Evidence map›Paper›PMID 29387948›Full record

ArticleMedical oncology (Northwood, London, England)2018

Expression of Hippo signaling pathway and Aurora kinase genes in chronic myeloid leukemia.

Ana Paula Zambuzi Cardoso Marsola, Belinda Pinto Simões, Leonardo Carvalho Palma, Maria Gabriela Berzoti-Coelho, Sandra Mara Burin, Fabíola Attié de Castro

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 21% of its field
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

16 citing papers in PubMed, 20 citations in OpenAlex.

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  14. The role of Aurora-A in human cancers and future therapeutics.American journal of cancer research · 2020
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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

6 authors at 1 institution in 1 country.

Ana Paula Zambuzi Cardoso MarsolaDepartment of Clinical Analysis, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo-USP, Café Avenue, Ribeirão Preto, SP, Brazil. anafarma_usp@yahoo.com.br.
Belinda Pinto SimõesDepartment of Internal Medicine, Ribeirão Preto Medical School, University of São Paulo-USP, 3900 Bandeirantes Avenue, Ribeirão Preto, SP, Brazil.
Leonardo Carvalho PalmaDepartment of Internal Medicine, Ribeirão Preto Medical School, University of São Paulo-USP, 3900 Bandeirantes Avenue, Ribeirão Preto, SP, Brazil.
Maria Gabriela Berzoti-CoelhoDepartment of Clinical Analysis, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo-USP, Café Avenue, Ribeirão Preto, SP, Brazil.
Sandra Mara BurinDepartment of Clinical Analysis, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo-USP, Café Avenue, Ribeirão Preto, SP, Brazil.
Fabíola Attié de CastroDepartment of Clinical Analysis, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo-USP, Café Avenue, Ribeirão Preto, SP, Brazil.
Universidade de São Paulo · BR

Funding

FAPESP 2015-21237-4).FAPESP FAPESP (2015-23555-3
6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm resulting from clonal expansion of hematopoietic stem cells positive for the Philadelphia chromosome. The CML pathogenesis is associated with expression of the BCR-ABL1 oncogene, which encodes the Bcr-Abl protein with tyrosine kinase activity, promoting the leukemic cell exacerbated myeloproliferation and resistance to apoptosis. CML patients are usually treated with tyrosine kinase inhibitors (TKI), but some of them acquire resistance or are refractory to TKI. Thus, it is still relevant to elucidate the CML pathogenesis and seek new therapeutic targets, such as the Hippo signaling pathway and cell cycle regulatory genes from the Aurora kinase family. The present study quantified the expression level of genes encoding components of the Hippo signaling pathway (LATS1, LATS2, YAP, and TAZ), AURKA and AURKB in CML patients at different stages of the disease, who were resistant or sensitive to imatinib mesylate therapy, and in healthy individuals. The expression levels of the target genes were correlated with the CML Sokal's prognostic score. The most striking results were the LATS2 and AURKA overexpression in CML patients, the overexpression of TAZ and AURKB in CML patients at advanced phases and TAZ in CML IM-resistant. The development of drugs and/or identification of tumor markers for the Hippo signaling pathway and the Aurora kinase family, either alone or in combination, can optimize CML treatment by enhancing the susceptibility of leukemic cells to apoptosis and leading to a better disease prognosis.

Indexed as

Gene Expression Regulation, LeukemicAdultAgedAged, 80 and overAurora Kinase AAurora Kinase BBiomarkers, TumorCase-Control StudiesDrug Resistance, NeoplasmFemaleFollow-Up StudiesHippo Signaling PathwayHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleAURKA protein, humanAURKB protein, humanAurora Kinase AAurora Kinase BBiomarkers, TumorImatinib MesylateProtein Kinase InhibitorsProtein Serine-Threonine KinasesAurora kinasesBCR–ABL1Chronic myeloid leukemiaHippo pathwayTyrosine kinase inhibitors

Identifiers

PMID29387948
OpenAlexW2785786008

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.