About

Shaista Aziz Patel joined the Ethnic Studies Department as an Assistant Professor in July 2018, specializing in Critical Muslim Studies. She holds a PhD in Social Justice Education and a graduate Certificate in Women and Gender Studies from the University of Toronto. Prior to her appointment at UCSD, she taught courses as a sessional instructor in Sociology and Women and Gender Studies at the University of Toronto. As an interdisciplinary scholar, her primary research interests encompass Critical Muslim, Dalit feminist, and critical Caste studies, as well as transnational feminist studies. Her work explores the complex entanglements of bodies, colonialism, race, caste, gender, religion, capitalism, and relations of labor across different spatialities and temporalities. She is particularly interested in teaching undergraduate and graduate courses in critical Muslim studies, critical caste studies, decolonial theory, and questions of solidarity, including movements from Palestine, North America, and Kashmir. Her scholarship addresses issues of non-Black, non-Indigenous people of color complicity in settler colonialism, white and Brahminical supremacies. Her publications include book chapters from Palgrave Macmillan, the University of British Columbia, McGill-Queen's University, and Fernwood Presses, as well as articles in various academic journals. She is also a co-editor of a forthcoming book titled 'Contestations and Compromise: Reading against Multiple Colonialities, Race, and Caste in the University,' to be published by the University of Alberta Press in 2025.

Research topics

• Medicine
• Internal medicine
• Oncology
• Computer Science
• Family medicine
• Biology
• Genetics
• Chemistry
• Cancer research
• Intensive care medicine
• Endocrinology
• Medical emergency
• Immunology
• Gastroenterology
• Bioinformatics
• Pharmacology
• Computational biology
• Emergency medicine
• Nursing

Selected publications

• Baseline tumor burden and outcomes in patients with rare cancers treated with immunotherapy (Southwest Oncology Group trial S1609)

  Cancer · 2026-03-27

  articleOpen access

  BACKGROUND: It has been suggested that baseline tumor burden may correlate with immune checkpoint inhibitor (ICI) outcome for individual tumor types in which ICIs are standardly used. The authors investigated whether pretreatment tumor burden correlates with overall survival (OS), progression-free survival (PFS), and tumor regression among patients who had rare cancers treated with dual ICIs. METHODS: Southwest Oncology Group study S1609 was a phase 2, National Cancer Institute/Southwest Oncology Group basket study (>1000 sites) evaluating nivolumab plus ipilimumab in 53 cohorts of patients who had rare/ultrarare malignancies (ClinicalTrials.gov identifier NCT02834013). Overall, 722 patients were included in this secondary analysis, all of whom had measurable disease (Response Evaluation Criteria in Solid Tumors, version 1.1). Baseline tumor burden, defined as the sum of the greatest dimensions of target lesions at study registration, was analyzed based on quartiles observed in the data. The number of target lesions was also considered a secondary tumor burden measure. End points included OS and PFS. RESULTS: Larger baseline tumor burden correlated with shorter OS, but not PFS (multivariable analysis). Higher baseline tumor burden quartiles had only a weak negative association with any tumor regression at first scan (Fisher exact test, p = .09), and multivariable analyses further indicated that both tumor burden and any tumor regression at first posttreatment scan were independently associated with OS in multivariable analysis (comparing a baseline tumor size ≥12.9 cm vs. 1.0-4.8 cm; hazard ratio, 1.64; 95% confidence interval, 1.02-1.72; p = .032), but there was no evidence of an interaction between tumor burden and any tumor regression at the first scan (p for interaction > .65). CONCLUSIONS: Larger baseline tumor burden was associated with worse OS, but not PFS, and was not predictive of tumor regression after dual ICI therapy in a large cohort with rare cancer types.

