Fouad Al‐Dayel

King Faisal Specialist Hospital & Research Centre

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Khawla S. Al‐Kuraya

King Faisal Specialist Hospital & Research Centre

224

Abdul K. Siraj

King Faisal Specialist Hospital & Research Centre

160

Sandeep Kumar Parvathareddy

King Faisal Specialist Hospital & Research Centre

Shahab Uddin

Qatar University

Rong Bu

King Faisal Specialist Hospital & Research Centre

Prashant Bavi

Ontario Institute for Cancer Research

Nasser Al‐Sanea

Princess Nourah bint Abdulrahman University

Maqbool Ahmed

Jinnah Postgraduate Medical Center

Luai H. Ashari

King Faisal Specialist Hospital & Research Centre

Alaa Abduljabbar

King Faisal Specialist Hospital & Research Centre

Cooperative Institutions

King Faisal Specialist Hospital & Research Centre

333

Alfaisal University

King Saud University

National Guard Health Affairs

King Abdulaziz Medical City

King Saud bin Abdulaziz University for Health Sciences

Universität Hamburg

University Medical Center Hamburg-Eppendorf

The University of Texas MD Anderson Cancer Center

King Abdullah International Medical Research Center

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Prognostic significance of DNMT3A alterations in Middle Eastern papillary thyroid carcinoma

European Journal of Cancer (2019)

Abdul K. Siraj Poyil Pratheeshkumar Sandeep Kumar Parvathareddy Rong Bu Tariq Masoodi

DNA methyltransferase

10.1016/j.ejca.2019.05.025

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Citations (17)

FISH analysis in chromophobe renal‐cell carcinoma

Diagnostic Cytopathology (2000)

M. Anwar Iqbal Mohammed Akhtar Cheryl Ulmer Fouad Al‐Dayel Malcolm C. Paterson

Loss of chromosomes 1, 2, 6, 10, 13, 17, and 21 is a characteristic finding in chromophobe renal-cell carcinoma (ChRCC). Previously, cytogenetic and molecular genetic techniques were used in demonstrating the chromosomal monosomies in ChRCCs. We performed interphase fluorescent in situ hybridization (FISH) using centromeric probes for chromosomes 1, 2, 6, and 10 on touch imprint smears from six histologically proven ChRCCs. All six ChRCC tumors showed one FISH signal corresponding to one copy number for each of these chromosomes. The percent cells with one FISH signal ranged from 48–88% (chromosome 1), 36–89% (chromosome 2), 26–98% (chromosome 6), and 64–99% (chromosome 10). In addition, 3 of the 6 cases were further studied with centromeric probes for chromosomes 13, 17, and 21. All three revealed monosomy of these three chromosomes. We conclude that interphase FISH performed on touch imprint smears is a relatively simple, rapid, and reliable method for detecting chromosome abnormalities which are specific for ChRCCs. Diagn. Cytopathol. 2000;22:3–6. © 2000 Wiley-Liss, Inc.

Monosomy

Chromophobe cell

Interphase

Chromosome 9

Chromosome 3

10.1002/(sici)1097-0339(200001)22:1<3::aid-dc2>3.3.co;2-s

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Colorectal carcinoma from Saudi Arabia. Analysis of MLH-1, MSH-2 and p53 genes by immunohistochemistry and tissue microarray analysis.

PubMed (2006)

Khawla S. Al‐Kuraya Prashant Bavi Adnan Ezzat Fouad Al‐Dayel Shahab Uddin

To document the incidence and role of p53 and DNA mismatch repair proteins in colorectal carcinomas, and to evaluate the relative frequency of major molecular pathways in colorectal cancers from Saudi Arabia.We collected the formalin fixed, paraffin embedded tissues from 154 colorectal tumors (83 patients from King Faisal Specialist Hospital and Research Centre and 71 from Saudi Aramco Dhahran Health Centre) between January 1989 and December 2003. We analyzed the p53 and mismatch repair gene expression (hMSH-2, hMLH-1) by immunohistochemistry in tissue microarray format.Expression loss of at least one mismatch repair gene was found in 33.8% of cases and significantly associated with the right-sided tumor location (p=0.0047). The p53 positivity was observed in 57.5% of tumors, and was inversely linked to expression loss of mismatch repair genes (p=0.0102).The strong confirmation of the previously established associations between tumor phenotype, and mismatch repair gene alteration provided strong evidence for the validity of our experimental approach. Together with the higher incidence of right sided location in Saudi (46.6%) than in Western colon cancers (34.9%), the observed high prevalence of mismatch gene expression loss in Saudi tumors argues for a higher importance of microsatellite instability in this population. If confirmed, it will be interesting to see whether an increased level of familial or sporadic microsatellite instability cases is causing this variation.

