Kah Min Tan
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Kah Min Tan has a total of 101 co-authors. Here are the top co-authors by number of shared publications:
- Boon Hao Hong
National Cancer Centre Singapore 1 , Singapore, Singapore
80 shared publications - Enya Hui Wen Ong
Division of Medical Sciences, National Cancer Centre Singapore, 30 Hospital Blvd, 168583, Singapore
80 shared publications - Melvin Lee Kiang Chua
National Cancer Centre Singapore/Duke-NUS Medical School, Singapore
80 shared publications - Amar U. Kishan
Department of Radiation Oncology, University of California Los Angeles, Los Angeles, USA
79 shared publications - Andrew Loblaw
Sunnybrook Health Sciences Centre, Toronto, ON M4N 3M5, Canada
79 shared publications - Benjamin Carlin
Department of Human Genetics, University of California
79 shared publications
Latest Publications
- 3 November 2026
- Published by American Association for Cancer Research (AACR) in Clinical Cancer Research
- p. OF1-OF11
Multi-institutional Patient-Level Comparison of Decipher Genomic Classifier and Artera Multimodal Artificial Intelligence in Prostate Cancer
Purpose: The Decipher Prostate Genomic Classifier (GC) and ArteraAI Multimodal Artificial Intelligence (MMAI) platform are widely used prognostic tools for localized prostate cancer, yet no direct comparison has been performed within the same patient cohort. Experimental Design: We sought to evaluate the concordance and prognostic value of GC and MMAI across multi-institutional cohorts totaling 688 patients with localized and oligometastatic prostate cancer. These included populations enriched for African American and East Asian patients. GC and MMAI scores were stratified into risk groups based on specimen type [biopsy or radical prostatectomy (RP)]. The primary endpoint was distant metastasis–free survival, measured from diagnosis to last follow-up or event. Results: GC and MMAI scores were significantly correlated across multiple cohorts. In Moffitt RP, biopsy, and National Cancer Centre Singapore cohorts, both MMAI and GC were prognostic alone and after adjusting for clinical variables. Multivariable analysis, including both biomarkers and clinical variables, showed that MMAI was significant even when accounting for GC in Moffitt RP and borderline in Moffitt biopsy. Analysis of concordant/discordant cases showed that patients who were high risk for both GC and MMAI did qualitatively worse. In pathway analysis, concordance with GC and MMAI was high for Moffitt RP and oligometastatic patients. Across both biopsy cohorts, although most biological pathways were concordant, there were consistent discordant signaling, metabolic, and DNA repair pathways. Conclusions: In the first direct patient-level comparison of GC and MMAI in prostate cancer, these biomarkers were found to demonstrate moderate correlation, and both biomarkers demonstrated prognostic value across diverse populations and disease states.
- 3 November 2026
- Published by American Association for Cancer Research (AACR) in Clinical Cancer Research
- p. OF1-OF11
Multi-institutional Patient-Level Comparison of Decipher Genomic Classifier and Artera Multimodal Artificial Intelligence in Prostate Cancer
Purpose: The Decipher Prostate Genomic Classifier (GC) and ArteraAI Multimodal Artificial Intelligence (MMAI) platform are widely used prognostic tools for localized prostate cancer, yet no direct comparison has been performed within the same patient cohort. Experimental Design: We sought to evaluate the concordance and prognostic value of GC and MMAI across multi-institutional cohorts totaling 688 patients with localized and oligometastatic prostate cancer. These included populations enriched for African American and East Asian patients. GC and MMAI scores were stratified into risk groups based on specimen type [biopsy or radical prostatectomy (RP)]. The primary endpoint was distant metastasis–free survival, measured from diagnosis to last follow-up or event. Results: GC and MMAI scores were significantly correlated across multiple cohorts. In Moffitt RP, biopsy, and National Cancer Centre Singapore cohorts, both MMAI and GC were prognostic alone and after adjusting for clinical variables. Multivariable analysis, including both biomarkers and clinical variables, showed that MMAI was significant even when accounting for GC in Moffitt RP and borderline in Moffitt biopsy. Analysis of concordant/discordant cases showed that patients who were high risk for both GC and MMAI did qualitatively worse. In pathway analysis, concordance with GC and MMAI was high for Moffitt RP and oligometastatic patients. Across both biopsy cohorts, although most biological pathways were concordant, there were consistent discordant signaling, metabolic, and DNA repair pathways. Conclusions: In the first direct patient-level comparison of GC and MMAI in prostate cancer, these biomarkers were found to demonstrate moderate correlation, and both biomarkers demonstrated prognostic value across diverse populations and disease states.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from The Proteogenomics of Prostate Cancer Radioresistance
Differentially abundant transcripts
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from The Proteogenomics of Prostate Cancer Radioresistance
Differentially abundant transcripts
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from The Proteogenomics of Prostate Cancer Radioresistance
Differential RNA abundance of driver cancer genes, using DEseq2 with the default parameter lfcThreshold = 0
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from The Proteogenomics of Prostate Cancer Radioresistance
Differential RNA abundance of driver cancer genes, using DEseq2 with the default parameter lfcThreshold = 0
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 5 from The Proteogenomics of Prostate Cancer Radioresistance
Ratios of single-base substitution types, for the two radioresistant cell line, in 3 replicates each
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 5 from The Proteogenomics of Prostate Cancer Radioresistance
Ratios of single-base substitution types, for the two radioresistant cell line, in 3 replicates each
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 7 from The Proteogenomics of Prostate Cancer Radioresistance
Association between CNA events in seven candidate genes and BCR, using a log-rank test
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 7 from The Proteogenomics of Prostate Cancer Radioresistance
Association between CNA events in seven candidate genes and BCR, using a log-rank test
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 3 from The Proteogenomics of Prostate Cancer Radioresistance
Supporting data for differential RNA abundance analysis
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 3 from The Proteogenomics of Prostate Cancer Radioresistance
Supporting data for differential RNA abundance analysis
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 2 from The Proteogenomics of Prostate Cancer Radioresistance
The difference in RNA abundance of a PCNA isoform (ENST00000379143.10) and POLD1 isoforms (ENST00000440232.7 and ENST00000596648.1)
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 2 from The Proteogenomics of Prostate Cancer Radioresistance
The difference in RNA abundance of a PCNA isoform (ENST00000379143.10) and POLD1 isoforms (ENST00000440232.7 and ENST00000596648.1)
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 5 from The Proteogenomics of Prostate Cancer Radioresistance
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 5 from The Proteogenomics of Prostate Cancer Radioresistance
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 14 from The Proteogenomics of Prostate Cancer Radioresistance
Supplementary Table 14 from The Proteogenomics of Prostate Cancer Radioresistance
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 14 from The Proteogenomics of Prostate Cancer Radioresistance
Supplementary Table 14 from The Proteogenomics of Prostate Cancer Radioresistance
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 1 from The Proteogenomics of Prostate Cancer Radioresistance
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 1 from The Proteogenomics of Prostate Cancer Radioresistance