Al-Moundhri et al. (2005) determined the prognostic effect of tumor suppressor proteins in Arab patients diagnosed with gastric carcinoma and studied the association of their expression with the clinico-pathological features. WAF1 expression was determined in 121 paraffin-embedded tumor blocks prepared from patients diagnosed with gastric cancer (mean age was 60.2 years, with 68.6% of the tumors being deeply penetrating T3 and T4 and 71% of the patients had advanced stages III and IV) in the period of 1995 to 2002 by immunohistochemical staining using monoclonal antibodies. Over-expression of p21, considered if more than 10% of the tumor cells showed nuclear staining, was found in 8.3% of the samples. A significant association was detected between p21 waf1 and p27 kip1, and its over-expression inversely correlated with T-stage.

A study was undertaken by Shi et al. (1996) to understand whether p21/Waf1 is involved in thyroid carcinogenesis in Saudi Arabia. Specimens from 57 thyroid tumors were used to look for deletions or point mutations in the p21 cDNA. Three different deletion mutations were found by electrophoretic analysis; a 450 bp deletion (nt.-5 to 445) starting from the initiation codon, a 388 bp deletion (nt.45-432) in three papillary carcinoma samples, and a 349 bp deletion (nt.93-441) in a papillary carcinoma. The latter two deletions resulted in a frameshift and a truncated protein, while the former deletion caused a complete blockage of protein synthesis. These deletions could not be detected in the genomic DNA, indicating a role for abnormal RNA splicing. SSCP analysis of the remaining samples revealed a SNP at codon 31 (AGC to AGA) in all the samples. Since all the deletions encompassed the second exon, an analysis of this exon as well as the exon-intron boundary was initiated. However, this exercise failed to reveal any mutation, apart from a point mutation 16-bp downstream from the splice donor site of the second intron in three out of the five samples. It was not clear whether this mutation played any role in the aberrant RNA splicing.

Al-Hadyan et al. (2012) studied the association between the p21 variant C31A and the risk of head and neck carcinoma.  Blood samples were obtained from 156 Saudi individuals affected with head and neck cancer as well as 251 healthy Saudi controls.  DNA was extracted and amplified.  The SNP was genotyped by direct sequencing.  The variant C31A of the CDK1A gene was found to have a statistically significant allelic association with head and neck cancer risk [p=0.04, OR=1.44 (1.02-2.03)].  Cancer cases and controls were found to be in Hardy-Weinberg equilibrium.