Institution
Quest Diagnostics
Company•Madison, New Jersey, United States•
About: Quest Diagnostics is a company organization based out in Madison, New Jersey, United States. It is known for research contribution in the topics: Population & Myeloid leukemia. The organization has 1016 authors who have published 1376 publications receiving 60259 citations.
Topics: Population, Myeloid leukemia, Mass spectrometry, Fluorescence in situ hybridization, Leukemia
Papers published on a yearly basis
Papers
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Daniel C. Koboldt1, Robert S. Fulton1, Michael D. McLellan1, Heather Schmidt1 +352 more•Institutions (35)
TL;DR: The ability to integrate information across platforms provided key insights into previously defined gene expression subtypes and demonstrated the existence of four main breast cancer classes when combining data from five platforms, each of which shows significant molecular heterogeneity.
Abstract: We analysed primary breast cancers by genomic DNA copy number arrays, DNA methylation, exome sequencing, messenger RNA arrays, microRNA sequencing and reverse-phase protein arrays. Our ability to integrate information across platforms provided key insights into previously defined gene expression subtypes and demonstrated the existence of four main breast cancer classes when combining data from five platforms, each of which shows significant molecular heterogeneity. Somatic mutations in only three genes (TP53, PIK3CA and GATA3) occurred at >10% incidence across all breast cancers; however, there were numerous subtype-associated and novel gene mutations including the enrichment of specific mutations in GATA3, PIK3CA and MAP3K1 with the luminal A subtype. We identified two novel protein-expression-defined subgroups, possibly produced by stromal/microenvironmental elements, and integrated analyses identified specific signalling pathways dominant in each molecular subtype including a HER2/phosphorylated HER2/EGFR/phosphorylated EGFR signature within the HER2-enriched expression subtype. Comparison of basal-like breast tumours with high-grade serous ovarian tumours showed many molecular commonalities, indicating a related aetiology and similar therapeutic opportunities. The biological finding of the four main breast cancer subtypes caused by different subsets of genetic and epigenetic abnormalities raises the hypothesis that much of the clinically observable plasticity and heterogeneity occurs within, and not across, these major biological subtypes of breast cancer.
9,355 citations
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TL;DR: The 2001 Bethesda System terminology reflects important advances in biological understanding of cervical neoplasia and cervical screening technology.
Abstract: ObjectivesThe Bethesda 2001 Workshop was convened to evaluate and update the 1991
Bethesda System terminology for reporting the results of cervical cytology.
A primary objective was to develop a new approach to broaden participation
in the consensus process.ParticipantsForum groups composed of 6 to 10 individuals were responsible for developing
recommendations for discussion at the workshop. Each forum group included
at least 1 cytopathologist, cytotechnologist, clinician, and international
representative to ensure a broad range of views and interests. More than 400
cytopathologists, cytotechnologists, histopathologists, family practitioners,
gynecologists, public health physicians, epidemiologists, patient advocates,
and attorneys participated in the workshop, which was convened by the National
Cancer Institute and cosponsored by 44 professional societies. More than 20
countries were represented.EvidenceLiterature review, expert opinion, and input from an Internet bulletin
board were all considered in developing recommendations. The strength of evidence
of the scientific data was considered of paramount importance.Consensus ProcessBethesda 2001 was a year-long iterative review process. An Internet
bulletin board was used for discussion of issues and drafts of recommendations.
More than 1000 comments were posted to the bulletin board over the course
of 6 months. The Bethesda Workshop, held April 30-May 2, 2001, was open to
the public. Postworkshop recommendations were posted on the bulletin board
for a last round of critical review prior to finalizing the terminology.ConclusionsBethesda 2001 was developed with broad participation in the consensus
process. The 2001 Bethesda System terminology reflects important advances
in biological understanding of cervical neoplasia and cervical screening technology.
