Last Update

2016-07-16T00:00:00.000Z

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Wrong Klas Wiman?

Prof. Klas G. Wiman

Professor of Molecular Cell and Tumor Biology At the Department

Oncology-Pathology

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Oncology-Pathology

Background Information

Employment History

Professor of Molecular Cell and Tumor Biology

Karolinska Institute

Affiliations

Member of the Nobel Assembly
Karolinska Institute

Founder
Aprea AB

Web References (62 Total References)


Board of Directors | Aprea

aprea.com [cached]

Klas G. Wiman M.D., Ph.D. Dr. Klas Wiman is one of the Co-Founders, and Professor of Molecular Cell and Tumor Biology at the Department of Oncology-Pathology, Karolinska Institutet. He has performed academic research on p53 since 1990 and published more than 90 scientific articles on this topic. He has been coordinator of an EU FP6 Integrated project with 23 research groups focused on mutant p53, and was editor of the books '25 Years of p53 Research', 2005, and 'p53 in the Clinics', 2012. He is member of the Nobel Assembly at Karolinska Institutet.


News | Aprea

aprea.com [cached]

APR-246, developed based on results from Professor Klas G. Wiman and colleagues at Karolinska Institutet, has been shown to reactivate mutant p53 - by reconverting mutant p53 into wild-type p53 protein conformation and function - and thereby induce programmed cell death in human cancer cells. APR-246 has demonstrated compelling pre-clinical antitumor activity in a wide variety of solid and hematological (blood) tumors, including ovarian cancer, small cell lung cancer, esophageal cancer and AML (acute myeloid leukemia), among others. Additionally, strong synergy has been seen with both traditional anticancer agents, such as chemotherapy, as well as newer mechanism-based anticancer drugs. In addition to pre-clinical testing, a Phase I clinical study has been completed, demonstrating a favorable safety profile and both biological and clinical responses in hematological tumors with p53 mutations.

...
APR-246 has been developed based on results from Professor Klas Wiman and colleagues at Karolinska Institutet, and has been shown to reactivate non-functional tumor suppressor protein p53 and induce programmed cell death in many human cancer cells.


News | Aprea

aprea.com [cached]

APR-246, developed based on results from Professor Klas G. Wiman and colleagues at Karolinska Institutet, has been shown to reactivate mutant p53 - by reconverting mutant p53 into wild-type p53 protein conformation and function - and thereby induce programmed cell death in human cancer cells. APR-246 has demonstrated compelling pre-clinical antitumor activity in a wide variety of solid and hematological (blood) tumors, including ovarian cancer, small cell lung cancer, esophageal cancer and AML (acute myeloid leukemia), among others. Additionally, strong synergy has been seen with both traditional anticancer agents, such as chemotherapy, as well as newer mechanism-based anticancer drugs. In addition to pre-clinical testing, a Phase I clinical study has been completed, demonstrating a favorable safety profile and both biological and clinical responses in hematological tumors with p53 mutations.

...
APR-246 has been developed based on results from Professor Klas Wiman and colleagues at Karolinska Institutet, and has been shown to reactivate non-functional tumor suppressor protein p53 and induce programmed cell death in many human cancer cells.


Aprea AB - Board

www.aprea.com [cached]

Klas G. Wiman

M.D., Ph.D., is one of the Co-Founders, and Professor of Molecular Cell and Tumor Biology at the Department of Oncology-Pathology, Karolinska Institutet. Wiman has performed academic research on p53 since 1990 and published more than 50 scientific articles on this topic. He has been coordinator of an EU FP6 Integrated project with 23 research groups focused on mutant p53, and editor of the book "25 Years of p53 Research" published in 2005. He is member of the Nobel Assembly at Karolinska Institutet.


Mutp53 - Karolinska Institutet, Sweden

www.mutp53.com [cached]

Prof. Klas Wiman Co-ordinator

Phone: +46-8-51779342

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