About

Juliet A. Williams is a Professor at UCLA specializing in feminist theory and politics, masculinities studies, gender discrimination law, and issues related to Title IX and education. Her work focuses on understanding and addressing gender-based discrimination and inequalities within educational and societal contexts. As a leading scholar in her field, she contributes to the development of feminist legal and political theory, emphasizing the importance of gender justice and policy reform.

Research topics

• Political Science
• Computer Science
• Sociology
• Law
• Public relations
• Computer Security
• Social Science
• Chemistry
• Cancer research
• Biology
• Linguistics
• Data science
• Social psychology
• Engineering ethics
• Pharmacology
• Biochemistry
• Medicine
• Gender studies
• Engineering
• Epistemology
• Aesthetics
• Psychology

Selected publications

• Solving for X: Gender Markers, the Law, and the Administrative State

  Signs · 2026-05-04

  article1st authorCorresponding
  PublisherDOI

• Not your mother's patriarchy? Reflections on the rise, fall, and unexpected return of a feminist keyword

  Feminist Theory · 2025-06-12 · 1 citations

  article1st authorCorresponding

  The 2016 election of Donald Trump to the US presidency breathed new life into a rhetorical relic of the feminist past: the term ‘patriarchy.’ Still, as relevant as the concept of patriarchy remains, the revival of this onetime radical feminist rallying cry hardly was foretold. Radical feminism has not fared well in the popular imagination, indelibly linked (among conservatives) to man-hating, and (among progressives) to transexclusionary politics. And while developments like the repeal of the settled right to abortion indicate that an unrelenting anti-feminist backlash has accomplished the seemingly impossible in turning back time, it hardly follows that feminists, too, should reach into the past in response. Accounting for the use of the term ‘patriarchy’ in the present requires understanding why it lost currency among feminists in the first place. This article argues that the term did not survive the intersectional turn in feminist studies—and for good reason. Reviving the term today risks repeating errors of the past, or worse, satisfying a nostalgic yearning for a time before the intersectional imperative. Abandoning the term carries its own dangers in enabling postfeminist denial of structural sexism. The article concludes with the hope that renewed interest in the term ‘patriarchy’ will provide a model of sorely needed intergenerational solidarity.

  PublisherDOI

• 104 (PB092): CDK2 heterobifunctional degraders co-degrade CDK2 and Cyclin E resulting in efficacy in CCNE1-amplified and overexpressed cancers

  European Journal of Cancer · 2024-10-01 · 1 citations

  articleSenior author
  PublisherDOI

• 295 (PB283): Predictive Markers of Response to the MDM2 Degrader KT-253

  European Journal of Cancer · 2024-10-01 · 1 citations

  articleSenior author
  PublisherDOI

• Supplementary Figure Legends from Discovery and Optimization of HKT288, a Cadherin-6–Targeting ADC for the Treatment of Ovarian and Renal Cancers

  2023-04-03

  preprintOpen access

  <p>This file contains the figure legends for supplementary figures S1-S7.</p>

  PublisherDOI

• Table S2 from Tumor Intrinsic Efficacy by SHP2 and RTK Inhibitors in KRAS-Mutant Cancers

  2023-04-03

  preprintOpen access

  <p>Supplementary Table 2: List of all cell lines in the CCLE where sensitivity to SHP099 was evaluated in 2D. Lineage and genetic status of KRAS and BRAF are shown. Blank cells represent cell line data where genetic or screening data do not exist. Data depicted in Figure 1B are IC50 values. This table includes all sensitivity data based on both IC50 and Amax data.</p>

  PublisherDOI

• Table S1 from Tumor Intrinsic Efficacy by SHP2 and RTK Inhibitors in KRAS-Mutant Cancers

