About

Dr. Takako Araki is an Associate Professor in the Division of Endocrinology, Diabetes and Metabolism at the University of Minnesota. Her research is dedicated to the quality improvement of pituitary perioperative patient care and the study of various pituitary disorders. She leads the Araki Lab, which focuses on understanding pituitary development and disorders, utilizing human iPS cells in their analysis. The lab investigates post-COVID pituitary dysfunction and aims to advance knowledge in pituitary-related health issues. The lab includes members such as Ryan Lawrence, a chemical engineering student; Mayu Tsuzuki, a study coordinator and lab manager; Gwyn Schmidt, an undergraduate student in Genetics, Cell Biology, and Development; Steven Sims, who investigates post-COVID pituitary dysfunction; Matthew Walters, a biochemistry graduate; and Joel Pardo, a medical scientist trainee with interests in research and gardening. The lab also collaborates with international researchers, including Dr. Ryusaku Matsumoto from Kyoto University, whose research involves in vitro analysis of pituitary development using human iPS cells.

Research topics

• Internal medicine
• Medicine
• Oncology
• Cancer research
• Urology
• Chemistry
• Biology
• Biochemistry
• Gynecology
• Surgery
• Molecular biology
• Intensive care medicine

Selected publications

• Rethinking the role of synergy calculations in the next century of drug combination discovery

  Med · 2026-05-01

  article
  PublisherDOI

• HLA Class I Expression is Associated with Increased Immune Cell Density and PTEN Loss in Prostate Cancer

  Molecular Cancer Research · 2026-05-01

  article

  Human leukocyte antigen Class I (HLA-I) downregulation in prostate cancer may contribute to tumor immune evasion. We digitally quantified HLA-I protein expression in a cohort of racially diverse and molecularly characterized prostatectomy specimens, as well as additional cohorts of metastatic hormone-sensitive (mHSPC) and castration-resistant prostate cancer (mCRPC). We confirm that HLA-I protein expression is negatively associated with intragenic methylation of major HLA-I genes, downregulated in tumor compared to benign glands, but not associated with race, genetic ancestry or clinicopathologic parameters in primary prostate cancer. Compared to matched primary tumor tissue, HLA-I expression is higher in HSPC pelvic lymph node metastases and increased primary tumor expression is inversely associated with metastasis among self-identified White, but not Black, patients. HLA-I expression in primary tumors is positively correlated with infiltrating immune cell densities, consistent with its established role in tumor cell immunogenicity. Surprisingly, primary tumors with PTEN loss show significantly higher HLA-I expression than those with intact PTEN, and this finding is validated in pre-clinical cell line and animal models, with a similar (nonsignificant) trend in mCRPC. Implications: The novel finding that PTEN loss is associated with higher tumoral HLA-I expression is concordant with observed increased immune cell infiltrates in tumors lacking PTEN, and may be relevant for precision medicine therapeutic approaches.

  PublisherDOI

• 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

• Supplementary Data 1 from Combination Treatment with Sipuleucel-T and Abiraterone Acetate or Enzalutamide for Metastatic Castration-Resistant Prostate Cancer: STAMP and STRIDE Trials

  2025-11-25

  articleOpen access1st authorCorresponding

  &lt;p&gt;Supplementary Data for Antonarakis et al&lt;/p&gt;

  PublisherOA PDFDOI

• Molecular alteration profiles characterize intraductal carcinoma of the prostate

