Evidence map›Paper›PMID 37438490›Full record

ArticleAnnals of hematology2023

Genomic and computational analysis of four novel variants of MPL gene in Congenital Amegakaryocytic Thrombocytopenia.

Anjali Shah, Chandan Kumar, Chandrakala Shanmukhaiah, Aruna Rajendran, Sangeeta Mudaliar, Susan Idicula-Thomas, Babu Rao Vundinti

Abstract read
PubMed Publisher
In one paragraph

Article in Annals of hematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

7 authors at 4 institutions in 1 country.

Anjali ShahDepartment of Cytogenetics, ICMR-National Institute of Immunohaematology, 13th floor, New Multi-storeyed building, KEM hospital Campus, Parel, Mumbai, Maharashtra, 400012, India.ORCID https://orcid.org/0000-0002-1343-177X
Chandan KumarBiomedical Informatics Centre, ICMR-National Institute for Research in Reproductive and Child Health, Mumbai, Maharashtra, 400012, India.ORCID https://orcid.org/0000-0002-7164-3105
Chandrakala ShanmukhaiahDepartment of Haematology, KEM Hospital, 10th Floor, New Multistoried Building, Parel, Mumbai, Maharashtra, 400012, India.
Aruna RajendranDepartment of Pediatric Hematology, Institute of Child Health and Hospital for Children, Chennai, India.
Sangeeta MudaliarBai Jerbai Wadia Hospital for Children, Mumbai, Maharashtra, India.
Susan Idicula-ThomasBiomedical Informatics Centre, ICMR-National Institute for Research in Reproductive and Child Health, Mumbai, Maharashtra, 400012, India.ORCID https://orcid.org/0000-0003-3766-6757
Babu Rao VundintiDepartment of Cytogenetics, ICMR-National Institute of Immunohaematology, 13th floor, New Multi-storeyed building, KEM hospital Campus, Parel, Mumbai, Maharashtra, 400012, India. vbaburao@hotmail.com.ORCID http://orcid.org/0000-0003-4783-2691
ICMR - National Institute of Immunohaemotology · INNational Institute for Research in Reproductive Health · INBai Jerbai Wadia Hospital for Children · INInstitute of Child Health · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Congenital amegakaryocytic thrombocytopenia (CAMT) is a rare, genetic, autosomal recessive disorder characterized by severe thrombocytopenia, due to inefficient bone marrow megakaryopoiesis eventually leading to aplasia. Majority of the cases are due to homozygous or compound heterozygous mutations in MPL gene encoding for thrombopoietin (THPO) receptor protein. CAMT can be diagnosed at early phase of life, with major complication of transfusion dependency and hematopoietic transplantation as only curative treatment. We have investigated the sequence variations in MPL gene of 7 bone marrow failure (BMF) subjects, who presented with clinically diverse phenotypes, through next generation sequencing (NGS). Plasma THPO levels were estimated using ELISA. Insilico sequence and structure-based analyses were performed to understand the structural and functional implications of mutations, identified through NGS. We studied 7 CAMT subjects suspected of BMF, who presented with severe thrombocytopenia followed by pancytopenia, bleeding manifestation and physical anomalies. The plasma THPO levels were significantly elevated (p<0.05) in all the cases. Molecular analysis by NGS identified 9 genomic mutations in MPL gene. These included 7 non-synonymous substitution, 1 nonsense substitution and 1 in-del mutations, of which 4 are novel mutations. Insilico analysis predicted damaging effects on THPO-R and its reduced affinity for THPO for all the identified mutations. CAMT is a rare disorder with diverse clinical phenotypes and diagnosis is challenging. The elevated plasma THPO levels should be considered for the primary diagnosis and prognosis of the disease. However, molecular analysis of MPL gene is important for the diagnosis and management of the disease through genetic counselling. Though the cytokines, THPO-R agonist are used for the treatment of CAMT, HSCT is the only curative therapy.

Indexed as

PancytopeniaThrombocytopeniaCongenital Bone Marrow Failure SyndromesGenomicsHumansReceptors, ThrombopoietinThrombopoietinMPL protein, humanReceptors, ThrombopoietinThrombopoietinCongenital amegakaryocytic thrombocytopeniaMPL geneNext generation sequencingPancytopeniaTHPO-R structureThrombopoietinThrombopoietin receptor

Identifiers

PMID37438490
OpenAlexW4384126621

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.