1

Qadah T, Finlayson J, Ghassemifar R: In vitro characterization of the α-thalassemia point mutation HBA2:c.95+1G>A (α2IVS1-1(G>A)). Hemoglobin, 2012, 36(1):38–46.

http://www.ncbi.nlm.nih.gov/pubmed/21967524

2

Qadah T, Finlayson J, Newbound C, Pell N, Jennens M, Holmes P, Grey D, Beilby J, Ghassemifar R.: A molecular tool to assess the pathological relevance of alpha-globin DNA variants. Pathology. 2012, 44(4):337-341.

http://www.ncbi.nlm.nih.gov/pubmed/22531344

3

Qadah T, Finlayson J, Newbound C, Pell N, Pascoe M, Greenwood L, Holmes P, Grey D, Beilby J, Ghassemifar R: Molecular and cellular characterization of a new α-thalassemia mutation (HBA2:c.94A>C) generating an alternative splice site and a premature stop codon. Hemoglobin. 2012, 36(3):244-52.

http://www.ncbi.nlm.nih.gov/pubmed/22524210

4

Ghassemifar R, Forster L, Qadah T, Finlayson J: Identification and Characterization of Two Novel and Differentially Expressed Isoforms of Human α2- and α1-Globin Genes. Hemoglobin. 2012, 36(3): p. 244-252.

http://www.ncbi.nlm.nih.gov/pubmed/22738435

5

Qadah T, Finlayson J, Dennis M, Ghassemifar R. Molecular and cellular analysis of three novel α2-globin gene promoter mutations [HBA2:c.-59C>T], [HBA2:c.-81C>A] and [HBA2:c.-91G>A] reveal varying patterns of transcriptional and translational activities. Pathology. 2014, 46(1):46-52.

http://www.ncbi.nlm.nih.gov/pubmed/24300714

6

Qadah T, Joly P, Finlayson J, Ghassemifar R Molecular and cellular analysis of a novel α2-globin mutation [HBA2:c.94A>G] shows activation of a cryptic splice site and generation of a premature termination codon. Hemoglobin. 2014, 38(1):13-8

http://www.ncbi.nlm.nih.gov/pubmed/24274170

7

Qadah T, Finlayson J, Emma N, Ghassemifar R: Molecular characterization of Hb Hamilton Hill (HBA2:c.388delC), a novel HBA2 variant generating a premature termination codon and truncated HBA2 chain. Hemoglobin, 2015; 39(2):88-94.

http://www.ncbi.nlm.nih.gov/pubmed/25791745

8

Qadah T, Finlayson J, Newbound C, Ghassemifar R: Experimental characterization of Hb Flurlingen (HBA2:c.177C>G,p.His>Gln) and Hb Boghé (HBA2:c.177C>A,p.His>Gln), reveals contradictory HBA2 expression and translation patterns despite identical amino acid substitutions.

Hemoglobin, 2015; 39(5):340-5.

https://www.ncbi.nlm.nih.gov/pubmed/26193975

9

Forster L, Ardakani RM, Qadah T, Finlayson J, Ghassemifar R: The effect of nonsense mediated decay on transcriptional activity within the novel β-thalassaemia mutation Hemoglobin Yala (HBB:c.129delT).

Hemoglobin, 2015;39(5):334-9.

https://www.ncbi.nlm.nih.gov/pubmed/26207313

10

Khojah A, Faidah H, Sami I, Qadah T: The Effect of Fetal Hemoglobin on RBC Parameters among Sickle Cell Anemia Patients: A Cross Sectional Study from Makkah City; Western Saudi Arabia.

Hematol Transfus Int J, 2016; 3(1): 00059. DOI: 10.15406/htij.2016.03.00059

http://medcraveonline.com/HTIJ/HTIJ-03-00059.php

1

Holmes P, Finlayson J, Ghassemifar R, Qadah T, Grey D, Figliomeni L, Newbound C, Pell N , Kersten M, Jennens M, Macaulay C, Greenwood L, Beilby J: Laboratory Diagnosis of a Beta Thalassemia Trait (HBB:c-78A>G) Masked by a Coexisting Alpha Globin Variant Hb Hekinan (HBA1:c.84G>T). HAA2010 conference, Poster no. 093. Auckland, New Zealand.

2

Qadah T, Finlayson J, Newbound C, Pell N, Jennens M, Holmes P, Ghassemifar R: A novel point mutation of alpha1 globin gene (IVSII-147 [HBA1:c.301-3 C>G]) causing mild alpha thalassemia phenotype. HAA2011 conference, Poster no. 238. Sydney, Australia.

http://www.ishapd.org/2011/volume1.pdf

3

Qadah T, Finlayson J, Ghassemifar R: Investigation of the impact of point mutations in the transcription initiation site of the alpha-1 globin gene. F1000 Posters 2011, 2:1792 (HAA2011 conference, Poster no. 239. Sydney, Australia).

http://f1000.com/posters/browse/summary/1089560

4

Qadah T, Finlayson J, Dennis M, Ghassemifar R: Molecular analysis of two novel HBA2 promoter point mutations causing down regulation of HBA2 Transcripts. F1000 Posters 2012, 3:1531 (HAA2012 conference, Poster no. 226. Melbourne, Australia)

http://f1000.com/posters/browse/summary/1092755

5

Forster L, Viprakasit V, Chinchang W, Riolueang S, Qadah T, Finlayson J, Ghassemifar R: In vitro analysis of the [HBB:c.129delT] beta thalassemia mutation (Haemoglobin Yala). HAA2012 conference, Poster no. 268. Melbourne, Australia.

http://www.fcconventions.com.au/HAA2012/p08.pdf

6

Ghassemifar R, Dennis M, Qadah T, Finlayson J. Experimental characterization of transcriptional activator and suppressor elements sites within the α-globin core and proximal promoter region.

Thalassemia International Federation congress, 2013, Abstract no. 204, Abo Dhabi, UAE

7

Ghassemifar R, Dennis M, Qadah T, Finlayson J. Experimental insertion of a 2nd TATA binding protein site at the position 73 prior to the translation initiation site significantly compensates the activity loss of the endogenous HBA2 TATA binding protein site.

Thalassemia International Federation congress, 2013, Abstract no. 209, Abo Dhabi, UAE

8

Talal Qadah, Reza Ghassemifar, Jill Finlayson. An in vitro model to investigate the pathologic significance of novel mutations in the alpha globin genes.
XXVIIth International Symposium on Technological Innovations in Laboratory Hematology 2014, Oral Abstract, The Hague, Netherlands, May 15-17, 3014

9

Khoja A & Qadah T. Effect of fetal hemoglobin (HbF) on the hematological parameters of sickle cell anemia patients from Makkah city, Saudi Arabia.

Accepted - HAA2016 conference, Ref. no. 321. Melbourne, Australia