Evidence map›Paper›PMID 26823817›Full record

ArticleInternational journal of clinical and experimental pathology2015

Evaluation of AKT phosphorylation and PTEN loss and their correlation with the resistance of rituximab in DLBCL.

Yihui Ma, Pengyu Zhang, Yi Gao, Huijie Fan, Mingzhi Zhang, Jingjing Wu

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Novel BAFF-Receptor Antibody to Natively Folded Recombinant Protein Eliminates Drug-Resistant Human B-cell MalignanciesClinical cancer research : an official journal of the American Association for Cancer Research · 2018
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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 2 institutions in 1 country.

Yihui MaDepartment of Pathology, Henan Key Laboratory for Tumour Pathology, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450002, Henan Province, P. R. China.
Pengyu ZhangDepartment of Endocrinology, Cancer Research Institute, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450002, Henan Province, P. R. China.
Yi GaoDepartment of Oncology, Cancer Research Institute, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450002, Henan Province, P. R. China.
Huijie FanDepartment of Oncology, Cancer Research Institute, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450002, Henan Province, P. R. China.
Mingzhi ZhangDepartment of Oncology, Cancer Research Institute, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450002, Henan Province, P. R. China.
Jingjing WuDepartment of Oncology, Cancer Research Institute, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450002, Henan Province, P. R. China.
Henan Cancer Hospital · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiffuse large B-cell lymphoma (DLBCL) is the most common subtype of lymphoma with quite high mortality. PTEN/PI3K/AKT signal pathway is constitutively activated and plays an oncogenic role in most tumors including non-Hodgkin's lymphoma (NHL). Since rituximab used in chemotherapy has been proved to improve the survival of DLBCL patients, rituximab resistance is a common clinical challenge in the treatment of DLBCL. The aims of the present study are to determine the different levels of several important biomarkers of PTEN/PI3K/AKT pathway in DLBCL patients who are resistant or sensitive to rituximab treatment, and investigate the potential clinical application of these biomarkers.

methods48 patients with DLBCL who were treated by rituximab-based chemotherapy were divided into 2 groups according to their reactions to rituximab. The expression of p-AKT, PTEN, and Ki-67 protein in 48 DLBCL tissues were detected using immunohistochemistry and analyzed for the clinical pathological significance and the resistance to rituximab. Meanwhile, PTEN gene deletion was detected also by FISH, and mutation of PIK3CA was performed by sequencing analysis.

resultsActivation of p-AKT in 12 of 48 (25.0%) and loss expression of PTEN in 15 of 48 (31.3%) DLBCL species were observed. P-AKT activation (P<0.05) and loss of PTEN expression (P<0.05) were significantly associative with high Ki-67 index. P-AKT and PTEN expression showed a significant negative correlation in all 48 DLBCL patients (r=-0.450, P<0.05), and the Spearman correlation coefficient in the resistant group (r=-0.769, P<0.05) was greater than in the sensitive group (r=-0.691, P<0.05).

conclusionRegulation of PTEN/PI3K/AKT signal pathway participates in the progression of DLBCL, and may be involved in the development of the resistance to rituximab for some DLBCL patients.

Indexed as

AdultAgedAged, 80 and overAntineoplastic AgentsBiomarkers, TumorDrug Resistance, NeoplasmFemaleHumansImmunohistochemistryIn Situ Hybridization, FluorescenceLymphoma, Large B-Cell, DiffuseMaleMiddle AgedPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktAntineoplastic AgentsBiomarkers, TumorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanRituximabAKTlymphomaPI3KPTENrituximab resistance

Identifiers

PMID26823817
PMCPMC4713603
OpenAlexW2418229423

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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.