Tumor necrosis factor induced protein 3 gene polymorphism and the susceptibility to chronic primary immune thrombocytopenia in Egyptian children: a case-control study
Background Primary immune thrombocytopenia (PIT) is an acquired auto-immune disease characterized by decreased platelet count with increased bleeding tendency. The tumor necrosis factor associated induced protein-3 (TNFAIP3) codes for the ubiquitin-modifying enzyme that is indispensable for limiting...
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| Veröffentlicht in: | Egyptian Journal of Medical Human Genetics 2021-02, Vol.22 (1), p.12-9, Article 12 |
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| creator | El-hady, Marwa Abd Mosallam, Dalia S. Anis, Shahira K. Mansour, Basma S. Yassa, Marianne E. |
| description | Background
Primary immune thrombocytopenia (PIT) is an acquired auto-immune disease characterized by decreased platelet count with increased bleeding tendency. The tumor necrosis factor associated induced protein-3 (TNFAIP3) codes for the ubiquitin-modifying enzyme that is indispensable for limiting inflammation. TNFAIP3 single-nucleotide polymorphisms (SNP) has been implicated in the susceptibility to multiple auto-immune diseases. We aimed to study the distribution of TNFAIP3 (
rs5029939 C>G
) SNP and the possible association of the studied polymorphism with the susceptibility to chronic PIT and the response to treatment in a sample of the Egyptian pediatric chronic PIT patients. This is a case-control study performed on 40 chronic PIT patients and 50 age- and gender-matched healthy controls. DNA samples from both groups were tested for TNFAIP3 (
rs5029939 C
>
G
) SNP using polymerase chain reaction-restriction fragment length polymorphism assay.
Results
TNFAIP3 (
rs5029939 C
>
G
) genotype distribution showed no statistically significant difference between PIT cases and controls [CC 77.5% vs. 82.5%, and CG 22% vs. 18%, respectively; OR (95% CI), 1.323 (0.470–0.723);
p
, 0.596]. The minor allele frequency (MAF) of
rs5029939
-
G
was comparable between the 2 groups (0.11 vs. 0.09) [OR (95% CI), 1.282 (0.484–3.397);
p
, 0.617]. No statistically significant difference was observed between chronic PIT patients carrying the mutant heterozygous genotype (CG) achieving complete response and those with no response [OR (95% CI), 1.667 (0.165-16.810);
p
> 0.05]. The MAF of
rs5029939
-
G
was comparable between both groups [OR (95% CI), 1.571 (0.175–14.111);
p
> 0.05].
Conclusion
This study showed no liability of patients carrying TNFAIP3 (
rs5029939 C
>
G
) polymorphism to develop chronic course of the disease or to achieve complete response to treatment. TNFAIP3 (
rs5029939 C < G
) SNP plays no role in either susceptibility to chronic PIT in the studied sample of Egyptian pediatric population or their response to treatment. |
