Topic
Growth factor receptor inhibitor
About: Growth factor receptor inhibitor is a research topic. Over the lifetime, 4730 publications have been published within this topic receiving 297500 citations.
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TL;DR: It is concluded that rab7 regulates the endocytic trafficking of the EGF·EGFR complex by regulating its lysosomal degradation.
155 citations
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TL;DR: It is found that sterile wounding initiates an innate immune response that increases resistance to overt infection and microbial colonization through activation of the epidermal growth factor receptor.
Abstract: We found that sterile wounding of human skin induced epidermal expression of the antimicrobial (poly)peptides human β-defensin–3, neutrophil gelatinase–associated lipocalin, and secretory leukocyte protease inhibitor through activation of the epidermal growth factor receptor. After skin wounding, the receptor was activated by heparin-binding epidermal growth factor that was released by a metalloprotease-dependent mechanism. Activation of the epidermal growth factor receptor generated antimicrobial concentrations of human β-defensin–3 and increased the activity of organotypic epidermal cultures against Staphylococcus aureus. These data demonstrate that sterile wounding initiates an innate immune response that increases resistance to overt infection and microbial colonization.
155 citations
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TL;DR: The results suggest that Npn-1 possesses a “heparin” mimetic site that is able to interact at least in part through ionic bonding with the heparin binding site on many of the proteins studied.
154 citations
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TL;DR: It is demonstrated that adenovirus-mediated expression of a soluble VEGF receptor in a remote organ could inhibit tumor angiogenesis and enhance apoptosis and thereby suppress tumor growth in vivo.
Abstract: Antiangiogenic therapy shows promise as a strategy for cancer treatment.
We constructed an adenovirus (AdVEGF-ExR) expressing the entire
extracellular domain of the human vascular endothelial growth factor
(VEGF) receptor ( flt-1 ) fused to the Fc portion of human
IgG. The soluble receptor secreted from AdVEGF-ExR-infected cells bound
to VEGF and inhibited VEGF-induced DNA synthesis in endothelial cells.
When human lung cancer cell line H157, which produces not only VEGF but
also fibroblast growth factor 2 and interleukin 8 at substantial
levels, was infected with AdVEGF-ExR, cell growth in
vitro was not affected. However, when H157 cells infected with
AdVEGF-ExR were injected s.c. into nude mice, tumor formation stopped
on the 10th day after reaching a certain size (about 100
mm 3 ), and tumor size declined gradually thereafter. When
AdVEGF-ExR was injected into skeletal muscle and uninfected H157 cells
were injected s.c., the soluble receptor was detectable in the
circulating blood for 3 weeks, tumor growth ceased after 10 days, and
tumor size declined thereafter. Histological examination revealed that
intratumor angiogenesis was markedly suppressed, and apoptosis was
enhanced. Using the same experimental protocol, a significant
suppression of tumor growth was also seen in four of five other lung
cancer cell lines, some of which secreted VEGF at nominal levels, at
least under normoxic conditions in vitro . Our results
demonstrate that adenovirus-mediated expression of a soluble VEGF
receptor in a remote organ could inhibit tumor angiogenesis and enhance
apoptosis and thereby suppress tumor growth in vivo .
Adenovirus-mediated overexpression of a soluble VEGF receptor in a
remote organ may have the potential to be a feasible and effective
strategy for cancer treatment.
154 citations
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TL;DR: The overall management of breast cancer will increasingly require an understanding of Breast cancer heterogeneicity, the biological nature of any given tumor as well the existence of increased personalized treatment options.
Abstract: Breast cancer is a heterogeneous disease with different molecular drivers regulating its growth, survival and treatment response. Drug development efforts have resulted in agents against new molecular targets that are active against only those tumors with the targeted molecular alteration or phenotype. The authors critically discuss the recently established and investigational strategies for the treatment of the main breast cancer subtypes. Breast cancer is a heterogeneous disease with different molecular drivers regulating its growth, survival and response to therapy. Breast cancer is divided in three major subtypes based on the pattern of expression of hormone receptors and HER2: luminal tumors (or HR positive), HER2 amplified tumors, and the remaining subtypes being collectively referred to as triple-negative breast cancer. While tumors within these subtypes have similar gene-expression patterns, clinical outcomes, and response to therapy, this division is far from perfect and subgroups within these groups are beginning to be identified. In terms of therapy, an increasingly rational drug development effort has resulted in agents against new molecular targets that are active against only those tumors with the targeted molecular alteration or phenotype. These agents include receptor and non-receptor tyrosine kinase inhibitors (HER1, HER2, HER3, insulin-like growth factor receptor, c-met, fibroblast growth factor receptor and HSP 90 inhibitors), intracellular signaling pathways (PI3K, AKT, mTOR), angiogenesis inhibitors and agents that interfere with DNA repair (PARP inhibitors). Thus, the overall management of breast cancer will increasingly require an understanding of breast cancer heterogeneicity, the biological nature of any given tumor as well the existence of increased personalized treatment options.
154 citations