About

Rana McKay is a Clinical Professor of Medicine at UC San Diego. Her research focuses on prostate cancer, including molecular changes, treatment strategies, and clinical outcomes. She has contributed to the characterization of molecular alterations in prostate cancer, the development of emerging approaches and unmet needs in the field, and the evaluation of various therapies such as immunotherapy, radiotherapy, and targeted treatments. Her work involves analyzing longitudinal molecular changes, genetic mutations, and treatment responses in patients with metastatic prostate cancer, aiming to improve therapeutic strategies and patient outcomes.

Research topics

• Medicine
• Internal medicine
• Oncology
• Genetics
• Biology
• Gastroenterology
• Classics
• Gynecology
• Surgery
• Computational biology
• Bioinformatics
• History
• Intensive care medicine

Selected publications

• B7-H3 Gene Expression Shapes Prognosis and Therapeutic Opportunities Across Prostate Cancer Patient Groups

  Clinical Cancer Research · 2026-04-21

  article

  PURPOSE: B7-H3 (CD276) represents a promising therapeutic target tested in high-risk localized and treatment-refractory metastatic prostate cancer (PC). To guide therapeutic development and treatment strategies, we examined prostate tumors and evaluated expression, molecular features, and overall survival (OS), accounting for tissue site, hormone-sensitivity status, and race. EXPERIMENTAL DESIGN: 8,157 PC samples with paired DNA/RNA were analyzed based on annotations by tissue site, self-reported race, and disease state: hormone-sensitive (HSPC), castration-resistant (CRPC), or neuroendocrine PC (NEPC). Expression quartiles were B7-H3-high (>75th percentile) or B7-H3-low (<25th percentile). OS was evaluated using Kaplan-Meier and Cox proportional hazards models. RESULTS: B7-H3 expression was broadly maintained but varied by tumor site, hormone-sensitivity status, and race. High expression aligned with AR-associated transcription factors (HOXB13, FOXA1), AR-associated pathogenic dysregulations (AR-V7, SPOP, FOXA1, TMPRSS2:ERG fusions), and actionable surface antigens (TROP2, NECTIN-4). Weak correlations were found for lineage-plastic program regulators (EZH2, SOX2, ASCL1) and NEPC-associated surface antigens (DLL3, CEACAM5). High B7-H3 expression in primary tumors and HSPCs portended adverse OS (HR: 1.342, 1.30, CI: 1.19-1.512, 1.15-1.46, q < 0.0001), although favorable in metastatic tumors (HR: 0.823, CI: 0.719-0.942, q = 0.0048). No significant differences in OS were observed among CRPCs and NEPCs, although OS varied by race, with poorest survival in Asian/Pacific Islander metastatic PC patients (HR = 3.72, CI: 1.49-9.29, q = 0.012). CONCLUSIONS: Maintained B7-H3 expression in various PC settings supports its viability as a target. Associations with AR-related molecular factors, surface antigens, and investigative targets for cell therapy or antibody-drug conjugates (ADC) suggest potential dual-targeting strategies.

