Evidence map›Paper›PMID 41221040›Full record

ReviewFrontiers in pharmacology2025

Potential signaling pathways, biomarkers, natural drugs, and chronic myeloid leukemia therapeutics.

Sultan Alqahtani

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2025. 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

1 author.

Sultan AlqahtaniDepartment of Basic Medical Sciences, College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Philadelphia chromosome signals BCR-ABL1 migration in myeloid clonal proliferation disorders such as chronic myeloid leukemia (CML). The crucial function of the Musashi2-Numb axis in deciding cell fate and its connection to significant signaling pathways like Hedgehog and Notch, which are necessary for the self-renewal pathways of CML stem cells, will be the subject of future research in this work. For this review, we conducted a PubMed search using the terms Musashi2-Numb, signaling pathways, and leukemia. As a result, we assembled several studies. Tyrosine kinase inhibitors like imatinib can kill and eradicate BCR-ABL1 translocated cells, but they cannot directly target BCR-ABL1 leukemia stem cells. The primary issue is stem cells' resistance to imatinib therapy. Since leukemia stem cells are thought to be treated by the Musashi2-Numb signaling pathway, a successful therapy approach may involve comprehending and controlling the downstream molecules and signaling pathway of BCR-ABL1 that are important in the survival and self-renewal of leukaemia stem cells. Here, we focused on the generalised perspectives of the drugs that target major signaling proteins and change elements or pathways downstream of BCR-ABL1 can effectively treat chronic leukemia stem cells. There are handful number of proteins such as Musashi2 which have substantial diagnostic use in leukemia treatment and strategy. After going through a number recent develeopments in CML and its therapeutics, I presented here an overview of the latest advancements in CML, natural drugs, biomarkers, potential signaling pathways, and treatment strategies.

Indexed as

biomarkerschronic myeloid leukemia (CML)CML therapeuticsdisease progressionmyeloid sarcomanatural drugspotential signaling pathways

Identifiers

PMID41221040
PMCPMC12598037

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.