  PublisherDOI

• microRNA-25 drives immune checkpoint therapy resistance by repressing innate and humoral immunity via Syndecan-3

  Nature Communications · 2026-05-20

  articleOpen access

  Immune checkpoint therapy (ICT) can induce durable tumor control but is limited by primary and acquired resistance. The mechanisms underlying immune-resistant tumor microenvironments (TMEs) remain incompletely understood. Here we show that deletion of microRNA-25 (miR-25) sensitizes tumors to ICT across multiple syngeneic mouse models. Single-cell transcriptomics reveals that miR-25 deficiency activates innate and humoral immunity by increasing major histocompatibility complex class II (MHC II) expression in tumor-associated macrophages (TAMs) and enhancing classical complement signaling in cancer-associated fibroblasts (CAFs). Complement activation shifts CAFs toward an inflammatory (iCAF) state, reduces suppressive crosstalk with TAMs, and promotes a pro-inflammatory TME. Mechanistically, miR-25 represses Syndecan-3 (SDC3) in response to interferon-γ (IFN-γ). Editing the miR-25 binding site in Sdc3 restores SDC3 expression and overcomes resistance. These findings identify miR-25-mediated SDC3 repression as a driver of immune resistance and suggest strategies to convert immune-cold tumors into ICT-responsive hot tumors, offering avenues to enhance ICT.

  PublisherDOI

• Molecular Translators as a Computational Primitive for Biomarker Discovery: Learnability Gains Under Conserved Information Ceilings

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-30

  articleSenior author

  Abstract Virtual molecular mapping systems such as MISO and GigaTIME introduce a potentially transformative primitive in computational pathology: translation of H&E whole-slide images into biologically structured molecular representations, learned on paired cohorts and deployed as an inference-time map. Despite sustained progress in machine learning, H&E-to-molecular-biomarker (e.g., gene mutation) prediction continues to exhibit recurrent field-level performance plateaus whose drivers remain poorly resolved. It remains unclear whether continued optimization targets a removable methodological limitation or instead presses against an intrinsic ceiling imposed by morphology. We develop a formal framework characterizing what deterministic translators can and cannot change. Histology-based biomarker modeling is governed by two constraints: method-limited gaps (finite labels, weak supervision, structured nuisance) and modality-limited ceilings (intrinsic slide-specific information in morphology). Because deterministic translation introduces no new slide-level measurements at inference, H&E information ceilings are conserved; however, translation can still improve finite-sample learnability, yielding an apparent information–performance paradox that we formalize as learnability gains under conserved information ceilings. We derive falsifiable signatures distinguishing these regimes and characterize them in controlled analytical experiments anchored to representative systems, including MISO and GigaTIME. We introduce an open-source toolkit comprising learning regime diagnosis, information-ceiling estimations, phase analyses, fidelity perturbation tests, and shortcut-confounding stress tests as an operational rubric for identifying and overcoming removable performance plateaus in translator-assisted molecular biomarker discovery and computational pathology.

  PublisherDOI

• DART/SWOG/NCI phase II anti-CTLA-4/PD-1 trial: clear cell carcinomas of ovary, endometrium, cervix

