Evidence map›Paper›PMID 42505403›Full record

ArticleCells2026

CaMKK2 Expression Correlates with High-Risk CLL Biology, and Pharmacologic Inhibition Is Associated with Reduced Leukemic Cell Survival and Nurse-like Cell Support In Vitro.

Shekeab Jauhari, Alicia D Cooper-Volkheimer, Vini Verma, Dilber Gökçe Kaplan, Fahmin Basher, J Brice Weinberg, Nelson J Chao, Luigi Racioppi

Abstract read
In one paragraph

Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Shekeab JauhariDivision of Hematological Malignancies and Cellular Therapy, Department of Medicine, Duke University, Durham, NC 27707, USA.
Alicia D Cooper-VolkheimerDivision of Hematological Malignancies and Cellular Therapy, Department of Medicine, Duke University, Durham, NC 27707, USA.ORCID 0000-0002-0275-4450
Vini VermaDivision of Hematological Malignancies and Cellular Therapy, Department of Medicine, Duke University, Durham, NC 27707, USA.
Dilber Gökçe KaplanDivision of Hematological Malignancies and Cellular Therapy, Department of Medicine, Duke University, Durham, NC 27707, USA.ORCID 0009-0008-2583-4593
Fahmin BasherDivision of Hematological Malignancies and Cellular Therapy, Department of Medicine, Duke University, Durham, NC 27707, USA.ORCID 0000-0002-6368-6762
J Brice WeinbergDivision of Hematology, Department of Medicine, Duke University, Durham, NC 27707, USA.
Nelson J ChaoDivision of Hematological Malignancies and Cellular Therapy, Department of Medicine, Duke University, Durham, NC 27707, USA.ORCID 0000-0001-6725-7220
Luigi RacioppiDivision of Hematological Malignancies and Cellular Therapy, Department of Medicine, Duke University, Durham, NC 27707, USA.ORCID 0000-0002-9207-6752

Funding

Creation of in vivo active chemical probes for CAMKK2 to treat cancerR01CA218442 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DREWRY, DAVID HAROLD · 2017 to 2019
$2.0M
HILLS research fund WBSE 391001259NCI NIH HHS R01 CA218442NIH-NCI/United States 5R01CA218442-03
6 · The paper itself

Abstract

BACKGROUND/

objectivesChronic lymphocytic leukemia (CLL) is characterized by clinical and biological heterogeneity shaped by intrinsic signaling programs and microenvironmental interactions. Established biomarkers, including IGHV mutation status and TP53 alterations, provide important clinical and molecular information, but do not fully capture the diversity of pathways that sustain leukemic cell fitness. Aberrant calcium signaling contributes to leukemic survival; however, the clinical relevance of Ca

methodsCaMKK2 expression was quantified in purified CD19

resultsElevated CaMKK2 expression was enriched in IGHV-unmutated CLL and associated with shorter time to treatment and inferior overall survival. Pharmacological inhibition of CaMKK2 was associated with reduced primary CLL viability in a dose-dependent manner and increased Annexin V/PI-defined total cell death with sensitivity correlating with CaMKK2 expression levels. Inhibition also attenuated CD163

conclusionsCaMKK2 expression is associated with IGHV-unmutated, high-risk CLL biology. Pharmacologic inhibition of CaMKK2 was associated with reduced leukemic cell viability and altered macrophage phenotypes in ex vivo systems. These findings are exploratory, derived from a limited cohort, and support further investigation into the role of CaMKK2 in CLL biology, but do not establish independent prognostic value or direct on-target causality.

Indexed as

Calcium-Calmodulin-Dependent Protein Kinase KinaseLeukemia, Lymphocytic, Chronic, B-CellApoptosisCell SurvivalHumansMutationCalcium-Calmodulin-Dependent Protein Kinase KinaseCAMKK2 protein, humancalcium signalingCaMKK2chronic lymphocytic leukemiaIGHV-unmutated CLLnurse-like cellstumor-associated macrophagetumor microenvironment

Identifiers

PMID42505403
PMCPMC13406266

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Registered trials

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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.