear - Cell Renal Cell Carcinoma (ccRCC)

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TLDR
Molecular analysis concerning acquired, non-genetic resistance to TKIs, with insight into specific biological processes in clear-cell renal cell carcinoma is focused on.
Abstract
Researchers have specified different subsets of tyrosine kinase inhibitors potential resistance mechanisms in clear-cell renal cell carcinoma. In most papers published until now, drug resistance is divided into intrinsic and acquired, and typically multi-drug resistance (MDR) protein is described. Herein, the authors focus on molecular analysis concerning acquired, non-genetic resistance to TKIs, with insight into specific biological processes.

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The epithelial-to-mesenchymal transition and cancer stem cells : a coalition against cancer therapies

TL;DR: The EMT process may facilitate the generation of cancer cells with the mesenchymal traits needed for dissemination as well as the self-renewal properties needed for initiation of secondary tumors.
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The role of tumor microenvironment in therapeutic resistance.

TL;DR: This review highlights myeloid cells, cancer-associated fibroblasts, and mesenchymal stem cells consisting of the tumor microenvironment, as well as the relevant signaling pathways that eventually render cancer cells to be therapeutically resistant.
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Potential molecular, cellular and microenvironmental mechanism of sorafenib resistance in hepatocellular carcinoma.

TL;DR: Systemic insight is provided into the potential molecular, cellular and microenvironmental mechanism of sorafenib resistance in hepatocellular carcinoma depending on abundant previous studies and reports.
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Molecular Biology of Osteosarcoma

TL;DR: Activity and safety of cabozantinib in osteosarcoma were studied, as well as sorafenib and pazopanib, and novel bifunctional molecules, of potential imaging and osteosARcoma targeting applications may be used in the future.

Epidermal growth factor-induced epithelio-mesenchymal transition in human breast carcinoma cells

TL;DR: In this article, the epidermal growth factor (EGF) was shown to increase the motility of PMC42-LA cells and increase the mesenchyme-associated extracellular matrix molecules fibronectin and chondroitin sulfate proteoglycan.
References
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Journal ArticleDOI

Sunitinib versus interferon alfa in metastatic renal-cell carcinoma.

TL;DR: Progression-free survival was longer and response rates were higher in patients with metastatic renal-cell cancer who received sunitinib than in those receiving interferon alfa.
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Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes

TL;DR: These functionally polarized cells, and similarly oriented or immature dendritic cells present in tumors, have a key role in subversion of adaptive immunity and in inflammatory circuits that promote tumor growth and progression.
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Sorafenib in advanced clear-cell renal-cell carcinoma.

TL;DR: As compared with placebo, treatment with sorafenib prolongs progression-free survival in patients with advanced clear-cell renal-cell carcinoma in whom previous therapy has failed; however, treatment is associated with increased toxic effects.
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A Perspective on Cancer Cell Metastasis

TL;DR: It is suggested that metastasis can be portrayed as a two-phase process: the first phase involves the physical translocation of a cancer cell to a distant organ, whereas the second encompasses the ability of the cancer cellto develop into a metastatic lesion at that distant site.
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