Research team Grandér/Pokrovskaja Tamm

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Molecular mechanisms of action of anti-cancer drugs and role of non-coding RNA in cancer

The aim of our research is to improve conditions for the use of anti-cancer drugs in patients with cancer. The group runs two major projects: studies on the mechanisms of cell death (and resistance) induced by well-known as well as novel anti-cancer drugs and the role of non-coding RNA in cancer.

Projects

Autophagy in anti-cancer therapy
Long non-coding RNAs in tumor development
STAT3 as a target for anti-cancer therapy
STAT1 and STAT3 - mechanisms of interaction and inhibition of signaling

Funding

  • Swedish Cancer Society (Autophagy in anti-cancer therapy and Therapy resistance)
  • The Swedish Childhood Cancer Foundation (Molecular mechanisms underlying pediatric leukemia development and treatment)
  • Swedish foundation for Strategic Research (Autophagy in anti-cancer therapy)
  • The Cancer Society in Stockholm (Drug development to overcome drug resistance and the Role of non-coding RNA in cancer)
  • Karolinska Institutet, KID (STAT3 as a target for anti-cancer therapy)
  • Karolinska Institutet, KID (Comprehensive analysis of non-coding RNAs in hematological malignancies)

Group members

Katja Pokrovskaja Tamm, PI, PhD, Associate Professor
Ann-Charlotte Björklund, Research Technician
Sander Busker, MSc, PhD student
Matheus Dyczynski, MSc, PhD student
Linda Vidarsdottir, Postdoc
Yasmin Yu, MSc, PhD student

Selected publications

Identification of novel small molecules that inhibit STAT3-dependent transcription and function.
Kolosenko I, Yu Y, Busker S, Dyczynski M, Liu J, Haraldsson M, et al
PLoS ONE 2017 ;12(6):e0178844

Tumor acidosis enhances cytotoxic effects and autophagy inhibition by salinomycin on cancer cell lines and cancer stem cells.
Pellegrini P, Dyczynski M, Sbrana F, Karlgren M, Buoncervello M, Hägg-Olofsson M, et al
Oncotarget 2016 Jun;7(24):35703-35723

Cell crowding induces interferon regulatory factor 9, which confers resistance to chemotherapeutic drugs.
Kolosenko I, Fryknäs M, Forsberg S, Johnsson P, Cheon H, Holvey-Bates E, et al
Int. J. Cancer 2015 Feb;136(4):E51-61

A pseudogene long-noncoding-RNA network regulates PTEN transcription and translation in human cells.
Johnsson P, Ackley A, Vidarsdottir L, Lui W, Corcoran M, Grandér D, et al
Nat. Struct. Mol. Biol. 2013 Apr;20(4):440-6

Proteomic screen reveals Fbw7 as a modulator of the NF-κB pathway.
Arabi A, Ullah K, Branca R, Johansson J, Bandarra D, Haneklaus M, et al
Nat Commun 2012 ;3():976

MiR-200c regulates Noxa expression and sensitivity to proteasomal inhibitors.
Lerner M, Haneklaus M, Harada M, Grandér D
PLoS ONE 2012 ;7(5):e36490

Involvement of miR17 pathway in glucocorticoid-induced cell death in pediatric acute lymphoblastic leukemia.
Harada M, Pokrovskaja-Tamm K, Söderhäll S, Heyman M, Grander D, Corcoran M
Leuk. Lymphoma 2012 Oct;53(10):2041-50

Glucocorticoid-induced cell death is mediated through reduced glucose metabolism in lymphoid leukemia cells.
Buentke E, Nordström A, Lin H, Björklund A, Laane E, Harada M, et al
Blood Cancer J 2011 Jul;1(7):e31

MiRNA-27a controls FBW7/hCDC4-dependent cyclin E degradation and cell cycle progression.
Lerner M, Lundgren J, Akhoondi S, Jahn A, Ng H, Akbari Moqadam F, et al
Cell Cycle 2011 Jul;10(13):2172-83

DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1.
Lerner M, Harada M, Lovén J, Castro J, Davis Z, Oscier D, et al
Exp. Cell Res. 2009 Oct;315(17):2941-52

Cell death induced by dexamethasone in lymphoid leukemia is mediated through initiation of autophagy.
Laane E, Tamm K, Buentke E, Ito K, Kharaziha P, Khahariza P, et al
Cell Death Differ. 2009 Jul;16(7):1018-29

Glucocorticoid-induced cell death is mediated through reduced glucose metabolism in lymphoid leukemia cells.
Buentke E, Nordström A, Lin H, Björklund A, Laane E, Harada M, et al
Blood Cancer J 2011 Jul;1(7):e31

Interferon alpha induces nucleus-independent apoptosis by activating extracellular signal-regulated kinase 1/2 and c-Jun NH2-terminal kinase downstream of phosphatidylinositol 3-kinase and mammalian target of rapamycin.
Panaretakis T, Hjortsberg L, Tamm K, Björklund A, Joseph B, Grandér D
Mol. Biol. Cell 2008 Jan;19(1):41-50