blood-cancer

New AML drug target discovered: CCDC137 fuels leukemia growth by stabilizing a cancer-promoting protein.

CCDC137 is overexpressed in AML and correlates with poor prognosis. CCDC137 stabilizes S100A6 protein, which then activates the PI3K/AKT signaling pathway driving AML cell proliferation and cell cycle progression. This CCDC137→S100A6→PI3K/AKT axis is a novel AML therapeutic target.

New AML drug target discovered: CCDC137 fuels leukemia growth by stabilizing a cancer-promoting protein.

Key Findings

CCDC137 overexpressed in AML; correlates with poor prognosis
CCDC137 stabilizes S100A6 protein by preventing its degradation
Stable S100A6 activates PI3K/AKT pathway
CCDC137 promotes AML cell proliferation and cell cycle progression
Novel therapeutic target identified for AML-specific therapy

Implications

Targeting CCDC137-S100A6-PI3K/AKT axis could provide a new therapeutic approach in AML, especially in combination with existing PI3K/AKT inhibitors.

Caveats

Preclinical cell line and mechanistic study; abstract-only. In vivo models and patient-derived AML samples needed for validation.

Source: Journal of leukocyte biology — 2026-04-02

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New AML drug target discovered: CCDC137 fuels leukemia growth by stabilizing a cancer-promoting protein.

Key Findings

Implications

Caveats

Read more

Landmark DCIS trial, CRC microbiome & AML combos

Colorectal Cancer Microbiome Discovery Platform

GBM Tumor Microenvironment Drug Target Atlas

BET Inhibitor Target Selectivity Database