3,122 citations
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Stanford University1, University of Göttingen2, University of Texas MD Anderson Cancer Center3, University of Rochester Medical Center4, St James's University Hospital5, University of Paris6, University of Düsseldorf7, University of Pavia8, Medical University of Vienna9, University of Chicago10, Quest Diagnostics11, University of Freiburg12, Cleveland Clinic13, Federal University of Ceará14, Nagasaki University15, University of Dundee16, VU University Medical Center17
TL;DR: This revised IPSS-R comprehensively integrated the numerous known clinical features into a method analyzing MDS patient prognosis more precisely than the initial IPSS and should prove beneficial for predicting the clinical outcomes of untreated MDS patients and aiding design and analysis of clinical trials in this disease.
2,310 citations
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University of Texas MD Anderson Cancer Center1, University of Rochester Medical Center2, Quest Diagnostics3, Washington University in St. Louis4, Memorial Sloan Kettering Cancer Center5, Roswell Park Cancer Institute6, Duke University7, University of Illinois at Chicago8, Rush University Medical Center9
TL;DR: Aberrant DNA methylation, which results in leukemogenesis, is frequent in patients with myelodysplastic syndromes (MDS) and is a potential target for pharmacologic therapy.
Abstract: BACKGROUND
Aberrant DNA methylation, which results in leukemogenesis, is frequent in patients with myelodysplastic syndromes (MDS) and is a potential target for pharmacologic therapy. Decitabine indirectly depletes methylcytosine and causes hypomethylation of target gene promoters.
METHODS
A total of 170 patients with MDS were randomized to receive either decitabine at a dose of 15 mg/m2 given intravenously over 3 hours every 8 hours for 3 days (at a dose of 135 mg/m2 per course) and repeated every 6 weeks, or best supportive care. Response was assessed using the International Working Group criteria and required that response criteria be met for at least 8 weeks.
RESULTS
Patients who were treated with decitabine achieved a significantly higher overall response rate (17%), including 9% complete responses, compared with supportive care (0%) (P < .001). An additional 12 patients who were treated with decitabine (13%) achieved hematologic improvement. Responses were durable (median, 10.3 mos) and were associated with transfusion independence. Patients treated with decitabine had a trend toward a longer median time to acute myelogenous leukemia (AML) progression or death compared with patients who received supportive care alone (all patients, 12.1 mos vs. 7.8 mos [P = 0.16]; those with International Prognostic Scoring System intermediate-2/high-risk disease, 12.0 mos vs. 6.8 mos [P = 0.03]; those with de novo disease, 12.6 mos vs. 9.4 mos [P = 0.04]; and treatment-naive patients, 12.3 mos vs. 7.3 mos [P = 0.08]).
CONCLUSIONS
Decitabine was found to be clinically effective in the treatment of patients with MDS, provided durable responses, and improved time to AML transformation or death. The duration of decitabine therapy may improve these results further. Cancer 2006. © 2006 American Cancer Society.
1,419 citations
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TL;DR: A critical role for telomere length in the overall fitness, reserve, and well being of the aging organism is demonstrated.
1,328 citations
Authors
Showing all 1029 results
Name | H-index | Papers | Citations |
---|---|---|---|
David Heber | 90 | 393 | 29672 |
Michael R. McClung | 86 | 286 | 28679 |
Vay Liang W. Go | 80 | 374 | 23536 |
Dan Jones | 72 | 320 | 18591 |
Michael K. Racke | 67 | 202 | 16048 |
Sue A. Ingles | 64 | 204 | 15372 |
Charles M. Rowland | 57 | 132 | 12064 |
Susanne M. Henning | 56 | 161 | 10416 |
Teresa M. Darragh | 56 | 180 | 12167 |
Michael J. McPhaul | 53 | 141 | 7933 |
Edward I. Ginns | 50 | 144 | 8163 |
Alex V. Levin | 49 | 293 | 9089 |
Delbert A. Fisher | 47 | 191 | 7720 |
Maren S. Fragala | 43 | 157 | 7338 |
Brendan M. Everett | 43 | 130 | 12462 |