Evidence map›Paper›PMID 32354950›Full record

ArticleIn vivo (Athens, Greece)

Optimal Response in a Patient With CML Expressing

Livia Manzella, Elena Tirrò, Silvia Rita Vitale, Adriana Puma, Maria Letizia Consoli, Loredana Tambè, Maria Stella Pennisi, Sandra DI Gregorio, Chiara Romano, Cristina Tomarchio and 2 more

Open access · diamondAbstract readCase Reports
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. The silent players: AtypicalOncology reports · 2025
    Review
  2. Article
  3. [Chronic myeloid leukemia with e6a2 fusion gene: a case report and literature review].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
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

12 authors at 2 institutions in 1 country.

Livia ManzellaDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy manzella@unict.it.
Elena TirròDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Silvia Rita VitaleDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Adriana PumaDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Maria Letizia ConsoliDivision of Hematology and Bone Marrow Transplant, A.O.U. Policlinico-Vittorio Emanuele, Catania, Italy.
Loredana TambèDivision of Hematology and Bone Marrow Transplant, A.O.U. Policlinico-Vittorio Emanuele, Catania, Italy.
Maria Stella PennisiDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Sandra DI GregorioDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Chiara RomanoDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Cristina TomarchioDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Francesco DI RaimondoDivision of Hematology and Bone Marrow Transplant, A.O.U. Policlinico-Vittorio Emanuele, Catania, Italy.
Fabio StagnoDivision of Hematology and Bone Marrow Transplant, A.O.U. Policlinico-Vittorio Emanuele, Catania, Italy.
Azienda Ospedaliero-Universitaria Policlinico - Vittorio Emanuele · ITUniversity of Catania · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimThe Philadelphia chromosome is considered the hallmark of chronic myeloid leukemia (CML). However, although most patients with CML are diagnosed with the e13a2 or e14a2 breakpoint cluster region (BCR)-Abelson 1 (ABL1) fusion transcripts, about 5% of them carry rare BCR-ABL1 fusion transcripts, such as e19a2, e8a2, e13a3, e14a3, e1a3 and e6a2. In particular, the e6a2 fusion transcript has been associated with clinically aggressive disease frequently presenting in accelerated or blast crisis phases; there is limited evidence on the efficacy of front-line second-generation tyrosine kinase inhibitors for this genotype. CASE REPORT: We describe a case of atypical BCR-ABL1 e6a2 fusion transcript in a 46-year-old woman with CML.

resultsThe use of primers recognizing more distant exons from the common BCR-ABL1 breakpoint region correctly identified the atypical BCR-ABL1 e16a2 fusion transcript. Treatment with second-generation tyrosine kinase inhibitor nilotinib was effective in this patient expressing the atypical e6a2 BCR-ABL1 fusion transcript.

Indexed as

RNA IsoformsAbnormal KaryotypeAntineoplastic AgentsCytogenetic AnalysisFemaleFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiddle AgedMolecular Targeted TherapyProtein Kinase InhibitorsPyrimidinesAntineoplastic AgentsBCR-ABL1 fusion protein, humanFusion Proteins, bcr-ablnilotinibProtein Kinase InhibitorsPyrimidinesRNA IsoformsBCR–ABL1CMLe6a2nilotinibTKI therapy

Identifiers

PMID32354950
PMCPMC7279803
OpenAlexW3021450623

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.