| doi_str_mv | 10.1186/s43042-020-00129-6 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_doaj_</sourceid><recordid>TN_cdi_proquest_journals_2670470110</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A679537695</galeid><doaj_id>oai_doaj_org_article_04d51c7077f24ea39846104dbcd206fe</doaj_id><sourcerecordid>A679537695</sourcerecordid><originalsourceid>FETCH-LOGICAL-c496t-3f8be04ebf2abb5478fa0ef7db520f8faf6f6bd89a1e8bfce73ccb972a1836c13</originalsourceid><addsrcrecordid>eNp9ks1u1DAQxyMEEmXhBThZ4pxiO14n4VZVBSpV4lLOlj_Gu14l9mI7h7wQz8m0qShICFmyPaP5_T2emaZ5z-glY4P8WERHBW8ppy2ljI-tfNFccDrSlgvBXv5xf928KeVEqdx3vbhoft4vc8okgs2phEK8thXtEN1iwZFzThVCJB05QARyTtOK4edjKDPR0ZF6BFKWYuFcgwlTqCupidhjTjFYpMOs80rCPC9IV3TPJtm1pjPEoPEVcnNYEdURmTC5DPET0cTqAq1NseY0kVIXt75tXnk9FXj3dO6a759v7q-_tnffvtxeX921Voyytp0fDFABxnNtzF70g9cUfO_MnlOPhpdeGjeMmsFgvIW-s9aMPdds6KRl3a653XRd0if1lL9KOqhHR8oHpXMNdgJFhdsz29O-91yA7sZBSIZOYx2n0gNqfdi0sIg_FihVndKSI6avuOyp6Clj9DnqoFE0RJ9q1nYOxaor2Y_YJYnbrrn8RxQuB3PASoEP6P8L4Bvw0NeSwf_-DKPqYWTUNjIKR0Y9joySCHUbVDA4HiA_Z_wf6hfGd8fO</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2670470110</pqid></control><display><type>article</type><title>Tumor necrosis factor induced protein 3 gene polymorphism and the susceptibility to chronic primary immune thrombocytopenia in Egyptian children: a case-control study</title><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Springer Nature OA Free Journals</source><creator>El-hady, Marwa Abd ; Mosallam, Dalia S. ; Anis, Shahira K. ; Mansour, Basma S. ; Yassa, Marianne E.</creator><creatorcontrib>El-hady, Marwa Abd ; Mosallam, Dalia S. ; Anis, Shahira K. ; Mansour, Basma S. ; Yassa, Marianne E.</creatorcontrib><description>Background
Primary immune thrombocytopenia (PIT) is an acquired auto-immune disease characterized by decreased platelet count with increased bleeding tendency. The tumor necrosis factor associated induced protein-3 (TNFAIP3) codes for the ubiquitin-modifying enzyme that is indispensable for limiting inflammation. TNFAIP3 single-nucleotide polymorphisms (SNP) has been implicated in the susceptibility to multiple auto-immune diseases. We aimed to study the distribution of TNFAIP3 (
rs5029939 C>G
) SNP and the possible association of the studied polymorphism with the susceptibility to chronic PIT and the response to treatment in a sample of the Egyptian pediatric chronic PIT patients. This is a case-control study performed on 40 chronic PIT patients and 50 age- and gender-matched healthy controls. DNA samples from both groups were tested for TNFAIP3 (
rs5029939 C
>
G
) SNP using polymerase chain reaction-restriction fragment length polymorphism assay.
Results
TNFAIP3 (
rs5029939 C
>
G
) genotype distribution showed no statistically significant difference between PIT cases and controls [CC 77.5% vs. 82.5%, and CG 22% vs. 18%, respectively; OR (95% CI), 1.323 (0.470–0.723);
p
, 0.596]. The minor allele frequency (MAF) of
rs5029939
-
G
was comparable between the 2 groups (0.11 vs. 0.09) [OR (95% CI), 1.282 (0.484–3.397);
p
, 0.617]. No statistically significant difference was observed between chronic PIT patients carrying the mutant heterozygous genotype (CG) achieving complete response and those with no response [OR (95% CI), 1.667 (0.165-16.810);
p
> 0.05]. The MAF of
rs5029939
-
G
was comparable between both groups [OR (95% CI), 1.571 (0.175–14.111);
p
> 0.05].
