Severe telomere shortening in Fanconi anemia complementation group L.


Journal

Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234

Informations de publication

Date de publication:
Jan 2021
Historique:
received: 06 10 2020
accepted: 16 12 2020
pubmed: 5 1 2021
medline: 21 5 2021
entrez: 4 1 2021
Statut: ppublish

Résumé

Fanconi Anemia (FA) is a rare genetic disease with the incidence of 1 in 360,000 and is characterised by bone marrow failure, physical abnormalities, pancytopenia, and high frequency of chromosomal breakage and increased risk of evolving into malignancy. Telomere plays an important role in genomic stability, ageing process and cancers. Telomere shortening has been reported in FA. We studied telomere length in FA subjects and compared with complementation groups. Chromosomal breakage analysis from PHA stimulated, MMC induced peripheral blood culture was carried out in 37 clinically diagnosed FA. Molecular study of FANCA, G, and L was done through Sanger sequencing and next generation sequencing. Telomere length was estimated using real time quantitative polymerase chain reaction (qPCR) method. Student t-test was applied to test the significance. A high frequency of chromosomal breakage was observed in all the patients compared to healthy controls. We found significantly shorter telomere length in all the three complementation groups compare to age matched healthy controls. Among all complementation groups, FANCL showed severe telomere shortening (P value 0.0001). A negative correlation was observed between telomere length and chromosomal breakage frequency (R = -0.3116). Telomere shortening is not uncommon in FA subjects. However the telomere length shortening is different in complementation groups as FANCL showed severe telomere shortening in FA subjects. Though BM transplantation is essential for the management of the FA subjects, the telomere length can be considered as biological marker to understand the prognosis of the disease as FA subjects primarily treated with androgens.

Identifiants

pubmed: 33394227
doi: 10.1007/s11033-020-06101-2
pii: 10.1007/s11033-020-06101-2
doi:

Substances chimiques

DNA-Binding Proteins 0
FANCA protein, human 0
FANCG protein, human 0
Fanconi Anemia Complementation Group A Protein 0
Fanconi Anemia Complementation Group G Protein 0
FANCL protein, human EC 2.3.2.27
Fanconi Anemia Complementation Group L Protein EC 2.3.2.27

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

585-593

Subventions

Organisme : Department of Science and Technology, Government of India(IN)
ID : EEQ/2016/000510;B.R.V.

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Auteurs

Anjali Shah (A)

Department of Cytogenetics, ICMR-National Institute of Immunohematology, 13th floor, New Multistoried Building, K.E.M. Hospital Campus, Mumbai, Maharashtra, 400012, India.

Merin George (M)

Department of Cytogenetics, ICMR-National Institute of Immunohematology, 13th floor, New Multistoried Building, K.E.M. Hospital Campus, Mumbai, Maharashtra, 400012, India.

Somprakash Dhangar (S)

Department of Cytogenetics, ICMR-National Institute of Immunohematology, 13th floor, New Multistoried Building, K.E.M. Hospital Campus, Mumbai, Maharashtra, 400012, India.

Aruna Rajendran (A)

Department of Hematology, Institute of Child Health and Hospital for Children, Egmore, Chennai, Tamil Nadu, India.

Sheila Mohan (S)

Pediatric Haematology Department, Apollo Children's Hospital, Chennai, Tamil Nadu, India.

Babu Rao Vundinti (BR)

Department of Cytogenetics, ICMR-National Institute of Immunohematology, 13th floor, New Multistoried Building, K.E.M. Hospital Campus, Mumbai, Maharashtra, 400012, India. vbaburao@hotmail.com.

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