Author
Kari Alitalo
Other affiliations: Mount Sinai Hospital, Toronto, Cornell University, Kyoto University ...read more
Bio: Kari Alitalo is an academic researcher from University of Helsinki. The author has contributed to research in topics: Angiogenesis & Vascular endothelial growth factor C. The author has an hindex of 174, co-authored 817 publications receiving 114231 citations. Previous affiliations of Kari Alitalo include Mount Sinai Hospital, Toronto & Cornell University.
Papers published on a yearly basis
Papers
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Patent•
03 Sep 2019TL;DR: In this article, the use of anti-Ang2 antibodies or antigen-binding fragments thereof for treating ischemia is discussed, and the methods are useful for reducing microvascular permeability, increasing micro-vascular perfusion, reducing inflammation in a tissue, and treating or ameliorating diseases associated with amchemia and/or reperfusion injury.
Abstract: The disclosure is directed to methods and uses of antibodies or antigen-binding fragments thereof against Angiopoietin-2 (Ang-2). Specifically, the disclosure is direct to the use of anti-Ang2 antibodies or antigen-binding fragments thereof for treating ischemia. The methods disclosed are useful for reducing microvascular permeability, increasing microvascular perfusion, reducing inflammation in a tissue, and treating or ameliorating diseases associated with ischemia and/or reperfusion injury. The disclosed methods are also useful for protecting solid organ transplant tissue and treating or preventing chronic tissue transplant rejection.
TL;DR: Results shed light on the mechanism of receptor activation by VEGF ligands and may help in designing chimeric proteins that could be used therapeutically to promote or inhibit angiogenesis.
Abstract: This Podcast features an interview with Kari Alitalo, author of a Research Article that appears in the 2 July 2013 issue of Science Signaling , on how two related growth factors trigger distinct biological outcomes despite binding to the same receptor. Ligands of the vascular endothelial growth factor (VEGF) family modulate the development and growth of blood and lymphatic vessels. Although the related VEGF ligands VEGF-B and placental growth factor (PlGF) both exert their biological activities by binding to VEGF receptor 1 (VEGFR-1), PlGF robustly induces angiogenesis, whereas VEGF-B triggers angiogenesis only weakly. Through domain swapping experiments, Anisimov et al . determined that the angiogenic activity of PlGF was conferred by a domain in PlGF that interacted with VEGFR-1, whereas the corresponding domain in VEGF-B did not. These results shed light on the mechanism of receptor activation by VEGF ligands and may help in designing chimeric proteins that could be used therapeutically to promote or inhibit angiogenesis.
01 Jan 2016
TL;DR: It is shown that the homogeneously staining regions of the COLO 320 HSR marker chromosome contain amplified c-myc, and amplification of c- myc has been accompanied by translocation of the gene from its normal position on chromosome 8 (8q24).
Abstract: Two human neuroendocrine tumor cell lines de- rived from a colon carcinoma contain either numerous double min- ute chromosomes (COLO 320 DM) or a homogeneously staining marker chromosome (COLO 320 HSR). We found amplification and enhanced expression of the cellular oncogene c-myc in both COLO 320 DM and HSR cells, and we were able to show that the homogeneously staining regions of the COLO 320 HSR marker chromosome contain amplified c-myc. From previous and present karyotypes, it appears that the homogeneously staining regions re- side on a distorted X chromosome. Therefore, amplification of c- myc has been accompanied by translocation of the gene from its normal position on chromosome 8 (8q24). Because double minute
Patent•
02 Feb 1998
TL;DR: In this paper, the authors propose a method to combine peptides VEGF-C purifies and isoles, capables de se lier a au moins une des tyrosine kinases suivantes: tyrosin kinase a recepteur KDR (VEGFR-2) and tyrosinesine kinase an recepteur Flt4 (VEgFR-3), which concerne egalement des analogues de tels peptides, presentant des activites biologiques de type VEGFs, and des po
Abstract: Polypeptides VEGF-C purifies et isoles, capables de se lier a au moins une des tyrosine kinases suivantes: tyrosine kinase a recepteur KDR (VEGFR-2) et tyrosine kinase a recepteur Flt4 (VEGFR-3). L'invention concerne egalement des analogues de tels peptides, presentant des activites biologiques de type VEGF-C ou VEGF ou qui sont des inhibiteurs de VEGF ou de VEGF-C, ainsi que des polynucleotides codant ces polypeptides, des vecteurs et cellules hotes qui contiennent ces polynucleotides, des compositions pharmaceutiques et reactifs pour diagnostic contenant ces polypeptides et des procedes pour produire et utiliser ces polypeptides.
Patent•
02 Sep 2009
TL;DR: In this paper, an invention concerne un anticorps isole, ou l'un de ses fragments, who se lie a un epitope extracellulaire d'un recepteur 4 du facteur de croissance des fibroblastes (FGFR4) who est exprime par une cellule de mammifere and qui bloque l'invasion by les cellules cancereuses.
Abstract: La presente invention concerne un anticorps isole, ou l'un de ses fragments, qui se lie a un epitope extracellulaire d'un recepteur 4 du facteur de croissance des fibroblastes (FGFR4) qui est exprime par une cellule de mammifere et qui bloque l'invasion par les cellules cancereuses. Le cas echeant, l'anticorps ou son fragment se lie a un epitope du FGFR4 lie par l'anticorps monoclonal F90-10C5 ou comprenant des regions determinant des complementarites identiques a celle de l'anticorps monoclonal F90-10C5. L'invention concerne egalement des procedes d'utilisation de l'anticorps ou de son fragment pour moduler l'invasion, la croissance interne, ou la metastase de cellules cancereuses et traiter le cancer affectant un sujet. L'invention concerne en outre un procede permettant d'identifier un anticorps ou un fragment d'anticorps inhibant le pouvoir invasif.
Cited by
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TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
51,099 citations
TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
28,811 citations
28 Jul 2005
TL;DR: PfPMP1）与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。
18,940 citations
TL;DR: It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration.
Abstract: Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.
12,395 citations
TL;DR: Amplification of the HER-2/neu gene was a significant predictor of both overall survival and time to relapse in patients with breast cancer, and had greater prognostic value than most currently used prognostic factors in lymph node-positive disease.
Abstract: The HER-2/neu oncogene is a member of the erbB-like oncogene family, and is related to, but distinct from, the epidermal growth factor receptor. This gene has been shown to be amplified in human breast cancer cell lines. In the current study, alterations of the gene in 189 primary human breast cancers were investigated. HER-2/neu was found to be amplified from 2- to greater than 20-fold in 30% of the tumors. Correlation of gene amplification with several disease parameters was evaluated. Amplification of the HER-2/neu gene was a significant predictor of both overall survival and time to relapse in patients with breast cancer. It retained its significance even when adjustments were made for other known prognostic factors. Moreover, HER-2/neu amplification had greater prognostic value than most currently used prognostic factors, including hormonal-receptor status, in lymph node-positive disease. These data indicate that this gene may play a role in the biologic behavior and/or pathogenesis of human breast cancer.
11,597 citations