Ganiraju C. Manyam

The University of Texas MD Anderson Cancer Center

Full Professor(heuristic)

interferon and immune responses · Immunology

h-index47

i10-index88

Publications556

Citations13,470

Grants

No NSF/NIH grants on record.

Career Trajectory

Research Cluster Map

Direct collaborators. Node size = influence, colour = community, dashed = past collaboration.

Potential Collaborators

Recent Publications

Last 2 years · showing 20 of 137

Abstract 1181: Transcriptomic analysis of NDRG1 amplification in aggressive breast cancer.
Cancer Research · 2026-04-03
644 Temporospatial Activation of Signal Transducer and Activator of Transcription 3 (STAT3) and its Transcriptome Signature in the Transition from Normal to Cancer in Colons of Patients at High Risk for Colorectal Cancer
Laboratory Investigation · 2026-03-01
Supplementary Figure S8 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S12 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S14 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S5 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S10 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Table S9 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S13 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S16 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S2 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S11 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S19 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S17 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S15 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S20 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Data 1 from SETD2 Loss and ATR Inhibition Synergize to Promote cGAS Signaling and Immunotherapy Response in Renal Cell Carcinoma
2025-11-25
Supplementary Figure S18 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Table S13 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25
Supplementary Figure S7 from SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
2025-11-25

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