  Journal for ImmunoTherapy of Cancer · 2026-02-01 · 1 citations

  articleOpen access

  BACKGROUND: Dual anti-CTLA-4/PD-1 inhibitors show efficacy in numerous malignancies. We are the first to report on the efficacy of ipilimumab-nivolumab immunotherapy in a dedicated cohort of patients with gynecologic clear cell carcinomas (CCCs), which are rare, aggressive cancers. METHODS: DART is a multicenter, multicohort phase II trial of ipilimumab (1 mg/kg intravenously every 6 weeks) plus nivolumab (240 mg intravenously every 2 weeks), with primary objective as Response Evaluation Criteria in Solid Tumors (RECIST)-based overall response rate (ORR). Secondary objectives were ORR by immune RECIST (iRECIST), progression-free survival (PFS), overall survival (OS), clinical benefit rate (CBR; overall response plus stable disease (SD) ≥6 months), and toxicity. RESULTS: Overall, in this cohort of 32 patients with gynecologic CCC (N=19 ovarian, N=8 endometrial, N=5 cervical; 1-8 prior therapies; 3 had prior PD-1 inhibitor exposure), an ORR of 9.38% was seen. This included two complete responses (CRs) (both ovarian origin) that are ongoing at >3 years and one partial response (PR). Overall ORR increased to 12.5% when including one PR by iRECIST criteria for a patient with cervical CCC lasting 26 months, with an OS of 32.0 months. The CBR was 21.88% overall for all 32 (7/32) evaluable patients with gynecologic CCC. This included two CR, one PR, and two patients with SD >6 months with ovarian CCC and one PR by iRECIST and one SD >6 months in two patients with cervical CCC. PFS for the seven patients with CBR was 63.6+, 47.8+, 40.5+, 50.8+, 7.4, 26, and 58.1+ months. Median OS was 21.7 months for all 32 evaluable patients. Seven of 32 patients (21.9%) discontinued therapy because of toxicity; there were no treatment-related deaths. CONCLUSIONS: Ipilimumab plus nivolumab demonstrated durable antitumor activity in certain patients with CCC of gynecological origin, particularly in those with CCC of ovarian origin. Safety is consistent with the known profile of ipilimumab and nivolumab. Correlative studies to better identify which patients will respond to combined ipilimumab and nivolumab are ongoing. TRIAL REGISTRATION NUMBER: NCT02834013.

  PublisherOA PDFDOI

• Abstract 1591: microRNA-25 drives initial resistance to immune checkpoint therapy by repressing innate and humoral immunity via Syndecan3

  Cancer Research · 2026-04-03

  article

  Abstract Immune Checkpoint Therapy (ICT) has demonstrated durable responses and long-lasting immunologic memory in cancer treatment. However, overcoming primary and acquired resistance remains a major challenge. Here, we show that CRISPR-Cas9-mediated deletion of miRNA-25 (miR-25) sensitizes tumors to cancer immunotherapy across three syngeneic mouse tumor models. Single-cell RNA sequencing (scRNA-seq) of the tumor microenvironment (TME) revealed that miR-25 deficiency induces innate immunity by upregulating major histocompatibility complex class II (MHC II) in antigen-presenting M1-like macrophages and enhances the classical complement cascade in cancer-associated fibroblasts (CAFs) to drive a humoral immune response. The complement activation polarizes CAFs from myofibroblastic CAFs (myCAFs) toward inflammatory CAFs (iCAFs) while simultaneously reduces immune-suppressive interactions between CAFs and tumor associated macrophages (TAMs). This shift results in a reduced macrophage population and fosters a pro-inflammatory, anti-tumor TME. Syndecan-3 (Sdc3), a membrane proteoglycan expressed in tumors, is repressed by miR-25 through miRISC (microRNA induced silencing complex) upon IFN-γ exposure. Using an adenine base editor (ABE8e) to mutate the miR-25 binding site in the 3’ untranslated region (3’ UTR) of Sdc3 effectively overcomes the resistance. The repression of SDC3 by miR-25 is further validated in five human cancer cell lines upon IFN-γ exposure but remains unaffected in non-cancerous cells. These findings identify miR-25 as a key driver of initial resistance through the repression of SDC3 and demonstrate that miR-25 deletion or stabilization of SDC3 could transform immune resistant "cold" tumors into immune responsive "hot" tumors, offering therapeutic avenues to enhance cancer immunotherapy. Citation Format: Zhouting Zhu, Wenyan Han, Yufei Deng, Zhaoyang Jia, Lujing Wu, Shweta Jakhmola, Gulshanbir Baidwan, Tongyun Wang, Dhenugen Logeswaran, Amanda Y. Sun, Bill Bray, Na Li, Lingling Wang, Hui Hui, Jiaqian Wu, Sandip Pravin Patel, Tariq M. Rana. microRNA-25 drives initial resistance to immune checkpoint therapy by repressing innate and humoral immunity via Syndecan3 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 1591.

