Evidence map›Paper›PMID 26208274›Full record

ArticlePloS one2015

Distribution of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Mutations in a Cohort of Patients Residing in Palestine.

Issa Siryani, Mohamed Jama, Nisreen Rumman, Hiyam Marzouqa, Moein Kannan, Elaine Lyon, Musa Hindiyeh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. A comprehensive review of cystic fibrosis in Africa and Asia.Saudi journal of biological sciences · 2023
    Review
  4. Article
  5. Article
  6. Review
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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

7 authors at 3 institutions in 2 countries.

Issa SiryaniCaritas Baby Hospital, Bethlehem, Palestine; Bethlehem University, Bethlehem, Palestine; Palestinian Forum for Medical Research (PFMR), Ramallah, Palestine.
Mohamed JamaARUP Institute for Clinical and Experimental Pathology, Salt Lake City, UT, United States of America.
Nisreen RummanCaritas Baby Hospital, Bethlehem, Palestine.
Hiyam MarzouqaCaritas Baby Hospital, Bethlehem, Palestine.
Moein KannanBethlehem University, Bethlehem, Palestine.
Elaine LyonARUP Institute for Clinical and Experimental Pathology, Salt Lake City, UT, United States of America; Department of Pathology, University of Utah, Salt Lake City, UT, United States of America.
Musa HindiyehCaritas Baby Hospital, Bethlehem, Palestine; Bethlehem University, Bethlehem, Palestine; Palestinian Forum for Medical Research (PFMR), Ramallah, Palestine.
Bethlehem University · PSARUP Institute for Clinical and Experimental PathologyUniversity of Utah · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis (CF) is an autosomal recessive inherited life-threatening disorder that causes severe damage to the lungs and the digestive system. In Palestine, mutations in the Cystic Fibrosis Transmembrane Conductance Regulator gene (CFTR) that contributes to the clinical presentation of CF are ill defined. A cohort of thirty three clinically diagnosed CF patients from twenty one different Palestinian families residing in the central and southern part of Palestine were incorporated in this study. Sweat chloride testing was performed using the Sweat Chek Conductivity Analyzer (ELITECH Group, France) to confirm the clinical diagnosis of CF. In addition, nucleic acid from the patients' blood samples was extracted and the CFTR mutation profiles were assessed by direct sequencing of the CFTR 27 exons and the intron-exon boundaries. For patient's DNA samples where no homozygous or two heterozygous CFTR mutations were identified by exon sequencing, DNA samples were tested for deletions or duplications using SALSA MLPA probemix P091-D1 CFTR assay. Sweat chloride testing confirmed the clinical diagnosis of CF in those patients. All patients had NaCl conductivity >60 mmol/l. In addition, nine different CFTR mutations were identified in all 21 different families evaluated. These mutations were c.1393-1G>A, F508del, W1282X, G85E, c.313delA, N1303K, deletion exons 17a-17b-18, deletion exons 17a-17b and Q1100P. c.1393-1G>A was shown to be the most frequent occurring mutation among tested families. We have profiled the underling mutations in the CFTR gene of a cohort of 21 different families affected by CF. Unlike other studies from the Arab countries where F508del was reported to be the most common mutation, in southern/central Palestine, the c.1393-1G>A appeared to be the most common. Further studies are needed per sample size and geographic distribution to account for other possible CFTR genetic alterations and their frequencies. Genotype/phenotype assessments are also recommended and finally carrier frequency should be ascertained.

Indexed as

MutationAdolescentAdultArabsChildChild, PreschoolCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorExonsFemaleGenotypeHumansInfantIntronsMaleYoung AdultCystic Fibrosis Transmembrane Conductance Regulator

Identifiers

PMID26208274
PMCPMC4514804
OpenAlexW1896304586

What OpenQuestion holds

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LicenceCC BY
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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.