ReviewMolecular biology reports2025
CaMKK2 as a therapeutic target to combat metastasis in glioblastoma.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
Glioblastoma, an aggressive primary brain malignancy associated with poor survival rate and limited curative interventions, posing significant challenges in clinical management. Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) is known to regulate various cellular processes including energy homeostasis and immune modulation under normal physiological conditions as well as promoting metastasis in several cancer types. This review delves into the intricate involvement of CAMKK2 in the virulence of glioblastoma. Several studies have suggested that CAMKK2 can be a potential biomarker and therapeutic target for glioblastoma. Differential expression of CAMKK2 across glioma grades highlights its potential utility in disease stratification. Specifically, elevated CAMKK2 expression in high-grade gliomas is associated with increased metastatic potential. Furthermore, CAMKK2 ha been implicated in promoting resistance to immune checkpoint blockade therapy, underscoring its protumorigenic role. Given its involvement in tumor progression metastasis, modulation of the tumor microenvironment, and therapy resistance, CAMKK2 represents a promising candidate for the development of novel glioblastoma treatment strategies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.