Presence of donor-specific DNA in plasma of kidney and liver-transplant recipients

Lo, Y.M. Dennis; Tein, Mark; Pang, Calvin C P; Yeung, Chung Kwong; Tong, Kwok Lung; Hjelm, N M

doi:10.1016/s0140-6736(05)79055-3

Cited by 275 publications

(209 citation statements)

References 5 publications

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“…Endogenous XIAP and OAS1 mRNA levels in untreated and INF-b-treated parental, U6 control or XIAP shRNA MDA-MB-231 cell lines were measured using quantitative RT-PCR as per the TaqMan method (Heid et al, 1996;Lo et al, 1999). The primer sets used for XIAP amplification were 5 0 -GGT GAT AAA GTA AAG TGC TTT CAC TGT-3 0 and 5 0 -TCA GTA GTT CTT ACC AGA CAC TCC TCA A-3 0 .…”

Section: Quantitative Rt-pcrmentioning

confidence: 99%

Loss of XIAP protein expression by RNAi and antisense approaches sensitizes cancer cells to functionally diverse chemotherapeutics

et al. 2004

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Stable expression of short-hairpin RNAs (shRNAs) directed against the X-linked inhibitor of apoptosis (XIAP) resulted in the generation of three MDA-MB-231 cell lines (XIAP shRNA cells) with reductions in XIAP mRNA and protein levels 485% relative to MDA-MB-231 cells stably transfected with the U6 RNA polymerase III promoter alone (U6 cells). This RNA interference (RNAi) approach dramatically sensitized these cells to killing by the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Importantly, loss of XIAP also sensitized the cells to killing by taxanes but had no additional effects on killing by carboplatin and doxorubicin. The increased sensitivity of the XIAP shRNA cells to killing by TRAIL and taxanes correlated with enhanced caspase cleavage and activation, including caspase-8, and robust processing of poly(ADP-ribose) polymerase and BID compared to U6 cells. Additionally, increasing XIAP levels by adenovirus-mediated expression protected both XIAP shRNA and U6 cells from TRAIL killing in a dose-dependent manner. The effects observed by stable RNAi with respect to TRAIL sensitization were also achieved following downregulation of XIAP in Panc-1 cells treated with a second-generation, mixed-backbone antisense oligonucleotide, AEG 35156/GEM640. These data indicate that reducing XIAP protein expression by either RNAi or antisense approaches increases cancer cell susceptibility to functionally diverse chemotherapeutic agents and supports the notion that downregulation of XIAP in vivo may synergize with disease-relevant chemotherapeutic regimes, including TRAIL and taxanes, to increase the effectiveness of antineoplastic agents.

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Section: Quantitative Rt-pcrmentioning

confidence: 99%

Loss of XIAP protein expression by RNAi and antisense approaches sensitizes cancer cells to functionally diverse chemotherapeutics

et al. 2004

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“…All three genes are frequently altered in various hematological malignancies. An excellent review (Drexler, 1998) (Garcia et al, 1999) and multiple myeloma (46%) (Tasaka et al, 1998;Lo et al, 1999;Ng et al, 1999;Gonzalez et al, 2000;Uchida et al, 2001). Controversy arises concerning the prognostic relevance of p16 INK4A /p14 ARF /p15 INK4B inactivation.…”

Section: Ink4 Family Of Proteinsmentioning

confidence: 99%

Tumor suppressor genes in normal and malignant hematopoiesis

2002

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“…Another promising new approach is determination of graftderived circulating cell-free DNA (GefDNA) [13][14][15]. As solid organ transplants are also genome transplants, GefDNA could be determined in plasma and used as a marker of allograft injury [9].…”

Section: Summary and Perspectivementioning

confidence: 99%

Therapeutic monitoring of immunosuppressive drugs in pediatric patients: special considerations

Weber

Dötsch

2016

Expert Review of Clinical Pharmacology

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Presence of donor-specific DNA in plasma of kidney and liver-transplant recipients

Cited by 275 publications

References 5 publications

Loss of XIAP protein expression by RNAi and antisense approaches sensitizes cancer cells to functionally diverse chemotherapeutics

Loss of XIAP protein expression by RNAi and antisense approaches sensitizes cancer cells to functionally diverse chemotherapeutics

Tumor suppressor genes in normal and malignant hematopoiesis

Therapeutic monitoring of immunosuppressive drugs in pediatric patients: special considerations

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