
Daniel Sargent
· Professor of History and Public PolicyVerifiedUniversity of California, Berkeley · Public Policy
Active 1939–2026
About
Daniel Sargent is a faculty member at the Goldman School of Public Policy at the University of California, Berkeley. His work focuses on history and public policy, contributing to the academic community through his research and teaching. As a professor of history and public policy, he is involved in exploring the intersections of historical analysis and policy development, aiming to inform and improve public policy through a historical perspective.
Research topics
- Horticulture
- Biology
- Genetics
- Gastroenterology
- Medicine
- Internal medicine
- Surgery
- Oncology
Selected publications
Communications Biology · 2026-01-14 · 2 citations
articleOpen accessGenomes record past climatic impact on species' range shifts, admixture, refugial isolation, and adaptative evolution. However, these processes are poorly understood in perennial herbaceous species forming a dominant group of temperate flora. We present a demographic history of the perennial herb woodland strawberry (Fragaria vesca L.) reconstructed from 200 genomes spanning most of its European range. Temporal population structure reveals a strong division into western and eastern genetic clusters along a longitudinal climatic gradient, with eastern core populations showing greater resilience during glaciations. Divergence patterns indicate that postglacial recolonization of western and eastern Europe occurred from distinct refugia in multiple waves. The current largest, admixed populations from the Mediterranean to northern Europe form a continuous chain maintained by east-west gene flow through Central Europe, with historical migration patterns indicating comparable connections during earlier interglacials. Our reconstruction of woodland strawberry's climatic history with high temporal resolution reveals how the late Pleistocene core-periphery dynamics shaped its survival and genome evolution under climate change. The data points to populations that are essential for maintaining the long term genetic diversity of the species and opens new avenues to understand climatic adaptation of temperate flora.
Developmental processes in the Rosaceae through the lens of DNA and RNA methylation
Planta · 2025-02-08 · 5 citations
reviewOpen accessAbstract Main conclusion This review discusses the DNA and RNA methylation pathways and their biological roles in Rosaceae developmental processes relevant for breeding and production. Abstract The Rosaceae is a plant family of great importance for human nutrition and health. Many traits and developmental processes of the Rosaceae are influenced by epigenetic methylation, functions of which are now being unravelled in several important species of this family. Methylation of DNA at the 5th position of cytosine (5mC) is a well-established epigenetic mark that affects important cellular processes such as gene expression and genome stability and is involved in a wide range of plant biological functions. Further to this, recent technological advances have uncovered other naturally occurring chemical modifications of DNA and RNA as additional layers of regulatory epigenetic information in plants. In this review we give a comprehensive summary of plant 5-methylcytosine DNA methylation mechanisms and review their components identified in species of the Rosaceae family. We detail and discuss the role of 5mC DNA methylation dynamics in Rosaceae developmental processes, including phase transition, bud development, bud dormancy, plant architecture, plant regeneration, fruit development, ripening and senescence. We then review recent advances in understanding the newly identified nucleic acid modifications, N 6 -adenosine methylation of DNA (6mA) and RNA (m 6 A) as additional epigenetic mechanisms. We summarise identified components of adenosine methylation pathways in the Rosaceae and discuss the emerging roles of this modification in plant development including recent findings in Rosaceous species. Integrating epigenetic aspects of plant development with plant genetics and physiology is crucial for understanding biological processes in Rosaceous plants.
The Economics of the Vietnam War
Cambridge University Press eBooks · 2024-10-31
book-chapter1st authorCorresponding2023-03-31
preprintOpen accessCCR Translation for This Article from Achieving Sufficient Accrual to Address the Primary Endpoint in Phase III Clinical Trials from U.S. Cooperative Oncology Groups
2023-03-31
preprintOpen accessSenior author<p>PDF file - 45KB</p>
2023-03-31
