Enter Your Search:
Results 1-3 (3)
Go to page number:
Select a Filter Below
Journal of Clinical Investigation (1)
Medical Science Monitor : International Medical Journal of Experimental and Clinical Research (1)
PLoS ONE (1)
Lahav, Meir (3)
Arenzana-Seisdedos, Fernando (1)
Beery, Einat (1)
Belyaeva, Inessa (1)
Brenner, Baruch (1)
Caruz, Antonio (1)
Dronichev, Vladimir (1)
Fujii, Nobutaka (1)
Gryaznov, Sergei (1)
Habler, Liliana (1)
Kushnir, Michal (1)
Lapidot, Tsvee (1)
Magerus, Aude (1)
Nagler, Arnon (1)
Nordenberg, Yardena (1)
Peled, Amnon (1)
Petit, Isabelle (1)
Ponomaryov, Tanya (1)
Rabinowitz, Claudette (1)
Rabizadeh, Esther (1)
Rinkevich, Baruch (1)
Samocha, Katty (1)
Sandbank, Judith (1)
Slavin, Shimon (1)
Szyper-Kravitz, Martin (1)
Taichman, Russell S. (1)
Uziel, Orit (1)
Weiss, Lola (1)
Weissmann-Brenner, Alina (1)
Zehavi, Tania (1)
Zipori, Dov (1)
Year of Publication
Rituximab associated neutropenia: Description of three cases and an insight into the underlying pathogenesis
Medical Science Monitor : International Medical Journal of Experimental and Clinical Research
To describe Rituximab associated neutropenia (RAN), and to explore its underlying mechanism.
We describe three patients with RAN. The effect of patient’s plasma on colony forming unit, Granulocyte-Monocyte (CFU-GM) was measured by the addition of plasma to the culture of a healthy bone-marrow. Repeated tests were performed after recovery of white count.
In the leukopenic period the patient’s plasma inhibited CFU growth completely. Control plasma did not have such an effect. Addition of patient’s cell supernatant to bone marrow cells did not change the number of CFU. The same effect was demonstrated in normal control. After recovery the patient’s plasma did not inhibit colony formation, similar to control.
RAN is a clinically significant side effect. It may take place during treatment or several months afterwards. Circulating antibodies in the plasma may be responsible for this unique BM toxicity.
rituximab; neutropenia; bone marrow; pathogenesis
Telomere Shortening Sensitizes Cancer Cells to Selected Cytotoxic Agents: In Vitro and In Vivo Studies and Putative Mechanisms
Telomere/telomerase system has been recently recognized as an attractive target for anticancer therapy. Telomerase inhibition results in tumor regression and increased sensitivity to various cytotoxic drugs. However, it has not been fully established yet whether the mediator of these effects is telomerase inhibition per se or telomere shortening resulting from inhibition of telomerase activity. In addition, the characteristics and mechanisms of sensitization to cytotoxic drugs caused by telomerase inhibition has not been elucidated in a systematic manner.
In this study we characterized the relative importance of telomerase inhibition versus telomere shortening in cancer cells. Sensitization of cancer cells to cytotoxic drugs was achieved by telomere shortening in a length dependent manner and not by telomerase inhibition per se. In our system this sensitization was related to the mechanism of action of the cytotoxic drug. In addition, telomere shortening affected also other cancer cell functions such as migration. Telomere shortening induced DNA damage whose repair was impaired after administration of cisplatinum while doxorubicin or vincristine did not affect the DNA repair. These findings were verified also in in vivo mouse model. The putative explanation underlying the phenotype induced by telomere shortening may be related to changes in expression of various microRNAs triggered by telomere shortening.
To our best knowledge this is the first study characterizing the relative impact of telomerase inhibition and telomere shortening on several aspects of cancer cell phenotype, especially related to sensitivity to cytotoxic drugs and its putative mechanisms. The microRNA changes in cancer cells upon telomere shortening are novel information. These findings may facilitate the development of telomere based approaches in treatment of cancer.
Induction of the chemokine stromal-derived factor-1 following DNA damage improves human stem cell function
Taichman, Russell S.
Journal of Clinical Investigation
The chemokine stromal-derived factor-1 (SDF-1) controls many aspects of stem cell function. Details of its regulation and sites of production are currently unknown. We report that in the bone marrow, SDF-1 is produced mainly by immature osteoblasts and endothelial cells. Conditioning with DNA-damaging agents (ionizing irradiation, cyclophosphamide, and 5-fluorouracil) caused an increase in SDF-1 expression and in CXCR4-dependent homing and repopulation by human stem cells transplanted into NOD/SCID mice. Our findings suggest that immature osteoblasts and endothelial cells control stem cell homing, retention, and repopulation by secreting SDF-1, which also participates in host defense responses to DNA damage.
Results 1-3 (3)
Go to page number:
Remove citation from clipboard
Add citation to clipboard
This will clear all selections from your clipboard. Do you wish proceed?
Clipboard is full! Please remove an item and try again.
PubMed Central Canada is a service of the
Canadian Institutes of Health Research
(CIHR) working in partnership with the National Research Council's
Canada Institute for Scientific and Technical Information
in cooperation with the
National Center for Biotechnology Information
U.S. National Library of Medicine
(NCBI/NLM). It includes content provided to the
PubMed Central International archive
by participating publishers.