  PublisherDOI

• Unlocking the potential of immunotherapy for patients with resectable non–small cell lung cancer

  Frontiers in Oncology · 2026-01-12

  articleOpen access1st author

  Following positive results in advanced and metastatic non-small cell lung cancer (NSCLC), there has been a move toward the application of immunotherapy in the treatment of locally advanced, resectable, oncogene driver-negative disease. To date, there have been eight Phase III trials across the adjuvant, neoadjuvant, and perioperative settings that demonstrate benefit with (chemo)-immunotherapy in patients with resectable NSCLC. Given the wealth of immunotherapy treatment regimens both available and under investigation in this setting, there is a need to determine the optimal timing of immunotherapy treatment (neoadjuvant, perioperative, or adjuvant) across disease stages to aid clinical decision-making. Established treatment guidelines often diverge, highlighting the need for a multidisciplinary team approach and consensus decision-making based on the latest evidence in the resectable setting. Finally, there is an unmet need surrounding the role of key predictive factors and response assessments, to assist clinicians in selecting patients for immunotherapy regimens. The aim of this review is to evaluate the current data and key considerations surrounding immunotherapy for the treatment of resectable NSCLC, including key parameters to inform de-escalating and escalating treatment approaches.

  PublisherOA PDFDOI

• Abstract 7594: Combining electronic health records, environmental, and genomics data for lung cancer risk prediction in Southern California.

  Cancer Research · 2026-04-03

  article

  Abstract Background: Lung cancer risk reflects intersecting clinical, environmental, and genomic factors, yet these data types are rarely integrated at the individual level. We assembled an EHR-based cohort in Southern California to build a predictive model of incident lung cancer diagnosis and to characterize the clinical, genomic, and neighborhood features that drive risk. Methods: We constructed a retrospective cohort of 7,151 adults from UC San Diego Health electronic health records (50.4% female, 65% ≥ 65 years) and linked approximately 40 clinical features to census-tract-level environmental and socioeconomic indicators from CalEnviroScreen, as well as genomic mutation status for ALK and EGFR. We compared 14 classifiers (logistic regression, random forest, XGBoost, and 11 PyTorch neural networks) using stratified five-fold cross-validation to predict lung cancer diagnosis. Hyperparameters for top performing models were optimized using Bayesian search in Optuna. Model performance was summarized using AUROC, accuracy, precision, recall, and F1, and feature importance was assessed using Shapley (SHAP) values. Results: Optimized XGBoost achieved the best cross-validated discrimination (AUROC 0.879), with accuracy 0.802, precision 0.744, and F1 0.694, outperforming linear and deep-learning baselines. Top-ranked features by SHAP included smoking intensity, cardiometabolic comorbidity, and age, with neighborhood unemployment, pesticide burden, and ozone levels contributing additional, though smaller, predictive signal, reinforcing the contribution of neighborhood disadvantage and pollution to lung cancer vulnerability in this regional cohort. Among genomically profiled patients, ALK-positive cases were diagnosed at a significantly younger age than ALK-wildtype cases (mean 56 vs 71 years, p=0.016), underscoring biologically distinct disease courses. Conclusion: An integrated gradient-boosting model leveraging EHR, environmental, and genomic data can meaningfully stratify individual lung cancer risk in a diverse regional cohort and elevate both clinical and neighborhood drivers of vulnerability. These findings support the use of routinely collected health and environmental data to guide targeted lung cancer screening and prevention efforts and motivate future work on external validation, time-varying exposures, and explicit fairness constraints across racial and socioeconomic groups. Citation Format: Gianni Pucillo, Sanye Naqvi, Allison Jue, Chandler Law, Sandip Patel, Uduak Z. George. Combining electronic health records, environmental, and genomics data for lung cancer risk prediction in Southern California [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 7594.

