Michael R. Grever
National Institutes of Health
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Featured researches published by Michael R. Grever.
Nature | 2000
Ash A. Alizadeh; Michael B. Eisen; R. Eric Davis; Izidore S. Lossos; Andreas Rosenwald; Jennifer C. Boldrick; Hajeer Sabet; Truc Tran; Xin Yu; John Powell; Liming Yang; Gerald E. Marti; Troy Moore; James I. Hudson; Lisheng Lu; David B. Lewis; Robert Tibshirani; Gavin Sherlock; Wing C. Chan; Timothy C. Greiner; Dennis D. Weisenburger; James O. Armitage; Roger A. Warnke; Ronald Levy; Wyndham H. Wilson; Michael R. Grever; John C. Byrd; David Botstein; Patrick O. Brown; Louis M. Staudt
Diffuse large B-cell lymphoma (DLBCL), the most common subtype of non-Hodgkins lymphoma, is clinically heterogeneous: 40% of patients respond well to current therapy and have prolonged survival, whereas the remainder succumb to the disease. We proposed that this variability in natural history reflects unrecognized molecular heterogeneity in the tumours. Using DNA microarrays, we have conducted a systematic characterization of gene expression in B-cell malignancies. Here we show that there is diversity in gene expression among the tumours of DLBCL patients, apparently reflecting the variation in tumour proliferation rate, host response and differentiation state of the tumour. We identified two molecularly distinct forms of DLBCL which had gene expression patterns indicative of different stages of B-cell differentiation. One type expressed genes characteristic of germinal centre B cells (‘germinal centre B-like DLBCL’); the second type expressed genes normally induced during in vitro activation of peripheral blood B cells (‘activated B-like DLBCL’). Patients with germinal centre B-like DLBCL had a significantly better overall survival than those with activated B-like DLBCL. The molecular classification of tumours on the basis of gene expression can thus identify previously undetected and clinically significant subtypes of cancer.
Journal of Clinical Oncology | 1990
Bruce D. Cheson; Peter A. Cassileth; David R. Head; Charles A. Schiffer; John M. Bennett; Clara D. Bloomfield; Richard D. Brunning; Robert Peter Gale; Michael R. Grever; Michael J. Keating
The National Cancer Institute (NCI) sponsored a workshop to develop a set of standardized diagnostic and response criteria for acute myeloid leukemia (AML) clinical trials. The French-American-British (FAB) classification was retained for diagnosing AML, with the addition of patients with bone marrow morphologic features of a myelodysplastic syndrome and less than 30% bone marrow blasts, but with greater than or equal to 30% blasts in the peripheral blood. In this report, there are four important subgroups of AML not defined in the FAB classification that are discussed: undifferentiated acute leukemia, MO (AML lacking definitive myeloid differentiation by morphology or conventional cytochemistry but with ultrastructural or immunophenotypic evidence for AML), mixed lineage leukemia, and hypocellular AML. Definitions of response for clinical trials are presented to facilitate comparisons among different studies. Complete remission is considered the only response worth reporting in phase III trials, since lesser responses do not improve survival. Partial remissions may be of interest to identify active new agents in phase I and II studies. Monoclonal antibodies and cytogenetic studies are not part of the routine assessment of remission or reassessment at relapse, and their role in the evaluation of patients with AML is currently being evaluated in clinical trials. Although we recognize that some of the definitions in this report are arbitrary, generalized use of these guidelines will make results of clinical trials more comparable and interpretable.
Journal of Clinical Oncology | 1995
Michael R. Grever; Kenneth J. Kopecky; M K Foucar; David R. Head; John M. Bennett; Robert E. Hutchison; W E Corbett; Peter A. Cassileth; Thomas M. Habermann; Harvey M. Golomb
PURPOSEnTherapy of hairy cell leukemia has markedly improved. Interferon alfa-2a and pentostatin are active agents. The National Cancer Institute organized an intergroup trial to compare these agents prospectively in untreated patients.nnnMETHODSnPatients were randomized to receive either interferon alfa-2a (3 x 10(6) U subcutaneously three times per week) or pentostatin (4 mg/m2 intravenously every 2 weeks). Patients who did not respond to initial treatment were crossed over.nnnRESULTSnOf 356 patients on study, 313 were eligible. Among interferon patients, 17 of 159 (11%) achieved a confirmed complete remission and 60 of 159 (38%) had a confirmed complete or partial remission. Among pentostatin patients, 117 of 154 (76%) achieved a confirmed complete remission and 121 of 154 (79%) had a confirmed complete or partial remission. Additional patients achieved criteria for complete remission, but lacked confirmatory follow-up evaluation. Response rates were significantly higher (P < .0001) and relapse-free survival was significantly longer with pentostatin than interferon (P < .0001). The median follow-up duration is 57 months (range, 19 to 82). Myelosuppression was more frequent with pentostatin (P = .013). A multivariate logistic regression analysis of the confirmed complete remissions on pentostatin showed the following factors to be important for achieving a complete remission: high hemoglobin level (two-tailed P = .024), young age (P = .0085), and no or little splenomegaly (P = .0029).nnnCONCLUSIONnBoth agents were well tolerated. Pentostatin produced higher response rates, and the responses were durable. Patient age and clinical status had an impact on outcome with pentostatin. Pentostatin is effective therapy for hairy cell leukemia.