  PublisherDOI

• Molecular Characterization of <i>KLK2</i> RNA Expression in Prostate Cancer

  Clinical Cancer Research · 2026-03-12

  article1st authorCorresponding

  PURPOSE: KLK2 is an androgen-regulated gene critical in prostate cancer biology with multiple KLK2-targeted therapies in clinical development. We investigated KLK2 RNA expression patterns and associations with molecular features to provide context for emerging KLK2-targeted treatments. EXPERIMENTAL DESIGN: DNA/RNA next-generation sequencing was performed on 7,078 prostate cancer specimens. KLK2-high/low RNA expression was defined as ≥75th/<25th percentiles (transcripts per million, TPM). KLK2 expression was evaluated across histologic subtypes, disease states, and metastatic sites, with correlative analyses of genomic alterations, RNA signatures, and clinical outcomes. RESULTS: KLK2 gene expression varied significantly by histology, with highest levels in adenocarcinoma (8.79 log2[TPM+1]) and minimal expression in histologic neuroendocrine prostate cancer (0.33 log2[TPM+1]). Expression was significantly higher in androgen deprivation therapy (ADT)/androgen receptor pathway inhibitor (ARPI)-sensitive versus ADT/ARPI-exposed tumors (8.97 vs. 8.38 log2[TPM+1], q<0.001). Localized tumors demonstrated higher expression than lymph node (8.93 vs. 8.76 log2[TPM+1]) or distant metastases (8.23 log2[TPM+1]), with visceral metastases showing the lowest levels. In the overall cohort, KLK2 expression correlated positively with androgen receptor signaling (r=0.25-0.47) and negatively with neuroendocrine signaling. High KLK2 expression was associated with significantly improved overall survival (93.9 vs. 74.4 months, hazard ratio 0.68, p<0.001) in the total cohort, with similar patterns in patients with ADT/ARPI-sensitive and ADT/ARPI-exposed disease. CONCLUSIONS: This large-scale clinico-genomic analysis reveals distinct KLK2 expression patterns across prostate cancer histologies, tumor sites, and clinical states. These findings provide a molecular framework understanding KLK2 as a therapeutic target in prostate cancer.

  PublisherDOI

• Concurrent tissue and circulating tumor DNA analysis in renal cell carcinoma: insights from a multimodal database

  The Oncologist · 2026-04-01

  articleOpen accessSenior author

  INTRODUCTION: Circulating tumor DNA (ctDNA) sequencing complements tissue-based next-generation sequencing (NGS), offering noninvasive and serial testing. We explore the mutational landscape of renal cell carcinoma (RCC) using matched tissue and ctDNA data to assess complementarity and clinical significance of molecular alterations. METHODS: From the Tempus multimodal database, we retrospectively analyzed de-identified data from patients with RCC with concurrent tissue (Tempus xT) and ctDNA testing (Tempus xF). Patients with xT and xF matched samples (collected ±90 days of one another) were included. We evaluated socio-demographic and clinical characteristics and selected pathogenic somatic short variants (PSSVs) and copy number variants (CNV). Analyses were restricted to the 104 genes shared by all assays. RESULTS: Among 392 patients, 66% (n = 259) had metastatic disease. The median time from tissue to blood collection was 21 days. The most common tissue sites were kidney (49%, n = 189) and bone (11%, n = 43). Frequently altered tissue-tested genes were: VHL (59%), PBRM1 (32%), and SETD2 (23%). Most frequently altered genes in ctDNA were TP53 (23%), VHL (18%), BAP1 (6%), and PBRM1 (5%); notably, 176 patients did not have any pathogenic or likely pathogenic variants detected in the 104 genes analyzed. Complementary ctDNA and tissue testing detected 6% more alterations than tissue testing alone, with greater concordance in metastatic cases. CONCLUSION: ctDNA testing offers complementary insights to tissue NGS in RCC, particularly in metastatic disease, suggesting the potential utility of ctDNA in advanced RCC. Longitudinal analysis may enhance delineation of biomarkers of response and resistance at mutation and ctDNA fraction levels.

  PublisherDOI

• Precision Diagnostics in Prostate Cancer Treatment (PREDICT): A Phase II Multiarm Biomarker-Based Study (Alliance A032102)

  JCO oncology advances. · 2026-04-01

  articleOpen accessSenior author
  PublisherDOI

• Figure S6 from Circulating and Intratumoral Immune Determinants of Response to Atezolizumab plus Bevacizumab in Patients with Variant Histology or Sarcomatoid Renal Cell Carcinoma

  2025-11-26

  articleOpen access

  &lt;p&gt;Supplementary Figure 6&lt;/p&gt;

  PublisherDOI

• Additive Clinical Utility of Microsatellite Instability and Tumor Mutational Burden to Predict Immune Checkpoint Inhibitor Effectiveness in Metastatic Castration-Resistant Prostate Cancer