  PublisherDOI

• BASECAMP-1 screening study: a model for efficient enrolment in precision oncology clinical trials

  BMJ Oncology · 2026-01-01

  articleOpen access

  Objective: Identifying eligible patients for precision oncology clinical trials is challenging, particularly for rare molecular subpopulations. To address this challenge, A2 Biotherapeutics developed BASECAMP-1 (NCT04981119), a non-interventional master screening study to identify patients eligible for interventional studies of logic-gated Tmod chimeric antigen receptor T-cell therapies. Eligible patients for these interventional trials have an advanced solid malignancy and are germline human leucocyte antigen (HLA)-A*02 heterozygous, with tumour-associated HLA-A loss of heterozygosity (LOH). HLA-A LOH occurs in ~16% of advanced solid malignancies; therefore, an efficient screening strategy is required. This report describes BASECAMP-1; compares the efficiency of two screening methods; and discusses the broader advantages of BASECAMP-1 beyond efficient enrolment. Methods and analysis: Patients are identified for BASECAMP-1 using two approaches. In the traditional approach, common for clinical trials, investigators consent and screen all patients who might be good candidates for cell therapy trials, with no prior knowledge of patient HLA-A type or LOH status. To further optimise our approach, we co-developed with Tempus AI (Tempus) the bioinformatic programme Aware, which identifies potentially eligible patients with tumour-associated HLA-A*02 LOH within a clinico-genomic database that includes linked genomic and transcriptomic sequencing and clinical data collected during routine care. Results: Over 42 months of using a traditional approach to identify eligible patients, 1918 patients at 13 study sites were consented and screened for BASECAMP-1; of these, 30 patients with tumour-associated HLA-A*02 LOH were enrolled (~0.7 participants per month). Over the last 30 months of that same period, Tempus Aware screening was implemented and 55 patients with tumour-associated HLA-A*02 LOH were enrolled (~1.8 participants per month). The bioinformatic approach identified more patients than the traditional approach and used sequencing results produced as part of the standard clinical tumour sequencing workflow, reducing resource use and study staff burden. Additional advantages of using a screening study, such as BASECAMP-1, include manufacturing efficiencies and collection of a large dataset of molecular and clinical parameters that can be used to supplement trial analyses. Conclusions: The BASECAMP-1 study demonstrates a clinico-genomic screening approach can more efficiently identify patients for precision oncology trials. Furthermore, precision oncology can be enhanced through collaborative data-sharing. Trial registration number: NCT04981119.

  PublisherOA PDFDOI

• Abstract 5333: Profiling membrane antigen expression of select antibody-drug conjugate (ADC) targets in <i>EGFR</i> -altered non-small cell lung cancer treated with osimertinib.

  Cancer Research · 2026-04-03

  articleSenior author

  Abstract Background: Resistance to EGFR-Tyrosine Kinase Inhibitors (TKIs) in patients with NSCLC represents an unmet clinical need. Bypass pathway upregulation is a key mechanism of resistance and represents a potential target for therapeutic agents such as Antibody-Drug Conjugates (ADCs). This study evaluates the RNA expression of select ADC targets in NSCLC patients treated with osimertinib (osi). Methods: The Tempus Lens Platform was used to identify a cohort (n=583 patients) of classical EGFR-altered NSCLC with DNA (xT) and RNA (xR) testing treated with first-line osi monotherapy (mono) or osi with chemotherapy (combo). RNA-seq data of select ADC membrane targets, including ERBB2, ERBB3, MET, NECTIN4, and TACSTD2 (TROP2) were quantified as transcripts per million (TPM), reported as log2(TPM + 1) and compared using Wilcoxon rank-sum test. Median RNA expression in each gene was defined relative to the pre-treatment EGFR-altered cohort. We examined real world overall survival (rwOS) and hazard ratio (HR) from Cox proportional hazards model. Results: Among 583 patients, median (range) age at diagnosis was 66 (27-88) years old while 68% were female. In all samples, the highest median gene expression was identified in ERBB2, MET, and TACSTD2 (TROP2) (7.46, 7.38, 7.57). When comparing first-line pre- and post-treatment samples, there was a significant increase in median gene expression of MET (7.23 vs 7.85; p&amp;lt;0.001) however decreases in median expression of NECTIN4 (5.22 vs 4.90; p=0.005) and ERBB2 (7.48 vs 7.38; p=0.021). In pre-osi mono patients (n=378), median rwOS was 29.8 months. Of the five genes assessed, only MET expression was associated with worse rwOS (HR 1.25; p=0.001). In the mono group, those with above-median MET expression at pre-treatment had a worse rwOS than those with below-median expression (26.1 vs. 31.5 months; p=0.007). Above-median MET expression was associated with worse rwOS compared to below median (HR 1.52; p=0.008). Conclusion: In patients with EGFR-altered NSCLC, we identified high expression of ERBB2, MET, and TACSTD2 (TROP2) in both pre- and post-treated samples. This may provide rationale for use of these ADC targets in second-line therapy, such as seen in recent approvals for trastuzumab deruxtecan in ERBB2-mutated, telisotuzumab vedotin in c-MET over-expressing, and datopotamab deruxtecan in EGFR-altered NSCLC. Notably, high MET pre-treatment expression was associated with poor survival outcome and appeared to be associated with post-osimertinib resistance. Further investigation is required to evaluate MET expression as a predictive biomarker for MET-targeting agents to overcome innate and acquired EGFR-TKI resistance. Citation Format: Kevin Lu, Tali Azenkot, Ellen B. Jaeger, Unnati Jariwala, Stamatina Fragkogianni, Jacob Mercer, Jyoti D. Patel, Sandip P. Patel. Profiling membrane antigen expression of select antibody-drug conjugate (ADC) targets in EGFR-altered non-small cell lung cancer treated with osimertinib [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 5333.

