Minimal information for studies of extracellular vesicles 2018 (MISEV2018): a position statement of the International Society for Extracellular Vesicles and update of the MISEV2014 guidelines
- C. Théry, K. Witwer, E. Zuba-Surma
- BiologyJournal of Extracellular Vesicles
- 23 November 2018
The MISEV2018 guidelines include tables and outlines of suggested protocols and steps to follow to document specific EV-associated functional activities, and a checklist is provided with summaries of key points.
Intercellular transfer of the oncogenic receptor EGFRvIII by microvesicles derived from tumour cells
- K. Al-Nedawi, B. Meehan, J. Rak
- BiologyNature Cell Biology
- 20 April 2008
It is shown that EGFRvIII can be 'shared' between glioma cells by intercellular transfer of membrane-derived microvesicles ('oncosomes'), which can contribute to a horizontal propagation of oncogenes and their associated transforming phenotype among subsets of cancer cells.
Endothelial expression of autocrine VEGF upon the uptake of tumor-derived microvesicles containing oncogenic EGFR
- K. Al-Nedawi, B. Meehan, R. Kerbel, A. Allison, J. Rak
- BiologyProceedings of the National Academy of Sciences
- 10 March 2009
It is proposed that oncogene-containing tumor cell-derived MVs could act as a unique form of angiogenesis-modulating stimuli and are capable of switching endothelial cells to act in an autocrine mode.
A reference map of the human binary protein interactome
- Katja Luck, Dae-Kyum Kim, M. Calderwood
- BiologyNature
- 23 February 2020
The utility of HuRI is demonstrated in identifying the specific subcellular roles of protein–protein interactions and in identifying potential molecular mechanisms that might underlie tissue-specific phenotypes of Mendelian diseases.
Acquired resistance to the antitumor effect of epidermal growth factor receptor-blocking antibodies in vivo: a role for altered tumor angiogenesis.
- A. Viloria-Petit, T. Crombet, R. Kerbel
- Biology, MedicineCancer Research
- 1 July 2001
The results suggest that variants displaying acquired resistance to anti-EGFR antibodies can emerge in vivo and can do so, at least in part, by mechanisms involving the selection of tumor cell subpopulations with increased angiogenic potential.
Continuous low-dose therapy with vinblastine and VEGF receptor-2 antibody induces sustained tumor regression without overt toxicity.
- G. Klement, S. Baruchel, R. Kerbel
- Biology, MedicineJournal of Clinical Investigation
- 2000
A combination therapy with DC101 and low-dose vinblastine resulted in full and sustained regressions of large established tumors, without an ensuing increase in host toxicity or any signs of acquired drug resistance during the course of treatment, which lasted for >6 months.
CD44 regulates hematopoietic progenitor distribution, granuloma formation, and tumorigenicity.
- R. Schmits, J. Filmus, T. Mak
- Medicine, BiologyBlood
- 15 September 1997
Tumor studies showed that SV40-transformed CD44-deficient fibroblasts were highly tumorigenic in nude mice, whereas reintroduction of CD44s expression into these fibro Blasts resulted in a dramatic inhibition of tumor growth.
Neutralizing antibodies against epidermal growth factor and ErbB-2/neu receptor tyrosine kinases down-regulate vascular endothelial growth factor production by tumor cells in vitro and in vivo:…
Therapeutic disruption of EGFR or ErbB2/neu protein function in vivo may result in partial suppression of angiogenesis, a feature that could enhance the therapeutic index of such agents in vivo and endow them with anti-tumor effects, the magnitude of which may be out of proportion with their observed cytostatic effects in monolayer tissue culture.
Mutant ras oncogenes upregulate VEGF/VPF expression: implications for induction and inhibition of tumor angiogenesis.
- J. Rak, Y. Mitsuhashi, R. Kerbel
- BiologyCancer Research
- 15 October 1995
The results suggest that dominantly acting ras oncogenes may contribute to the growth of solid tumors in vivo not only by a direct effect on tumor cell proliferation but also indirectly, i.e., by facilitating tumor angiogenesis.
Oncogenic events regulate tissue factor expression in colorectal cancer cells: implications for tumor progression and angiogenesis.
It is reported that in human colorectal cancer cells, TF expression is under control of 2 major transforming events driving disease progression, in a manner dependent on MEK/mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3'-kinase (PI3K).
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