Zgheib et al. 2013 studied the association of xenobiotic metabolizing genes and breast cancer risk by calculating the frequency of CYP2E1*5B (rs3813867 and rs2031920), CYP2E1*6 (rs6413432), NAT2*5 (rs1799929), NAT2*6 (rs1799930), GSTP1 6624 A>G (rs1695), GSTM1 215bp deletion, and GSTT1 480bp deletion in 227 breast cancer patients of Lebanese origin. The control group included in the study consisted of 99 unrelated women without breast cancer. No significant statistical differences were observed in the variant distribution of xenobiotic metabolizing genes between cases and controls.

Salem et al. 2011 investigated the GSTM1 and GSTT1 genotype frequencies in Bahraini, Lebanese, and Tunisian Arabs using multiplex PCR-based methods. GSTM1 and GSTT1 wild or null genotypes were determined in 167 Bahraini, 141 Lebanese, and 186 Tunisian subjects by identifying the presence of specific DNA bands on 1.5% agarose gel. Comparable GSTM1 null genotype frequencies were observed among Bahraini (49.7%) and Lebanese (52.5%) subjects. Tunisians had a slightly higher frequency of GSTM1 null genotype (63.4%). GSTT1 null genotype frequency among Bahraini subjects (28.7% ) were observed to be lower compared to that of Lebanese (37.6%) and Tunisians (37.1%) subjects. Statistically significant difference in frequencies noted in this study while comparing Bahraini and Tunisian GSTM1 null genotypes was attributed to the ethnic diversity observed in those populations.

Al-Moundhri et al. (2009) carried out a molecular study on the combined analysis of polymorphisms GSTM1/G1 and IL-1B/IL-1RN genes in gastric adenocarcinoma. A total of 107 control subjects and 107 gastric cancer patients were included in this study. Al-Moundhri et al. (2009) did not find any statistically significant associations between the GSTM1/G1 or IL-1B-31 genes and gastric cancer risk. However, they found a statistical association between the presence of the IL-1RN*2 allele and gastric cancer (odds ratio 2.2, 95% confidence interval=1.2-3.7, P=0.01). Combined analysis showed that a combination of the null GSTM1 genotype and carriers of IL-1RN*2 was associated with a statistically significant correlation with gastric cancer (odds ratio=3.6, 95% confidence interval=1.4-9.4, P=0.008). Al-Moundhri et al. (2009) suggested that the individual variation in both the antioxidative property of GSTM1 and the cellular inflammatory modulator IL-1RN may predispose individuals to an increased risk of gastric cancer.

In Saudi Arabia, Evans et al. (1996) determined the frequency of GSTM1 gene deletion within a group of healthy Saudis (804 men) and within another group of Saudi patients with coronary atherosclerosis (88 males and 2 females).  The mean age for the first group was 27.4 _SD 6.4 years, while the mean age for the second group was 56.4 _SD 12.1 years.  The GSTM1 null phenotype was detected in 56% of the individuals from the healthy group and in 63% of patient group.  This study found the difference between the two groups to be statistically insignificant; therefore having low enzymatic activity does not count as a predisposing factor for coronary atherosclerosis according to this study.

McLellan et al. (1997) found that two Saudi individuals with ultrarapid GSTM1 enzyme activity were heterozygous for a tandem GSTM1 gene duplication; thus, they carried three GSTM1 genes.  They suggested that the duplication was generated as the reciprocal product of the homologous unequal crossing-over event that produces the null allele.

Bu et al. (2004) studied the frequencies of alleles and genotypes for CYP1A1, NAT2, GSTs, MTHFR, MTR (MS), and NQO*1 genes among Arabs.  Of the studied group, 95% were from Saudi Arabia, and 5% were from Jordan, Syria, Lebanon, and Yemen.  The mean age was 37 years, and male to female ratio was (25:1).  The frequencies of the null genotypes for the GSTT1 and GSTM1 genes were 25% and 55%, respectively.  The frequency of the 1578G allele was 40% and that of the 2293T allele was 13% in Arabs.

Using multiplex polymerase chain reaction, Abu-Amero et al. (2006) examined the association between GSTT1 and GSTM1 deletion and coronary artery disease among smokers.  A total of 1054 Saudi CAD patients and 762 Saudi controls were genotyped.  A significant association was found between the T null M null, T null M mild, and T mild M null genotypes with CAD independent of smoking interaction.  In CAD patients 30% had the T wild M wild genotype, 27% had the T wild M null genotype, 8% had the T null M wild genotype, and 36% had the T null M null genotype.  Also smoking, age, hypercholesterolemia and hypertriglyceridemia, diabetes mellitus, family history of CAD, hypertension, and obesity where all associated with CAD.  Few years later, Abu-Amero et al. (2009) investigated the prevalence of GSTM1 and GSTT1 deletion genotypes in spontaneous optic neuropathies.  A total of 108 Saudi patients with optic neuropathies and 120 control individuals, also Saudis, were included in the study.  All three GST deletion phenotypes (T0M1, T1M0, and T0M0) were found to be significantly more prevalent among the patient group than the control.  In addition, at least one deletion genotype was significantly greater for each type of spontaneous optic neuropathy.  Abu-Amero et al. (2009) suggested that GST deletion phenotypes may be involved in the pathogenesis of these optic neuropathies by way of the role that GST plays in detoxifying endogenous compounds and in inactivating endogenous end products formed during oxidative stress.