  PublisherDOI

• A phase II basket trial of Dual Anti-CTLA-4 and Anti-PD-1 Blockade in Rare Tumors (DART) SWOG S1609: vaginal cancer sub cohort results

  Journal of Gynecologic Oncology · 2026-01-01

  articleOpen access

  OBJECTIVE: The SWOG S1609 Dual Anti-CTLA-4 &amp; Anti-PD-1 blockade in Rare Tumors (DART) trial is the first basket study to include a sub-cohort assessing ipilimumab and nivolumab in patients with primary vaginal cancers with differing histology. METHODS: DART is a prospective, open-label, multicenter, multi-cohort phase II clinical trial of ipilimumab (1 mg/kg intravenously) 6 weekly plus nivolumab (240 mg intravenously) 2 weekly across multiple rare tumor cohorts, with the vagina cohort (any vaginal histology) reported here. The primary endpoint was objective response rate (ORR) per RECISTv1.1; progression-free survival (PFS), overall survival (OS), clinical benefit rate (CBR; overall response plus stable disease [SD] ≥6 months), and toxicity are secondary endpoints. RESULTS: Seven evaluable patients (median age, 60 years; performance status 0-1; no prior exposure to immunotherapy) were analyzed, of whom 3 had adenocarcinoma, 2 had squamous cell carcinoma (SCC), one had small-cell carcinoma and one had undifferentiated histology. The ORR was 29%, with 1 patient (14%) with undifferentiated histology achieving complete response (lasting 14.8 months) and 1 patient with SCC histology (14%) attaining a partial response (lasting 45.2 months). The CBR was 43%. The 6-month PFS rate was 43% and the median OS was 11.7 months. Five patients (71.4%) experienced an adverse event (AE) with 4 (57.1%) having grade 3-4 AE's. CONCLUSION: Ipilimumab plus nivolumab showed efficacy (ORR was 29% and CBR of 43%) and durability (one patient with prolonged SD >6 months) in a sub cohort of patients with vaginal cancer of differing histology without new safety signals. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02834013.

  PublisherOA PDFDOI

Frequent coauthors

• Razelle Kurzrock

  Medical College of Wisconsin Cancer Center

  133 shared

• Jonathan W. Riess

  UC Davis Comprehensive Cancer Center

  97 shared

• Heather A. Wakelee

  81 shared

• Michael J. Dennis

  80 shared

• Young Kwang Chae

  Northwestern University

  80 shared

• Mizuki Nishino

  80 shared

• George R. Blumenschein

  The University of Texas MD Anderson Cancer Center

  74 shared

• Mark M. Awad

  Dana-Farber Cancer Institute

  74 shared