  2023-04-03

  preprintOpen access

  <p>Supplementary Table 1: List of all cell lines in the CCLE (Cancer Cell Line Encyclopedia) where sensitivity to SHP2 (PTPN11) knockdown was evaluated in 2D. Lineage, and genetic status of KRAS and BRAF are shown. Blank cells represent cell line data where genetic or sensitivity data do not exist. Values depicted are the ATARIS quantile normalized z-score. Additional details on the methodology of the screen are published (58).</p>

  PublisherDOI

• Supplementary Figure Legends from Discovery and Optimization of HKT288, a Cadherin-6–Targeting ADC for the Treatment of Ovarian and Renal Cancers

  2023-04-03

  preprintOpen access

  <p>This file contains the figure legends for supplementary figures S1-S7.</p>

  PublisherOA PDFDOI

• Data from Distinct Transcriptional Programming Drive Response to MAPK Inhibition in <i>BRAF</i><sup>V600</sup>-Mutant Melanoma Patient-Derived Xenografts

  2023-04-03

  preprintOpen access

  <div>Abstract<p>Inhibitors targeting <i>BRAF</i> and its downstream kinase MEK produce robust response in patients with advanced <i>BRAF</i><sup>V600</sup>-mutant melanoma. However, the duration and depth of response vary significantly between patients; therefore, predicting response <i>a priori</i> remains a significant challenge. Here, we utilized the Novartis collection of patient-derived xenografts to characterize transcriptional alterations elicited by <i>BRAF</i> and MEK inhibitors <i>in vivo</i>, in an effort to identify mechanisms governing differential response to MAPK inhibition. We show that the expression of an <i>MITF</i>-high, “epithelial-like” transcriptional program is associated with reduced sensitivity and adaptive response to <i>BRAF</i> and MEK inhibitor treatment. On the other hand, xenograft models that express an MAPK-driven “mesenchymal-like” transcriptional program are preferentially sensitive to MAPK inhibition. These gene-expression programs are somewhat similar to the <i>MITF</i>-high and -low phenotypes described in cancer cell lines, but demonstrate an inverse relationship with drug response. This suggests a discrepancy between <i>in vitro</i> and <i>in vivo</i> experimental systems that warrants future investigations. Finally, <i>BRAF</i><sup>V600</sup>-mutant melanoma relies on either MAPK or alternative pathways for survival under <i>BRAF</i> and MEK inhibition <i>in vivo</i>, which in turn predicts their response to further pathway suppression using a combination of <i>BRAF</i>, MEK, and ERK inhibitors. Our findings highlight the intertumor heterogeneity in <i>BRAF</i><sup>V600</sup>-mutant melanoma, and the need for precision medicine strategies to target this aggressive cancer.</p></div>

  PublisherDOI

• Figure S2 from Distinct Transcriptional Programming Drive Response to MAPK Inhibition in <i>BRAF</i><sup>V600</sup>-Mutant Melanoma Patient-Derived Xenografts

  2023-04-03

  preprintOpen access

  <p>Overlap in differentially expressed genes upon MAPK inhibition among PDX models</p>

  PublisherDOI

Frequent coauthors

• Matthew J. Meyer

  Centre Hospitalier Universitaire Amiens-Picardie

  64 shared

• Jeffrey A. Engelman

  Novartis Institutes for BioMedical Research

  51 shared

• Xiamei Zhang

  50 shared

• Hui Gao

  48 shared

• Darrin D. Stuart

  Scorpion Therapeutics (United States)

  40 shared

• David A. Ruddy

  37 shared

• Peter S. Hammerman

  35 shared

• Daniel P. Rakiec

  32 shared

Labs

• Gender StudiesPI

Education

• B.A.

  Harvard University

Awards & honors

• Kenneth L. Sokoloff Fellow, UCLA Center for American Politic…
• Ms. Magazine Writers’ Workshop for Feminist Scholars (2009)
• UC ACCORD Faculty Research Seed Grant (2007)
• Faculty Co-Lead, UCLA Mellon Social Justice Curriculum, $5 m…