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Christian R. Geest

Researcher at University of Amsterdam

Publications -  7
Citations -  772

Christian R. Geest is an academic researcher from University of Amsterdam. The author has contributed to research in topics: Chronic lymphocytic leukemia & Leukemia. The author has an hindex of 6, co-authored 7 publications receiving 681 citations.

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The clinically active BTK inhibitor PCI-32765 targets B-cell receptor- and chemokine-controlled adhesion and migration in chronic lymphocytic leukemia

TL;DR: The data indicate that inhibition of BTK by PCI-32765 overcomes BCR- and chemokine-controlled integrin-mediated retention and homing of malignant B cells in their growth- and survival-supporting lymph node and bone marrow microenvironment, which results in clinically evident CLL regression.
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Resistance to ABT-199 induced by microenvironmental signals in chronic lymphocytic leukemia can be counteracted by CD20 antibodies or kinase inhibitors

TL;DR: A major clinical problem in chronic lymphocytic leukemia (CLL) is development of chemoresistance, which can be caused by genetic lesions but is also strongly influenced by the leukemic microenvironment.
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Tipping the Noxa/Mcl-1 Balance Overcomes ABT-737 Resistance in Chronic Lymphocytic Leukemia

TL;DR: The Noxa/Mcl-1 balance determines sensitivity to ABT-737 in CD40-stimulated CLL cells, and these data provide a rationale to investigate the combination of drugs which enhance the NoxA/M cl-1 Balance with ABT -737 to eradicate CLL in chemoresistant niches.
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Tight control of MEK-ERK activation is essential in regulating proliferation, survival, and cytokine production of CD34+-derived neutrophil progenitors

TL;DR: A novel role is identified in regulating the balance between proliferation and apoptosis during neutrophil differentiation, and the need for tight control of MEK-ERK activation is suggested to prevent the development of bone marrow failure.
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Mammalian target of rapamycin activity is required for expansion of CD34+ hematopoietic progenitor cells

TL;DR: It is shown that mTOR inhibition by rapamycin reduces the expansion of committed myeloid progenitors, but leaves the more primitive hematopoietic compartment unaffected, indicating that mammalian target ofRapamycin activity is essential for expansion of CD34+ hematopolietic progenitor cells during myelopoiesis.