Imatinib tackles lymphoma via the PDGFRβ+ pericyte

Chute, John P.; Himburg, Heather A.

doi:10.1182/blood-2013-05-501205

Cited by 9 publications

(6 citation statements)

References 7 publications

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“…One way is to construct a drug delivery carrier that targets pericyte-overexpressed markers (NG2 proteoglycan, aminopeptidase A [APA]) to enhance the delivery efficacy of conventional anticancer drugs (docetaxel and doxorubicin), such as nanoparticles and liposomes conjugated to pericyte-targeting peptides (37,38). The other way is to target the pericyte itself by blockade of PDGFR-β on the pericyte membrane, including aptamers competing against PDGF (39) and PDGFR-β inhibitors (40,41). As NG2, APA, and PDGFR-β are also overexpressed in CAFs (42)(43)(44), the effect of these 2 pericyte-targeting approaches on CAFs is still unclear.…”

Section: Discussionmentioning

confidence: 99%

Pericyte-targeting prodrug overcomes tumor resistance to vascular disrupting agents

Chen

Lei

Shi

et al. 2017

Journal of Clinical Investigation

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Section: Discussionmentioning

confidence: 99%

Pericyte-targeting prodrug overcomes tumor resistance to vascular disrupting agents

Chen

Lei

Shi

et al. 2017

Journal of Clinical Investigation

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“…One approach to target pericytes is the use of ibrutinib that not only improves the permeability of blood-brain barrier but also prolongs animal survival by enhancing chemotherapeutic effectiveness [ 498 ]. Some other investigations have confirmed that the inhibition of PDGFRβ + pericytes with imatinib (a specific tyrosine kinase inhibitor) achieved pericytes depletion and delayed lymphoma growth in both murine allograft and human xenograft models [ 499 , 500 ]. Clinically, the main purpose of applying imatinib is to inhibit tumor angiogenesis, but this scheme often showed modest or no effect as a single agent or in combination with chemotherapy (NCT01738139, NCT00785785) [ 501 , 502 ].…”

Section: Targeted Therapy Based On Tumor Stromamentioning

confidence: 99%

Targeting the tumor stroma for cancer therapy

et al. 2022

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Tumors are comprised of both cancer cells and surrounding stromal components. As an essential part of the tumor microenvironment, the tumor stroma is highly dynamic, heterogeneous and commonly tumor-type specific, and it mainly includes noncellular compositions such as the extracellular matrix and the unique cancer-associated vascular system as well as a wide variety of cellular components including activated cancer-associated fibroblasts, mesenchymal stromal cells, pericytes. All these elements operate with each other in a coordinated fashion and collectively promote cancer initiation, progression, metastasis and therapeutic resistance. Over the past few decades, numerous studies have been conducted to study the interaction and crosstalk between stromal components and neoplastic cells. Meanwhile, we have also witnessed an exponential increase in the investigation and recognition of the critical roles of tumor stroma in solid tumors. A series of clinical trials targeting the tumor stroma have been launched continually. In this review, we introduce and discuss current advances in the understanding of various stromal elements and their roles in cancers. We also elaborate on potential novel approaches for tumor-stroma-based therapeutic targeting, with the aim to promote the leap from bench to bedside.

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“…Protein tyrosine kinases (PTKs) contribute in signal transduction pathways that regulate various cellular processes such as growth, metabolism, differentiation, adhesion and apoptosis. Deregulation of PTK activity has been associated with the pathogenesis of various cancers as well as other inflammatory diseases (Chute and Himburg, 2013;Dolman et al, 2012;Falke et al, 2015;Wallace and Gewin, 2013). Imatinib is a multi-targeted tyrosine kinase inhibitor (TKI) that is used as molecularly targeted therapy in different types of cancer.…”

Section: Introductionmentioning

confidence: 99%