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排序方式: 共有598条查询结果,搜索用时 15 毫秒
91.
Kroef MJ; Fibbe WE; Mout R; Jansen RP; Haak HL; Wessels JW; Van Kamp H; Willemze R; Landegent JE 《Blood》1993,81(7):1849-1854
Interstitial deletions of the long arm of chromosome 5 are among the most characteristic abnormalities observed in myeloid disorders. To assess the lineage involvement of peripheral blood cells from patients with a 5q--anomaly, purified neutrophils, monocytes, T lymphocytes, and B lymphocytes were analyzed for loss of heterozygosity using six different highly polymorphic mininucleotide and dinucleotide (CA) repeat sequences from the 5q31 to 5q33 region. Ten patients were screened by polymerase chain reaction (PCR) amplification and proved to be informative for at least one marker. Six patients showed a complete or partial disappearance of an allele in myeloid cells, whereas cells of lymphoid lineages exhibited full heterozygosity. The other patients displayed no allelic loss, indicating that the informative markers were located outside the deleted chromosomal segments. In addition, three female patients who were also polymorphic for the BstXI site in the PGK- 1 gene were analyzed for the methylation status of this gene. Clonality of hematopoiesis, as determined by non-random X-chromosome inactivation, followed the same cell pattern as the 5q-specific allelic losses. In conclusion, using tumor-specific and clonal markers, we have demonstrated that the 5q- anomaly is restricted to cells of myeloid origin, leaving lymphoid cells unaffected. 相似文献
92.
Thomas Condamine Vinit Kumar Indu R. Ramachandran Je-In Youn Esteban Celis Niklas Finnberg Wafik S. El-Deiry Rafael Winograd Robert H. Vonderheide Nickolas R. English Stella C. Knight Hideo Yagita Judith C. McCaffrey Scott Antonia Neil Hockstein Robert Witt Gregory Masters Thomas Bauer Dmitry I. Gabrilovich 《The Journal of clinical investigation》2014,124(6):2626-2639
Myeloid-derived suppressor cells (MDSCs) dampen the immune response thorough inhibition
of T cell activation and proliferation and often are expanded in pathological conditions.
Here, we studied the fate of MDSCs in cancer. Unexpectedly, MDSCs had lower viability and
a shorter half-life in tumor-bearing mice compared with neutrophils and monocytes. The
reduction of MDSC viability was due to increased apoptosis, which was mediated by
increased expression of TNF-related apoptosis–induced ligand receptors (TRAIL-Rs)
in these cells. Targeting TRAIL-Rs in naive mice did not affect myeloid cell populations,
but it dramatically reduced the presence of MDSCs and improved immune responses in
tumor-bearing mice. Treatment of myeloid cells with proinflammatory cytokines did not
affect TRAIL-R expression; however, induction of ER stress in myeloid cells recapitulated
changes in TRAIL-R expression observed in tumor-bearing hosts. The ER stress response was
detected in MDSCs isolated from cancer patients and tumor-bearing mice, but not in control
neutrophils or monocytes, and blockade of ER stress abrogated tumor-associated changes in
TRAIL-Rs. Together, these data indicate that MDSC pathophysiology is linked to ER stress,
which shortens the lifespan of these cells in the periphery and promotes expansion in BM.
Furthermore, TRAIL-Rs can be considered as potential targets for selectively inhibiting
MDSCs. 相似文献
93.
Vanaja Mummaneni Sanjeev Kaul Linus N. Igwemezie David R. Newell David Porter Huw Thomas A. Hilary Calvert Benjamin Winograd Rashmi H. Barbhaiya 《Journal of pharmacokinetics and pharmacodynamics》1996,24(4):313-325
The bioequivalence of etoposide phosphate, a prodrug of etoposide, to etoposide was assessed in a randomized, crossover study
in 29 patients with histologically established solid tumors that had failed conventional treatment. Cohorts of patients received
one treatment course each of etoposide and etoposide phosphate which consisted of a 100 mg/m2 per day etoposide equivalent dose infused iv over 1 hr on a Day 1 to 5 schedule of treatment. The second course was administered
21 days later or on recovery of blood cell counts. Plasma and urine samples were collected over 24 hr on Day 1 of each course
and assayed for etoposide content by a validated HPLC/UV method. Resulting data were subjected to noncompartmental pharmacokinetic
analysis. Hematology profiles were obtained by collecting blood samples prior to the first course and twice a week after each
course. The pharmacodynamics and pharmacokinetics of etoposide were virtually identical after the two treatments. The point
estimates (90% confidence intervals) for nadir WBC, granulocytes, hemoglobin, and platelets expressed as % decrease from the
baseline, and for the pharmacokinetic parameters, Cmax, and AUC0-∞, after intravenous etoposide phosphate relative to etoposide were 100% (96%, 105%), 97% (91%, 103%), 95% (82%, 109%), 95%
(84%, 106%), 107% (101%, 113%), and 113% (107%, 119%), respectively. Therefore, etoposide phosphate is bioequivalent to etoposide
based on pharmacokinetic and pharmacodynamic assessments. 相似文献
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