preprintOpen access<div>Abstract<p><b>Purpose:</b> Assessing impact of poor accrual on premature trial closure requires a relevant metric. We propose defining accrual sufficiency on apparent ability to address primary endpoints (PE) rather than attaining accrual targets.</p><p><b>Experimental Design:</b> All phase III trials open January 1, 1993, to December 31, 2002, by five U.S. oncology Clinical Trials Cooperative Groups (CTCG) were evaluated for accrual sufficiency and scientific results. Sufficient accrual included meeting accrual target, CTCGs documentation attesting adequate accrual, or conclusive results at interim analysis; insufficient accrual included poor accrual as cited closure reason or other reasons rendering a trial unable to address its primary endpoints. Closure rates based on our accrual sufficiency definition are compared with rates of meeting accrual targets and addressing the primary endpoints. A percentage of target accrual above which trials commonly answer the intended scientific question was identified to serve as an alternative to meeting full target accrual in designating accrual success.</p><p><b>Results:</b> Of 238 eligible trials, 158 (66%) closed with sufficient accrual. Among 80 trials with insufficient accrual, 70 (29%) closed specifically because of poor accrual. Inadequate accrual rates are overemphasized when defining accrual success solely by meeting accrual targets. Nearly 75% of trials conclusively addressed the primary endpoints with positive results in 39% of trials. Exceeding 80% of target accrual serves as a reliable proxy for answering the intended scientific question.</p><p><b>Conclusions:</b> Approximately one third of phase III trials closed with insufficient accrual to address the primary endpoints, primarily due to poor accrual. Defining accrual sufficiency broader than meeting accrual targets represents a fairer account of trial closures. <i>Clin Cancer Res; 18(1); 256–62. ©2011 AACR</i>.</p></div>
2023-03-31
preprintOpen access<p>PDF file - 108KB, Predictive value of specific KRAS mutations in patients with BRAF-wild type resected stage III colon cancer treated with adjuvant FOLFOX chemotherapy with vs without cetuximab. Unadjusted hazard ratios (HR) for disease-free survival by KRAS mutation strata are shown for patients who were randomized during the period when KRAS-mutated and -wild type tumors were eligible. HR < 1 indicates benefit from cetuximab. No estimates produced due to insufficient sample size in one subgroup.</p>
2023-03-31
preprintOpen access<div>Abstract<p><b>Purpose:</b> We examined the prognostic impact of specific <i>KRAS</i> mutations in patients with stage III colon adenocarcinoma receiving adjuvant FOLFOX alone or combined with cetuximab in a phase III trial (N0147). Analysis was restricted to <i>BRAF</i>–wild-type tumors, because <i>BRAF</i> mutation was associated with poor prognosis, and <i>BRAF</i> and <i>KRAS</i> mutations are mutually exclusive.</p><p><b>Experimental Design:</b> The seven most common <i>KRAS</i> mutations in codon 12 and codon 13 were examined in 2,478 <i>BRAF</i>–wild-type tumors. Because <i>KRAS</i> mutations in codon 12 (<i>n</i> = 779) or 13 (<i>n</i> = 220) were not predictive of adjuvant cetuximab benefit, study arms were pooled for analysis. Disease-free survival (DFS) was evaluated by HRs using Cox models.</p><p><b>Results:</b><i>KRAS</i> mutations in codon 12 (multivariate HR, 1.52; 95% confidence interval, CI, 1.28–1.80; <i>P</i> < 0.0001) or codon 13 (multivariate HR, 1.36; 95% CI, 1.04–1.77; <i>P</i> = 0.0248) were significantly associated with shorter DFS compared with patients with wild-type <i>KRAS</i>/<i>BRAF</i> tumors, independent of covariates. <i>KRAS</i> codon 12 mutations were independently associated with proficient mismatch repair (<i>P</i> < 0.0001), proximal tumor site (<i>P</i> < 0.0001), low grade, age, and sex, whereas codon 13 mutations were associated with proximal site (<i>P</i> < 0.0001).</p><p><b>Conclusion:</b><i>KRAS</i> mutations in either codon 12 or 13 are associated with inferior survival in patients with resected stage III colon cancer. These data highlight the importance of accurate molecular characterization and the significant role of <i>KRAS</i> mutations in both codons in the progression of this malignancy in the adjuvant setting. <i>Clin Cancer Res; 20(11); 3033–43. ©2014 AACR</i>.</p></div>
2023-03-31
supplementary-materialsOpen access<p>PDF file - 81KB, Table S1. Multivariable logistic regression models showing the association of clinicopathologic and molecular characteristics with KRAS codon 12 or 13 mutation status in 2,478 BRAF-wild type stage III colon cancers.</p>
2023-03-31
preprintOpen accessSenior author<p>PDF file - 12KB, Plots of observed versus expected 1-year survival probabilities for N9841 based on models for each metric and a model with no metric, adjusting for treatment arm and sum of baseline tumor measurements.</p>
Recent grants
Cancer and Leukemia Group B Statistical Center
NIH · $95.3M · 1982–2015
Cancer Risk Assessment, Early Detection, and Interception Research Program
NIH · $127.2M · 1997–2030
NIH · $154.4M · 2014–2026
Methodology for development, validation, and use of novel endpoints in oncology
NIH · $1.2M · 2014–2020
Frequent coauthors
- 1059 shared
Richard M. Goldberg
Applied Physical Sciences (United States)
- 656 shared
Steven R. Alberts
Mayo Clinic
- 417 shared
Jacqueline Benedetti
Université de Caen Normandie
- 417 shared
Qian Shi
Mayo Clinic
- 408 shared
Marc Buyse
- 402 shared
Greg Yothers
University of Pittsburgh
- 396 shared
Frank A. Sinicrope
Mayo Clinic in Arizona
- 366 shared
Carmen J. Allegra
University of Florida Health
Labs
Education
- 1996
PhD, Biostatistics
University of Minnesota System
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