Microsatellite Instability

Tissue microarray

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Citations (15)

Prevalence, spectrum, and founder effect of BRCA1 and BRCA2 mutations in epithelial ovarian cancer from the Middle East

Human Mutation (2019)

Abdul K. Siraj Rong Bu Kaleem Iqbal Nabil Siraj Wael Al‐Haqawi

Germline mutations in breast cancer susceptibility gene 1 and 2 have previously been estimated to contribute to 13-18% of all epithelial ovarian cancer (EOC). To characterize the prevalence and effect of BRCA1 and BRCA2 mutations in Middle Eastern EOC patients, BRCA mutation screening was performed in 407 unselected ovarian cancer patients using targeted capture and/or Sanger sequencing. A total of 19 different pathogenic variants (PVs) were identified in 50 (12.3%) women. Nine PVs were recurrent accounting for 80% of cases with PVs (40/50) in the entire cohort. Founder mutation analysis revealed only two mutations (c.4136_4137delCT and c.1140dupG) sharing the same haplotypes thus representing founder mutations in the Middle Eastern population. Identification of the mutation spectrum, prevalence, and founder effect in Middle Eastern population facilitates genetic counseling, risk assessment, and development of a cost-effective screening strategy.

Founder effect

BRCA2 Protein

10.1002/humu.23736

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Citations (14)

Supplementary Figure 2 from Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer

Shahab Uddin Maqbool Ahmed Prashant Bavi Raafat El-Sayed Nasser Al‐Sanea

Supplementary Figure 2 from Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer

Degradation

10.1158/0008-5472.22375167.v1

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Data from Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer

Shahab Uddin Maqbool Ahmed Prashant Bavi Raafat El-Sayed Nasser Al‐Sanea

<div>Abstract<p>S-phase kinase protein 2 (SKP2), an F-box protein, targets cell cycle regulators including cycle-dependent kinase inhibitor p27Kip1 via ubiquitin-mediated degradation. SKP2 is frequently overexpressed in a variety of cancers. We investigated the role of SKP2 and its ubiquitin-proteasome pathway in colorectal carcinoma using a panel of cell lines, clinical samples, and the NUDE mouse model. Using immunohistochemical analysis on a large tissue microarray of 448 samples, an inverse association of SKP2 expression with p27Kip1 protein levels was seen. A colorectal cancer (CRC) subset with high level of SKP2 and low level of p27Kip1 showed a decreased overall survival (<i>P</i> = 0.0057). Treatment of CRC cell lines with bortezomib or expression of small interfering RNA of SKP2 causes down-regulation of SKP2 and accumulation of p27Kip1. Furthermore, treatment of CRC cells with bortezomib causes apoptosis by involving the mitochondrial pathway and activation of caspases. In addition, treatment of CRC cells with bortezomib down-regulated the expression of XIAP, cIAP1, and survivin. Finally, treatment of CRC cell line xenografts with bortezomib resulted in growth inhibition of tumors in NUDE mice via down-regulation of SKP2 and accumulation of p27Kip1. Altogether, our results suggest that SKP2 and the ubiquitin-proteasome pathway may be potential targets for therapeutic intervention for treatment of CRC. [Cancer Res 2008;68(9):3379–88]</p></div>

Survivin

SKP2

XIAP

Protein Degradation

Tissue microarray

10.1158/0008-5472.c.6497727

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Congenital acinar dysplasia. Familial cause of a fatal respiratory failure in a neonate.

PubMed (2003)

Kefah A. Al-Senan Abdulhakiem Kattan Fouad Al‐Dayel

Pulmonary hypoplasia is a rare cause of pulmonary insufficiency, and has a significant rate of morbidity and mortality among affected infants. In most cases, pulmonary hypoplasia is secondary to underlying abnormalities. These may include space occupying lesions, as in infants with congenital diaphragmatic hernia; malformation of chest wall resulting in a small thoracic cavity; severe and prolonged oligohydramnios; and neuromuscular disorders, which prevent normal fetal chest expansion. All lead to poor lung development. Primary pulmonary hypoplasia as a result of congenital acinar dysplasia is exceedingly rare and is diagnosed by exclusion of all known etiologies of secondary pulmonary hypoplasia.