Conclusion
This study showed no liability of patients carrying TNFAIP3 (
rs5029939 C
>
G
) polymorphism to develop chronic course of the disease or to achieve complete response to treatment. TNFAIP3 (
rs5029939 C < G
) SNP plays no role in either susceptibility to chronic PIT in the studied sample of Egyptian pediatric population or their response to treatment.</description><identifier>ISSN: 2090-2441</identifier><identifier>ISSN: 1110-8630</identifier><identifier>EISSN: 2090-2441</identifier><identifier>DOI: 10.1186/s43042-020-00129-6</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Autoimmune diseases ; China ; Diseases ; Egypt ; Enzymes ; Gene frequency ; Gene polymorphism ; Genetic aspects ; Genetic research ; Idiopathic thrombocytopenic purpura ; Immunological diseases ; Medical research ; Medicine ; Medicine & Public Health ; Medicine, Experimental ; Necrosis ; Patients ; PCR-RFLP and Egyptian children ; Pediatrics ; Polymorphism ; Primary immune thrombocytopenia (PIT) ; Restriction fragment length polymorphism ; rs5029939 C < G ; Single nucleotide polymorphisms ; Single-nucleotide polymorphism ; Statistical analysis ; Susceptibility ; Thrombocytopenia ; Tumor necrosis factor ; Tumor necrosis factor associated induced protein 3 (TNFAIP3) ; Tumor necrosis factor-TNF ; Ubiquitin</subject><ispartof>Egyptian Journal of Medical Human Genetics, 2021-02, Vol.22 (1), p.12-9, Article 12</ispartof><rights>The Author(s) 2021</rights><rights>COPYRIGHT 2021 Springer</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-3f8be04ebf2abb5478fa0ef7db520f8faf6f6bd89a1e8bfce73ccb972a1836c13</citedby><cites>FETCH-LOGICAL-c496t-3f8be04ebf2abb5478fa0ef7db520f8faf6f6bd89a1e8bfce73ccb972a1836c13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,27922,27923</link.rule.ids></links><search><creatorcontrib>El-hady, Marwa Abd</creatorcontrib><creatorcontrib>Mosallam, Dalia S.</creatorcontrib><creatorcontrib>Anis, Shahira K.</creatorcontrib><creatorcontrib>Mansour, Basma S.</creatorcontrib><creatorcontrib>Yassa, Marianne E.</creatorcontrib><title>Tumor necrosis factor induced protein 3 gene polymorphism and the susceptibility to chronic primary immune thrombocytopenia in Egyptian children: a case-control study</title><title>Egyptian Journal of Medical Human Genetics</title><addtitle>Egypt J Med Hum Genet</addtitle><description>Background
Primary immune thrombocytopenia (PIT) is an acquired auto-immune disease characterized by decreased platelet count with increased bleeding tendency. The tumor necrosis factor associated induced protein-3 (TNFAIP3) codes for the ubiquitin-modifying enzyme that is indispensable for limiting inflammation. TNFAIP3 single-nucleotide polymorphisms (SNP) has been implicated in the susceptibility to multiple auto-immune diseases. We aimed to study the distribution of TNFAIP3 (
rs5029939 C>G
) SNP and the possible association of the studied polymorphism with the susceptibility to chronic PIT and the response to treatment in a sample of the Egyptian pediatric chronic PIT patients. This is a case-control study performed on 40 chronic PIT patients and 50 age- and gender-matched healthy controls. DNA samples from both groups were tested for TNFAIP3 (
rs5029939 C
>
G
) SNP using polymerase chain reaction-restriction fragment length polymorphism assay.
Results
TNFAIP3 (
rs5029939 C
>
G
) genotype distribution showed no statistically significant difference between PIT cases and controls [CC 77.5% vs. 82.5%, and CG 22% vs. 18%, respectively; OR (95% CI), 1.323 (0.470–0.723);
p
, 0.596]. The minor allele frequency (MAF) of
rs5029939
-
G
was comparable between the 2 groups (0.11 vs. 0.09) [OR (95% CI), 1.282 (0.484–3.397);
p
, 0.617]. No statistically significant difference was observed between chronic PIT patients carrying the mutant heterozygous genotype (CG) achieving complete response and those with no response [OR (95% CI), 1.667 (0.165-16.810);
p
> 0.05]. The MAF of
rs5029939
-
G
was comparable between both groups [OR (95% CI), 1.571 (0.175–14.111);
p
> 0.05].