  Clinical Cancer Research · 2025-12-04 · 1 citations

  articleOpen access

  PURPOSE: Immune checkpoint inhibitors (ICI) have shown limited efficacy in unselected patients with metastatic castration-resistant prostate cancer (mCRPC). However, ICIs are approved for biomarker-defined subsets: microsatellite instability-high (MSI-H) and/or high tumor mutational burden (TMB-H). The efficacy of ICIs in TMB-H but not MSI-H disease remains unclear, and limited data exist evaluating ICI outcomes associated with blood-based MSI (bMSI) in mCRPC. EXPERIMENTAL DESIGN: This study used the United States-based deidentified Flatiron Health-Foundation Medicine prostate cancer Clinico-Genomic Database. Patients with tissue-assessed MSI (tMSI) and TMB (tTMB) status by an algorithm supporting an FDA-approved CDx for pembrolizumab were included if treated with single-agent ICI. Separately, outcomes on ICI associated with bMSI were assessed, including if treated with single-agent ICI or taxane. RESULTS: Among 2,965 patients with mCRPC, tMSI-H (3.2%) was nearly always also tTMB ≥10 mut/Mb (4.7%). In 84 ICI-treated patients, time to next treatment (TTNT) and overall survival (OS) were more favorable in tMSI-H with any TMB [TTNT HR, 0.18; 95% confidence interval (CI), 0.09-0.37 and OS HR, 0.32; 95% CI, 0.15-0.66] and tTMB ≥10 without tMSI-H (TTNT HR, 0.18; 95% CI, 0.04-0.48 and OS HR, 0.20; 95% CI, 0.05-0.77) compared with tTMB <10 without tMSI-H group. In intrapatient assessments, patients with tTMB ≥10 had more favorable TTNT with subsequent ICI versus prior taxane. Detection of bMSI-H was associated with more favorable TTNT on ICI (HR, 0.34; 95% CI, 0.14-0.83) and OS (HR, 0.21; 95% CI, 0.06-0.75) when tumor fraction ≥1%. CONCLUSIONS: These findings add support for tTMB and tMSI in predicting ICI monotherapy benefit in mCRPC and provide evidence supporting bMSI testing when tissue is unavailable.

  PublisherOA PDFDOI

• Supplementary Data from A Phase I Study of Combination Olaparib and Radium-223 in Men with Metastatic Castration-Resistant Prostate Cancer (mCRPC) with Bone Metastases (COMRADE)

  2025-11-27

  articleOpen accessSenior author

  &lt;p&gt;Supplementary methods, Tables S1-S3, Figures S1 and S2&lt;/p&gt;

  PublisherDOI

• Figure S9 from Circulating and Intratumoral Immune Determinants of Response to Atezolizumab plus Bevacizumab in Patients with Variant Histology or Sarcomatoid Renal Cell Carcinoma

  2025-11-26

  articleOpen access

  &lt;p&gt;Supplementary Figure 9&lt;/p&gt;

  PublisherDOI

• Table S3 from Circulating and Intratumoral Immune Determinants of Response to Atezolizumab plus Bevacizumab in Patients with Variant Histology or Sarcomatoid Renal Cell Carcinoma

  2025-11-26

  articleOpen access

  &lt;p&gt;Supplementary table 3&lt;/p&gt;

  PublisherDOI

• Figure S12 from Circulating and Intratumoral Immune Determinants of Response to Atezolizumab plus Bevacizumab in Patients with Variant Histology or Sarcomatoid Renal Cell Carcinoma

  2025-11-26

  articleOpen access

  &lt;p&gt;Supplementary Figure 12&lt;/p&gt;

  PublisherDOI

Recent grants

• Cancer Control Program

  NIH · $40.3M · 1996–2031

Frequent coauthors

• Toni K. Choueiri

  Dana-Farber Cancer Institute

  564 shared

• Elisabeth I. Heath

  222 shared

• Wanling Xie

  Harvard University

  214 shared

• Lauren C. Harshman

  194 shared

• Sabina Signoretti

  166 shared

• Bradley A. McGregor

  166 shared

• Ziad Bakouny

  Dana-Farber Cancer Institute

  164 shared

• Eliezer M. Van Allen

  Broad Institute

  159 shared

Education

• Ph.D., Microbiology and Immunology

  University of California, San Diego

  2003

• M.S., Microbiology and Immunology

  University of California, San Diego

  1998

• B.S., Microbiology and Immunology

  University of California, San Diego

  1996