Annals of Oncology | 2008
Miguel A. Villalona-Calero; Gregory A. Otterson; M. G. Wientjes; Frank Weber; T. Bekaii-Saab; D. Young; Anthony J. Murgo; Robert T. Jensen; T. K. Yeh; Y. Wei; Y. Zhang; Charis Eng; Michael R. Grever; Jessie L.-S. Au
BACKGROUNDnThe purpose of this study was to evaluate the potential of noncytotoxic doses of suramin to reverse chemotherapy resistance in advanced chemonaive and chemoresistant non-small-cell lung cancer patients.nnnPATIENTS AND METHODSnPatients received paclitaxel (Taxol) (200 mg/m(2)) and carboplatin (area under the concentration-time curve 6 mg/ml/min) every 3 weeks. The total suramin per cycle dose was calculated using a nomogram derived from the preceding phase I trial to obtain the desirable plasma concentration range of 10-50 microM.nnnRESULTSnThirty-nine response-assessable chemonaive patients (arm A) received 213 cycles. Thirty-eight cycles were administered to 15 patients with demonstrated resistance to paclitaxel and carboplatin (arm B). The pattern/frequency of toxic effects was similar to those expected for paclitaxel/carboplatin, and pharmacokinetic analyses (199 cycles) showed suramin plasma concentrations maintained between 10 and 50 microM in 94% of cycles. In arm A, response evaluation criteria in solid tumors (RECIST) response rate was 36% (95% confidence interval 22% to 54%; two complete, 12 partial); 15 patients (38%) had disease stabilization for > or =4 months; median progression-free survival (intention to treat) was 6.4 months; median overall survival (OS) 10.4 months and 1-year survival rate 38%. In arm B, no RECIST responses occurred; four patients had disease stabilization for > or =4 months; median OS was 132 days and 1-year survival rate 7%. Plasma basic fibroblast growth factor levels were higher in chemopretreated/refractory patients compared with chemonaive patients (P = 0.05). Sequence analysis of the EGFR tyrosine kinase domain in a long-term disease-free survivor revealed an ATP-binding pocket mutation (T790M).nnnCONCLUSIONSnNoncytotoxic suramin did not increase paclitaxel/carboplatins toxicity and the suramin dose was predicted from clinical parameters. No clinically significant reversal of primary resistance was documented, but a modulatory effect in chemotherapy-naive patients cannot be excluded. Controlled randomization is planned for further evaluation of this treatment strategy.
Blood | 1996
Bruce D. Cheson; John M. Bennett; Michael R. Grever; Neil E. Kay; Michael J. Keating; Susan O'Brien; Kanti R. Rai
Journal of the National Cancer Institute | 1994
Joseph J. Casciari; Melinda G. Hollingshead; Michael C. Alley; Joseph G. Mayo; Louis Malspeis; Seiji Miyauchi; Michael R. Grever; John N. Weinstein
Clinical Cancer Research | 2003
Miguel A. Villalona-Calero; M. Guillaume Wientjes; Gregory A. Otterson; Steven Kanter; Donn Young; Anthony J. Murgo; Beth Fischer; Carrie Dehoff; Danny Chen; Teng-Kuang Yeh; SaeHeum Song; Michael R. Grever; Jessie L.-S. Au
The cancer journal from Scientific American | 1996
Edward A. Sausville; Kimberly L K Duncan; Adrian M. Senderowicz; Jacqueline Plowman; Paul A. Randazzo; Richard A. Kahn; Louis Malspeis; Michael R. Grever
Journal of the National Cancer Institute | 1990
Michael R. Grever; John Crowley; Sydney E. Salmon; Richard McGee; Eric H. Kraut; Saundra S. Buys; Saul E. Rivkin
Journal of Clinical Oncology | 2004
C. A. Rhoades; Eric H. Kraut; D. Schuller; Y. Zhang; Kenneth K. Chan; K. Lang; C. Eng; Michael R. Grever