Tumor dormancy induction

Tumor dormancy induction refers to mechanisms by which cancer cells cease proliferating yet survive in a metabolically adapted, reversible state of growth arrest, often triggered by microenvironmental stresses, immune pressure, and specific signaling pathways. Central regulators—including p38 MAPK, TGF-β2, BMP-7, unfolded protein response proteins, and others—initiate transcriptional programs in dormant cells, enabling their persistence under adverse conditions (such as limited nutrients or immune attack). These cells can remain undetectable for years but retain potential to reactivate and cause tumor relapse, particularly after therapy. Understanding tumor dormancy induction is critical for developing novel cancer treatments aimed at eradicating minimal residual disease and preventing recurrence[1][2][3][4][5].

Other names

Cellular dormancyTumor mass dormancyDormant cancer cell (DCC) inductionDisseminated tumor cell dormancy

Not applicable to the "tumor dormancy induction" process per se. However, drugs targeting relevant pathways act by: Inducing cell cycle arrest and senescence (e.g., via p38 MAPK, p21, p27 activation); Modulating ERK/p38 signaling ratios to maintain or disrupt dormancy; Suppressing proliferative signals: inhibition of PI3K/AKT, ERK, Wnt pathways; induction of p38 signaling; Enhancing unfolded protein response (UPR) or ER stress adaptations for cell survival; Targeting stemness markers or cancer stem cell populations for elimination.