Khabaz et al. (2016) analyzed the association between GSTM1 gene polymorphism and colorectal cancer.  DNA was obtained from the tissue samples of 83 colorectal cancer patients and 35 healthy controls.  Subsequently, PCR and gene sequencing assays were carried out.  It was found that 83% of the colorectal cancer cases carried the null genotype (GSTM1*0/*0) while the remaining 17% were either the GSTM1wt/wt or GSTM1wt/*0 genotypes.  In comparison, only 65% of the controls carried the null genotype.  The authors found a statistically significant association between the GSTM1 null genotype and the risk of colorectal cancer in Saudi patients [p=0.03706, OR=2.57 (1.04-6.35)].  

Al-Achkar et al. (2014) we investigated the associations of polymorphisms in the cytochrome P450 gene (CYP1A1) and the glutathione S-transferase genes (GSTM1 and GSTT1) with chronic myelogenous leukemia (CML).  A total of 126 patients with CML and 172 healthy volunteers were genotyped.  Logistic regression analyses showed significant risk of CML associated with CYP1A1 Val allele [odds ratio (OR) 3.3, 95% confidence intervals (CI) 1.96-5.53], (p < 0.0001) while CYP1A1 Val/Val homozygotes were observed only in the CML patients.  There was statistically significant difference in the frequency of GSTM1 and GSTT1 null genotypes.  The GSTT1-null genotype was slightly higher in 27% of CML cases and 17% of controls (OR 1.98, 95% CI 1.12-3.5) (p < 0.020).  The GSTM1 null was higher in 43% of CML cases and 23% of controls (OR 2.55, 95% CI 1.54-4.22) (p < 0.00024).  Individuals carrying the CYP1A1 Ile/Val (AG) and GSTM1 null genotype have 9.9 times higher risk to be CML than those carrying CYP1A1 Ile/Ile (AA) and GSTM1 present genotype (OR 9.9, 95% CI 2.7-36.3) (p < 0.0001).  Al-Achkar et al. (2014) concluded that the association of the GSTM1 null genotype, either alone or in combination with GSTT1 null, with CYP1AI heterozygous leads to the CML risk.

Khedhaier et al. (2003) did not find direct correlation between GSTM1 gene deletion and the breast carcinoma onset in Tunisians through investigating the susceptibility and prognostic implications of the GSTM1 and GSTT1 gene deletions in 309 unrelated Tunisian patients with breast carcinoma and 242 healthy control subjects. However, an increase in the disease-free survival (DFS) was seen for patients carrying both gene deletions for GSTT1 and GSTM1.

In order to test the hypothesis that genetic polymorphism of glutathione S-transferase mu 1 (GSTM1) and/or S-transferase theta 1 (GSTT1) are associated with chronic obstructive pulmonary disease (COPD) in smokers, Faramawy et al. (2009) carried out a case-control study on 34 patients with COPD and 34 matched controls. Results indicated a carrier frequency of null GSTM1 genotype to be 52.9% among cases compared to 26.5% in controls. Carriers of null GSTM1 were found to be at much higher risk of developing COPD (OR, 3.13; 95% CI, 1.1-8.6). In case of GSTT1, the frequency of carriers of null GSTT1 genotype was found to be 50% among cases compared to 44.1% in the control group. Carriers of null GSTT1 were found to be at minor risk of developing COPD when compared with carriers of the wild GSTT1 genotype (OR, 1.3; 95% CI, 0.5-3.3). Furthermore, Faramawy et al. (2009) found that the risk of developing COPD was increased among carrier of null GSTT1 and GSTM1 haplotype (OR, 3.6; 95% CI, 1.1-11.6). Faramawy et al. (2009) concluded that carriers of null GSTM1 genotype were at high risk of developing COPD especially when they were null GSTT1 and GSTM1 haplotype.

Hussain et al. (2012) compared the frequency of GSTM1 gene deletion between 30 hypertensive patients (30 patients) and non-hypertensive individuals (33 controls). This study found no significant association between the null GSTM1 genotype and hypertension, and, therefore, concluded that null GSTM1 was not a significant risk factor for hypertension.