Conclusion
This study showed no liability of patients carrying TNFAIP3 (
rs5029939 C
>
G
) polymorphism to develop chronic course of the disease or to achieve complete response to treatment. TNFAIP3 (
rs5029939 C < G
) SNP plays no role in either susceptibility to chronic PIT in the studied sample of Egyptian pediatric population or their response to treatment.</description><subject>Autoimmune diseases</subject><subject>China</subject><subject>Diseases</subject><subject>Egypt</subject><subject>Enzymes</subject><subject>Gene frequency</subject><subject>Gene polymorphism</subject><subject>Genetic aspects</subject><subject>Genetic research</subject><subject>Idiopathic thrombocytopenic purpura</subject><subject>Immunological diseases</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Medicine, Experimental</subject><subject>Necrosis</subject><subject>Patients</subject><subject>PCR-RFLP and Egyptian children</subject><subject>Pediatrics</subject><subject>Polymorphism</subject><subject>Primary immune thrombocytopenia (PIT)</subject><subject>Restriction fragment length polymorphism</subject><subject>rs5029939 C < G</subject><subject>Single nucleotide polymorphisms</subject><subject>Single-nucleotide polymorphism</subject><subject>Statistical analysis</subject><subject>Susceptibility</subject><subject>Thrombocytopenia</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor associated induced protein 3 (TNFAIP3)</subject><subject>Tumor necrosis factor-TNF</subject><subject>Ubiquitin</subject><issn>2090-2441</issn><issn>1110-8630</issn><issn>2090-2441</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNp9ks1u1DAQxyMEEmXhBThZ4pxiO14n4VZVBSpV4lLOlj_Gu14l9mI7h7wQz8m0qShICFmyPaP5_T2emaZ5z-glY4P8WERHBW8ppy2ljI-tfNFccDrSlgvBXv5xf928KeVEqdx3vbhoft4vc8okgs2phEK8thXtEN1iwZFzThVCJB05QARyTtOK4edjKDPR0ZF6BFKWYuFcgwlTqCupidhjTjFYpMOs80rCPC9IV3TPJtm1pjPEoPEVcnNYEdURmTC5DPET0cTqAq1NseY0kVIXt75tXnk9FXj3dO6a759v7q-_tnffvtxeX921Voyytp0fDFABxnNtzF70g9cUfO_MnlOPhpdeGjeMmsFgvIW-s9aMPdds6KRl3a653XRd0if1lL9KOqhHR8oHpXMNdgJFhdsz29O-91yA7sZBSIZOYx2n0gNqfdi0sIg_FihVndKSI6avuOyp6Clj9DnqoFE0RJ9q1nYOxaor2Y_YJYnbrrn8RxQuB3PASoEP6P8L4Bvw0NeSwf_-DKPqYWTUNjIKR0Y9joySCHUbVDA4HiA_Z_wf6hfGd8fO</recordid><startdate>20210208</startdate><enddate>20210208</enddate><creator>El-hady, Marwa Abd</creator><creator>Mosallam, Dalia S.</creator><creator>Anis, Shahira K.</creator><creator>Mansour, Basma S.</creator><creator>Yassa, Marianne E.</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</general><general>SpringerOpen</general><scope>C6C</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>DOA</scope></search><sort><creationdate>20210208</creationdate><title>Tumor necrosis factor induced protein 3 gene polymorphism and the susceptibility to chronic primary immune thrombocytopenia in Egyptian children: a case-control study</title><author>El-hady, Marwa Abd ; Mosallam, Dalia S. ; Anis, Shahira K. ; Mansour, Basma S. ; Yassa, Marianne E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-3f8be04ebf2abb5478fa0ef7db520f8faf6f6bd89a1e8bfce73ccb972a1836c13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Autoimmune diseases</topic><topic>China</topic><topic>Diseases</topic><topic>Egypt</topic><topic>Enzymes</topic><topic>Gene frequency</topic><topic>Gene polymorphism</topic><topic>Genetic aspects</topic><topic>Genetic research</topic><topic>Idiopathic thrombocytopenic purpura</topic><topic>Immunological diseases</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Medicine, Experimental</topic><topic>Necrosis</topic><topic>Patients</topic><topic>PCR-RFLP and Egyptian children</topic><topic>Pediatrics</topic><topic>Polymorphism</topic><topic>Primary immune thrombocytopenia (PIT)</topic><topic>Restriction fragment length polymorphism</topic><topic>rs5029939 C < G</topic><topic>Single nucleotide polymorphisms</topic><topic>Single-nucleotide polymorphism</topic><topic>Statistical analysis</topic><topic>Susceptibility</topic><topic>Thrombocytopenia</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor associated induced protein 3 (TNFAIP3)</topic><topic>Tumor necrosis factor-TNF</topic><topic>Ubiquitin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>El-hady, Marwa Abd</creatorcontrib><creatorcontrib>Mosallam, Dalia S.</creatorcontrib><creatorcontrib>Anis, Shahira K.