Astrid Olsnes Kittang kartlegger kjemokin-nettverket i akutt myelogen leukemi

Astrid Olsnes Kittang

Astrid Olsnes Kittang (f. 1975) fra Oslo, tok medisinsk embetseksamen ved det Jagiellonske Universitetet i Krakow, Polen i 2000. Senere fullførte hun sin PhD i 2008 ved Institutt for Indremedisin, seksjon for hematologi, under Øystein Bruseruds forskningsgruppe. Nå har hun en 50 % postdoc-stilling ved samme seksjon. I tillegg arbeider Kittang som assistentlege ved Medisinsk avdeling, Haukeland Universitetssykehus.

Akutt myelogen Leukemi (AML) er en krefttype som har utspring i beinmargen. En pasient som har AML vil ha en overproduksjon av umodne hvite blodceller (leukemiceller). Denne opphopningen av leukemiceller vil etterhvert hindre utviklingen av de normale blodcellene i beinmargen. Dette vil snarlig få alvorlige konsekvenser for pasienten.

Kjemokiner er små proteiner som påvirker cellevandringen i kroppen. Disse proteinene vil dermed også styre leukemicellenes utvikling og spredning. Utfordringen er å få kjemokinene til å ha en negativ effekt på leukemicellene, altså redusere kreftens utvikling og spredning.  

"The Chemokine Network in Acute Myelogenous Leukemia: Molecular Mechanisms Involved in Leukemogenesis and Therapeutic Implications."
Dette er tittelen på Kittangs nypubliserte artikkel, den femte i rekken.

Se "Abstract":

Curr Top Microbiol Immunol. 2010 Apr 1. [Epub ahead of print]

The Chemokine Network in Acute Myelogenous Leukemia: Molecular Mechanisms Involved in Leukemogenesis and Therapeutic Implications.

Kittang AO, Hatfield K, Sand K, Reikvam H, Bruserud O.

Division of Hematology, Department of Medicine, Haukeland University Hospital, 5021, Bergen, Norway.

Abstract

Acute myelogenous leukemia (AML) is a bone marrow disease in which the leukemic cells show constitutive release of a wide range of CCL and CXCL chemokines and express several chemokine receptors. The AML cell release of various chemokines is often correlated and three release clusters have been identified: CCL2-4/CXCL1/8, CCL5/CXCL9-11, and CCL13/17/22/24/CXCL5. CXCL8 is the chemokine usually released at highest levels. Based on their overall constitutive release profile, patients can be classified into distinct subsets that differ in their T cell chemotaxis towards the leukemic cells. The release profile is modified by hypoxia, differentiation status, pharmacological interventions, and T cell cytokine responses. The best investigated single chemokine in AML is CXCL12 that binds to CXCR4. CXCL12/CXCR4 is important in leukemogenesis through regulation of AML cell migration, and CXCR4 expression is an adverse prognostic factor for patient survival after chemotherapy. Even though AML cells usually release high levels of several chemokines, there is no general increase of serum chemokine levels in these patients and the levels are also influenced by patient age, disease status, chemotherapy regimen, and complicating infections. However, serum CXCL8 levels seem to partly reflect the leukemic cell burden in AML. Specific chemokine inhibitors are currently being developed, although redundancy and pleiotropy of the chemokine system are obstacles in drug development.

PMID: 20376612 [PubMed - as supplied by publisher]