Evidence map›Paper›PMID 31093876›Full record

ArticleMolecular biology reports2019

The prognostic impact of hypermethylation for a panel of tumor suppressor genes and cell of origin subtype on diffuse large B-cell lymphoma.

Samir A Shawky, Mohamed H El-Borai, Hussein M Khaled, Iman Guda, Marwa Mohanad, Mona S Abdellateif, Abdel-Rahman N Zekri, Abeer A Bahanasy

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Article in Molecular biology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Samir A ShawkyTissue Culture and Cytogenetics Unit, Pathology Department, National Cancer Institute, Cairo University, 1 Fom El-Khalig Street, Cairo, Egypt.
Mohamed H El-BoraiTissue Culture and Cytogenetics Unit, Pathology Department, National Cancer Institute, Cairo University, 1 Fom El-Khalig Street, Cairo, Egypt.
Hussein M KhaledSurgical Oncology Unit, Pathology Department, National Cancer Institute, Cairo University, Cairo, Egypt.
Iman GudaMedical Oncology Department, National Cancer Institute, Cairo University, Cairo, Egypt.
Marwa MohanadBiochemistry Department, College of Pharmaceutical Sciences and Drug Manufacturing, Misr University for Science and Technology, 6th of October City, Egypt.
Mona S AbdellateifMedical Biochemistry and Molecular Biology, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt.
Abdel-Rahman N ZekriVirology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt.
Abeer A BahanasyTissue Culture and Cytogenetics Unit, Pathology Department, National Cancer Institute, Cairo University, 1 Fom El-Khalig Street, Cairo, Egypt. chaya2000@hotmail.com.
Cairo University · EGMisr University for Science and Technology · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diffuse Large B-cell lymphoma (DLBCL) is an aggressive disease with heterogeneous outcome and marked variable response to chemotherapy. We assessed promoter hypermethylation (PM) for a panel of tumor suppressor genes in 75 DLBCLs compared to 20 lymphoid hyperplasia (LH) and 30 normal control, using methylation specific PCR. Results were correlated to patients' clinic-pathological characteristics, immunophenotyping, and patients' outcome. DAPK1, RUNX3, MT1G, MGMT, CDH1 and p16 PM were detected in 38.7% (29/75), 49.3% (37/75), 46.7% (35/75), 44% (33/75), 49.3% (37/75) and 42.7% (32/75);respectively, of DLBCL patients compared to LH group (P < 0.05). Aberrant PM of RUNX3, MGMT, CDH1 and p16 was significantly higher in non-germinal central B-cell like (non-GCB) compared to GCB (58.3% vs. 33.3%, 56.2% vs. 22.2, 62.5% vs. 25.9, and 56.2% vs. 18.5%, respectively). PM of studies genes in DLBCL associated significantly with worse survival outcome and resistance to chemotherapy (P ≤ 0.01). In non-GCB group, DAPK1, MT1G, RUNX3, CDH1 and p16 PM associated significantly with reduced DFS (P ≤ 0.004) and OS (P ≤ 0.015). Multivariate analysis indicated that RUNX3 and CDH1 PM were independent prognostic factors for OS (P = 0.03 and 0.04; respectively), while DAPK1, RUNX3 and MT1G PM were independent prognostic factors for DFS (P = 0.002, 0.037& 0.007; respectively). DAPK1, RUNX3, MT1G, CDH1 and p16 PM are promising prognostic and/or predictive markers for non-GCB independent of IPI. Upregulation of those genes using new demethylating agents is a promising approach that sensitize chemoresistant DLBCL patients, especially the non-GCB subtype.

Indexed as

AdultAgedAntigens, CDAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsCadherinsCore Binding Factor Alpha 3 SubunitDeath-Associated Protein KinasesDisease-Free SurvivalDNA MethylationDoxorubicinFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansLymphoma, Large B-Cell, DiffuseAntigens, CDAntineoplastic AgentsCadherinsCDH1 protein, humanCore Binding Factor Alpha 3 SubunitDAPK1 protein, humanDeath-Associated Protein KinasesDoxorubicinMetallothioneinMT1G protein, humanRunx3 protein, humanCDH1 and p16DAPK1Diffuse large B cell lymphomaMT1GNon-GCBPromotor methylationRUNX3

Identifiers

PMID31093876
OpenAlexW2946343472

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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.