Pulmonary Hypoplasia

Etiology

Bronchopulmonary Dysplasia

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Citations (9)

High Prevalence of Fatty Acid Synthase Expression in Colorectal Cancers in Middle Eastern Patients and Its Potential Role as a Therapeutic Target

The American Journal of Gastroenterology (2009)

Shahab Uddin Azhar R. Hussain Maqbool Ahmed Jehad Abubaker Nasser Al‐Sanea

OBJECTIVES: Many human epithelial cancers, particularly those with a poor prognosis, express high levels of fatty acid synthase (FASN), a key metabolic enzyme linked to synthesis of membrane phospholipids in cancer cells. Overexpression of FASN is linked with activation of the phosphatidylinositol-3′-kinase (PI3 K)/AKT pathway. However, the role of FASN in colorectal cancer (CRC) has not been fully elucidated. We investigated the expression of FASN and determined its functional association with the PI3/AKT pathway in CRC. METHODS: Expression of FASN and its associated targets were studied by immunohistochemistry on 448 CRC tumors in a tissue microarray (TMA) format. Analysis of apoptosis and cell cycle was evaluatedin vitrousing CRC cell lines by flow cytometry and DNA fragmentation assays. Protein expression was determined by immunohistochemistry and western blotting.In vivoxenograft studies were performed using CRC cell lines and NUDE mice. RESULTS: Correlation of FASN with various clinicopathological parameters on 448 CRC samples was assessed. Activated AKT was found in 294/409 (71.9%) of CRC and was associated with FASN overexpression. FASN expression was observed in 27.1% (109/403) of Middle Eastern CRC. Additionally, FASN expression was significantly more common in tumors characterized by microsatellite instability (MSI) than in those characterized by microsatellite stability (MSS) (P< 0.01). Ourin vitrodata using HCT-15, an MSI CRC cell line, showed a better apoptotic response after inhibition of FASN activity as compared with Colo-320, an MSS CRC cell line. Finally, treatment of HCT-15 cell line xenografts with C-75 resulted in growth inhibition of tumors in NUDE mice via downregulation of FASN and AKT activity. CONCLUSIONS: These data identify FASN as a potential biomarker and a novel therapeutic target in distinct molecular subtypes of CRC.

Tissue microarray

10.1038/ajg.2009.230

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Citations (42)

Epstein – Barr virus infection is not the sole cause of high prevalence for Hodgkin's lymphoma in Saudi Arabia

Leukemia & lymphoma/Leukemia and lymphoma (2006)

Khawla S. Al‐Kuraya Rajeswari Narayanappa Fouad Al‐Dayel Hassan El‐Solh Adnan Ezzat

The age-adjusted incidence of Hodgkin's lymphoma (HL) is markedly higher in Saudi Arabia than in the USA, and accounts for 10.5% of all neoplasias in children aged 15 years or older in Saudi Arabia. Epstein-Barr virus (EBV) infection has been suspected to cause high HL incidence in developing countries. To investigate the role of EBV for the high frequency of HL in Saudi Arabia, we analysed 169 HLs from Saudi Arabia and 30 HLs from Europe for EBV infection by in situ hybridization with fluorescence in-conjugated EBV on tissue microarray sections. All Saudi Arabian and European HLs were analysed in one experiment under identical conditions. Unexpectedly, our data show only minor, insignificant differences in EBV infection rates between Saudi Arabian (42 out of 147 informative cases 28.6%) and European HL (nine out of 30 informative cases; 30%; P = 0.8752). Within the Saudi Arabian population, EBV infection was most frequently seen in mixed cellularity HL (52.4%). This was significantly more frequent than in nodular sclerosing HL (26.1%; P = 0.0236). EBV positivity was unrelated to patient prognosis. In conclusion, our data strongly suggest that EBV is not the main cause for the high prevalence of HL in Saudi Arabia. This would be consistent with a major role of genetic susceptibility genes for HL in these populations. The Saudi Arabian population, with high consanguinity and large families, would prove ideal for identifying HL susceptibility genes.

Epstein–Barr virus infection

10.1080/10428190500286879

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Citations (18)

MOESM1 of Germline POLE and POLD1 proofreading domain mutations in endometrial carcinoma from Middle Eastern region

Figshare (2019)

Abdul K. Siraj Sandeep Kumar Parvathareddy Rong Bu Kaleem Iqbal Sarah Siraj

Additional file 1: Table S1. Functional analysis of POLE and POLD1 genes using Gene Ontology (GO).

Proofreading

10.6084/m9.figshare.11358257

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