Recent Advances in Anti-Angiogenic Therapy of Cancer

Samant, Rajeev S.; Shevde, Lalita A.

doi:10.18632/oncotarget.234

Cited by 122 publications

(105 citation statements)

References 136 publications

(130 reference statements)

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“…Many cellular and molecular components of the tumor microenvironment have emerged as attractive targets for therapeutic strategies among carcinomas. MMPs have been implicated in many processes involved in tumor progression, such as antiangiogenesis (31,32). Despite the wealth of preclinical studies using MMP1 as a therapeutic target, clinical trials of MMP inhibitors in cancer therapy have proved to be disappointing (33).…”

Section: Discussionmentioning

confidence: 99%

Oncogenic KIT-containing exosomes increase gastrointestinal stromal tumor cell invasion

Atay

Banskota

Crow

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

145

107

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During tumor development, constant interplay occurs between tumor cells and surrounding stromal cells. We report evidence that gastrointestinal stromal tumor (GIST) cells invade the interstitial stroma through the release of the oncogenic protein tyrosine kinase (KIT)-containing exosomes, which triggers the phenotypic conversion of progenitor smooth muscle cells to tumor-promoting cells. These recipient cells display morphologic changes and acquire tumor-associated phenotypes, including enhanced adhesion to extracellular matrix proteins, activation of intracellular pathways downstream of KIT, expression of Interstitial Cell of Cajal-like markers, and release of various matrix metalloproteinases (MMPs), particularly MMP1. This report shows stimulation of MMP1 production by stromal cells via uptake of tumorderived exosomes, which leads to tumor cell invasion. Exosomes derived from GIST patients but not healthy donors show enhanced MMP1 secretion by smooth muscle cells and tumor cell invasion, whereas selective blocking of exosome-mediated MMP1 secretion decreases tumor invasiveness. Our study indicates that exosome release and subsequent MMP1 induction creates a positive feedback mechanism established between tumor and stromal cells that drives GIST development and offers unique insights for potential therapeutic strategies to block GIST progression and metastatic spread.ICC | crosstalk | microvesicles | tumor microenvironment

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Section: Discussionmentioning

confidence: 99%

Oncogenic KIT-containing exosomes increase gastrointestinal stromal tumor cell invasion

Atay

Banskota

Crow

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

145

107

View full text Add to dashboard Cite

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“…First of all, the influx of tumor-specific T-cells may be hampered by abnormal vascularization [25,26]. In both a xenograft transplant model and an immune refractory spontaneous murine model this problem could be overcome by treatment with low dose of gamma irradiation [25], or by targeting VEGF (vascular endothelial growth factor) [27]. However, even when the effector cells are inside the tumor they may encounter several immune suppressive hurdles before they can reach and kill the tumor cells [28].…”

Section: Treatment Of Advanced or End-stage Cancer May Fail Due To Immentioning

confidence: 99%

The importance of correctly timing cancer immunotherapy

Nejad

Welters

Arens

et al. 2016

Expert Opinion on Biological Therapy

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Introduction:The treatment options for cancer-surgery, radiotherapy and chemotherapy-are now supplemented with immunotherapy. Previously underappreciated but now gaining strong interest are the immune modulatory properties of the three conventional modalities. Moreover, there is a better understanding of the needs and potential of the different immune therapeutic platforms. Key to improved treatment will be the combinations of modalities that complete each other's shortcomings. Area covered: Tumor-specific T-cells are required for optimal immunotherapy. In this review, the authors focus on the correct timing of different types of chemotherapeutic agents or immune modulators and immunotherapeutic drugs, not only for the activation and expansion of tumor-specific Tcells but also to support and enhance their anti-tumor efficacy. Expert opinion: At an early phase of disease, clinical success can be obtained using single treatment modalities but at later disease stages, combinations of several modalities are required. The gain in success is determined by a thorough understanding of the direct and indirect immune effects of the modalities used. Profound knowledge of these effects requires optimal tuning of immunomonitoring. This will guide the appropriate combination of treatments and allow for correct sequencing the order and interval of the different therapeutic modalities. ARTICLE HISTORY

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“…Similarly, the movement of vascular endothelial cells represents an important aspect of angiogenesis and is a target for therapies designed to limit the size of tumors in patients with cancer (1,2). Cell migration can also be involved in pathological processes such as the metastasis of tumor cells to sites that are distant from the primary tumor (3).…”

mentioning

confidence: 99%

The Role of Microtubules and Their Dynamics in Cell Migration

Ganguly

Yang

Sharma

et al. 2012

Journal of Biological Chemistry

112

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Background: Microtubule effects on cell migration are poorly understood. Results: Tubulin mutations or drug treatments that suppress microtubule dynamics impede cell locomotion. Depolymerizing microtubules does not inhibit movement, but it becomes random. Conclusion: Microtubules act to restrain cell movement and specify directionality. Significance: Drugs have dose-dependent effects on microtubule behavior, cell migration, and mitosis. Understanding these actions will lead to more effective drug use.

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Recent Advances in Anti-Angiogenic Therapy of Cancer

Cited by 122 publications

References 136 publications

Oncogenic KIT-containing exosomes increase gastrointestinal stromal tumor cell invasion

Oncogenic KIT-containing exosomes increase gastrointestinal stromal tumor cell invasion

The importance of correctly timing cancer immunotherapy

The Role of Microtubules and Their Dynamics in Cell Migration

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