</creatorcontrib><creatorcontrib>Mansour, Basma S.</creatorcontrib><creatorcontrib>Yassa, Marianne E.</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Egyptian Journal of Medical Human Genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>El-hady, Marwa Abd</au><au>Mosallam, Dalia S.</au><au>Anis, Shahira K.</au><au>Mansour, Basma S.</au><au>Yassa, Marianne E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor necrosis factor induced protein 3 gene polymorphism and the susceptibility to chronic primary immune thrombocytopenia in Egyptian children: a case-control study</atitle><jtitle>Egyptian Journal of Medical Human Genetics</jtitle><stitle>Egypt J Med Hum Genet</stitle><date>2021-02-08</date><risdate>2021</risdate><volume>22</volume><issue>1</issue><spage>12</spage><epage>9</epage><pages>12-9</pages><artnum>12</artnum><issn>2090-2441</issn><issn>1110-8630</issn><eissn>2090-2441</eissn><abstract>Background
Primary immune thrombocytopenia (PIT) is an acquired auto-immune disease characterized by decreased platelet count with increased bleeding tendency. The tumor necrosis factor associated induced protein-3 (TNFAIP3) codes for the ubiquitin-modifying enzyme that is indispensable for limiting inflammation. TNFAIP3 single-nucleotide polymorphisms (SNP) has been implicated in the susceptibility to multiple auto-immune diseases. We aimed to study the distribution of TNFAIP3 (
rs5029939 C>G
) SNP and the possible association of the studied polymorphism with the susceptibility to chronic PIT and the response to treatment in a sample of the Egyptian pediatric chronic PIT patients. This is a case-control study performed on 40 chronic PIT patients and 50 age- and gender-matched healthy controls. DNA samples from both groups were tested for TNFAIP3 (
rs5029939 C
>
G
) SNP using polymerase chain reaction-restriction fragment length polymorphism assay.
Results
TNFAIP3 (
rs5029939 C
>
G
) genotype distribution showed no statistically significant difference between PIT cases and controls [CC 77.5% vs. 82.5%, and CG 22% vs. 18%, respectively; OR (95% CI), 1.323 (0.470–0.723);
p
, 0.596]. The minor allele frequency (MAF) of
rs5029939
-
G
was comparable between the 2 groups (0.11 vs. 0.09) [OR (95% CI), 1.282 (0.484–3.397);
p
, 0.617]. No statistically significant difference was observed between chronic PIT patients carrying the mutant heterozygous genotype (CG) achieving complete response and those with no response [OR (95% CI), 1.667 (0.165-16.810);
p
> 0.05]. The MAF of
rs5029939
-
G
was comparable between both groups [OR (95% CI), 1.571 (0.175–14.111);
p
> 0.05].
Conclusion
This study showed no liability of patients carrying TNFAIP3 (
rs5029939 C
>
G
) polymorphism to develop chronic course of the disease or to achieve complete response to treatment. TNFAIP3 (
rs5029939 C < G
) SNP plays no role in either susceptibility to chronic PIT in the studied sample of Egyptian pediatric population or their response to treatment.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><doi>10.1186/s43042-020-00129-6</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2090-2441 |
| ispartof | Egyptian Journal of Medical Human Genetics, 2021-02, Vol.22 (1), p.12-9, Article 12 |
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| language | eng |
| recordid | cdi_proquest_journals_2670470110 |
| source | DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature OA Free Journals |
| subjects | Autoimmune diseases China Diseases Egypt Enzymes Gene frequency Gene polymorphism Genetic aspects Genetic research Idiopathic thrombocytopenic purpura Immunological diseases Medical research Medicine Medicine & Public Health Medicine, Experimental Necrosis Patients PCR-RFLP and Egyptian children Pediatrics Polymorphism Primary immune thrombocytopenia (PIT) Restriction fragment length polymorphism rs5029939 C < G Single nucleotide polymorphisms Single-nucleotide polymorphism Statistical analysis Susceptibility Thrombocytopenia Tumor necrosis factor Tumor necrosis factor associated induced protein 3 (TNFAIP3) Tumor necrosis factor-TNF Ubiquitin |
| title | Tumor necrosis factor induced protein 3 gene polymorphism and the susceptibility to chronic primary immune thrombocytopenia in Egyptian children: a case-control study |
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