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ZBTB7B – Prostate Cancer

This summary reviews the evidence linking ZBTB7B to prostate cancer. Two independent multi‐patient studies provide converging evidence: a whole‑genome sequencing study of 27 tumors (PMID:31884093) and a transcriptome‑wide association study in 79,194 prostate cancer cases with 61,112 controls (PMID:39878408).

The overall clinical validity of the association is rated as Strong because both studies independently implicate ZBTB7B. The WGS study revealed novel focal amplifications and deletions of ZBTB7B in a cohort of 27 tumors (PMID:31884093), while the TWAS identified statistically significant expression differences linking the gene to disease risk in a very large case‑control analysis (PMID:39878408).

In terms of genetic evidence, the association is supported by recurrent genomic alterations and differential mRNA levels in prostate tissue. Although no specific coding variant was reported with a full HGVS annotation for ZBTB7B in these studies, the collective data derived from both focal copy number changes and gene expression profiles lend strong support to its role in the disease. Given the complex and multifactorial nature of prostate cancer susceptibility, the inheritance mode is best described as autosomal dominant with risk alleles contributing to disease predisposition.

Experimental evidence further strengthens the role of ZBTB7B by showing that its dysregulation can alter glycolytic activity and modulate immune escape in cancer models. Functional studies in xenograft and in vitro systems demonstrated that perturbation of the ZBTB7B‐glycolysis axis impacts tumor immune evasion, providing moderate experimental support for its involvement in tumorigenesis (PMID:39107297).

No significant conflicting data has been reported, and the corroborative findings across genomic and functional studies consolidate the association between ZBTB7B and prostate cancer. Both the genetic and experimental evidence, while addressing distinct aspects of tumor biology, converge on a role for ZBTB7B in promoting oncogenic processes in prostate tissue.

Key take‑home sentence: The integrated genomic and functional evidence supports the clinical utility of ZBTB7B as a significant biomarker and potential therapeutic target in prostate cancer.

References

  • Life sciences • 2020 • Whole‑genome sequencing of prostate cancer reveals novel mutation‑driven processes and molecular subgroups PMID:31884093
  • The Prostate • 2025 • Transcriptome‑Wide Association Study Identified Novel Blood Tissue Gene Biomarkers for Prostate Cancer Risk PMID:39878408
  • Cell death & disease • 2024 • ALDH1A1 promotes immune escape of tumor cells through ZBTB7B‑glycolysis pathway PMID:39107297

Evidence Based Scoring (AI generated)

Gene–Disease Association

Strong

27 tumor samples analyzed (PMID:31884093) and a transcriptome-wide study in 79,194 PCa cases (PMID:39878408) provide robust evidence for the association.

Genetic Evidence

Strong

Recurrent focal amplifications/deletions and significant expression differences in large cohorts support the genetic linkage between ZBTB7B and prostate cancer.

Functional Evidence

Moderate

Functional studies in cancer models indicate that disruption of ZBTB7B affects glycolytic flux and immune escape, aligning with tumorigenic processes (PMID:39107297).