  Cancer · 2025-12-28

  article

  BACKGROUND: Intraductal carcinoma of the prostate (IDC-P) is an intra-acinar and/or intraductal neoplastic epithelial proliferation that is a distinct histological entity according to the 2016 World Health Organization (WHO) classification system. Clinically, it is associated with higher grade tumors and a more aggressive disease course. However, the molecular underpinnings of IDC-P are not well elucidated. METHODS: This study identified radical prostatectomy (RP) cases from the Caris Life Sciences database, classified as prostatic adenocarcinoma with grade group 4/5 or with the words "cribriform," "necrosis," or "intraductal" in the pathology report. Digitized hematoxylin-eosin slides underwent central pathology review by a board-certified genitourinary pathologist to identify the presence of IDC-P according to the 2022 WHO classification. IDC-P cases (n = 175) were compared to non-IDC-P cases (n = 5334). Prostatic tumor specimens were sequenced via next-generation DNA/RNA sequencing. RESULTS: Compared to non-IDC-P cases, the IDC-P cohort had significantly more mutations in MUTYH (4.5% vs. 1.4%; p < .01), FANCA (2.7% vs. 0.5%; p < .01), NBN (2.5% vs. 0.6%; p < .05), and MTOR (0.6% vs. 0.1%; p < .05). IDC-P tumors were enriched for DLL3 and CEACAM5 expression, with lower expression of STEAP1, TROP2, ERBB2, PSCA, and B7-H3, compared to non-IDC-P tumors. IDC-P had significantly higher neuroendocrine prostate cancer signature scores and IFN-γ signature scores, and similar androgen receptor signature scores, compared to non-IDC-P. The tumor microenvironment of IDC-P had significantly higher cell fractions of M2 macrophages and fewer dendritic cells. CONCLUSIONS: IDC-P possesses a distinct molecular and immunological profile. Understanding these molecular underpinnings is crucial for the development of personalized treatment strategies for histologically distinct prostate cancer subsets.

  PublisherDOI

• Supplementary Figure 1 from Unique Spectrum of Activating &lt;i&gt;BRAF&lt;/i&gt; Alterations in Prostate Cancer

  2025-11-25

  articleOpen accessSenior author

  &lt;p&gt;Supplementary Figure 1&lt;/p&gt;

  PublisherDOI

• Supplementary Table 1 from Metastatic Prostate Cancers with &lt;i&gt;BRCA2&lt;/i&gt; versus &lt;i&gt;ATM&lt;/i&gt; Mutations Exhibit Divergent Molecular Features and Clinical Outcomes

  2025-11-25

  articleOpen accessSenior author

  &lt;p&gt;Composition and rates of all detectable genomic features detectable through the Caris diagnostic platform.&lt;/p&gt;

  PublisherDOI

• Table S4 from PSMA-positive Circulating Tumor Cell Detection and Outcomes with Abiraterone or Enzalutamide Treatment in Men with Metastatic Castrate-resistant Prostate Cancer

  2025-11-25

  articleOpen access

  &lt;p&gt;CTC biomarker group incidence by PSMA optimal cutoff (AR-v7, chromosomal instability (CIN), and neuroendocrine (NE) at baseline (N=97) and progression (N=57).&lt;/p&gt;

  PublisherDOI

• Supplementary Fig. 1 from Combination Treatment with Sipuleucel-T and Abiraterone Acetate or Enzalutamide for Metastatic Castration-Resistant Prostate Cancer: STAMP and STRIDE Trials

  2025-11-25

  articleOpen access1st authorCorresponding

  &lt;p&gt;Supplementary Fig 1 Analysis of Survival by Baseline Median PSA across the two studies using the study-specific median and quartiles.&lt;/p&gt;

  PublisherOA PDFDOI

• Supplementary Table 3 from Metastatic Prostate Cancers with &lt;i&gt;BRCA2&lt;/i&gt; versus &lt;i&gt;ATM&lt;/i&gt; Mutations Exhibit Divergent Molecular Features and Clinical Outcomes

  2025-11-25

  articleOpen accessSenior author

  &lt;p&gt;Comparisons of WTS profiles between ATMm and BRCA2m to the HRP group.&lt;/p&gt;

  PublisherDOI

Recent grants

• The aberrant androgen receptor underlies abiraterone/enzalutamide resistance

  NIH · $1.5M · 2015–2020

Frequent coauthors

• Mario A. Eisenberger

  673 shared

• Michael A. Carducci

  627 shared

• Samuel R. Denmeade

  502 shared

• Channing J. Paller

  Sidney Kimmel Comprehensive Cancer Center

  484 shared

• Jun Luo

  Johns Hopkins University

  443 shared

• Hao Wang

  402 shared

• Kenneth J. Pienta

  326 shared

• Changxue Lu

  Johns Hopkins Medicine

  304 shared

Labs

• Araki LabPI