BK polyomavirus association with colorectal cancer development.

The development of human neoplasms can be provoked by exposure to one of several viruses. Burkitt lymphoma, cervical carcinoma, and hepatocellular carcinoma are associated with Epstein-Barr, human papilloma, and hepatitis B virus infections, respectively. Over the past three decades, many studies have attempted to establish an association between colorectal cancer and viruses, with debatable results. The aim of the present research was to assess the presence of BK polyomavirus (BKV) DNA and protein in colorectal cancer samples from patients in the Western Province of Saudi Arabia. DNA extracted from archival samples of colorectal cancer tissues was analyzed for BKV sequences using polymerase chain reaction (PCR)-based techniques. In addition, expression of a BKV protein was assessed using immunohistochemical staining. None of the tumor and control samples examined tested positive for BKV DNA in PCR assays. Furthermore, immunohistochemical staining failed to detect viral proteins in both cancer and control specimens. These results may indicate that BKV is not associated with the development of colorectal adenocarcinoma in patients in the Western Province of Saudi Arabia.

GSTM1 gene polymorphism and the risk of colorectal cancer in a Saudi Arabian population.

The enzyme glutathione S-transferase Mu 1 (GSTM1) is encoded by the GSTM1 gene. Polymorphisms in GSTM1 affect the detoxifying function of the enzyme variants. This forms the basis of the debate about the impact of the GSTM1 null/present genotype on colorectal carcinoma risk. We tested the potential influence of GSTM1 polymorphisms on the development of colorectal cancer. DNA extracted from 83 samples taken from patients that were previously diagnosed as having colorectal carcinoma and from 35 control subjects who did not have colorectal carcinoma were amplified. GSTM1 genotypes were determined by DNA sequencing. The current study revealed that the majority (69/83, 83%) of colorectal cancer cases harbored the null genotype (GSTM1*0/*0), and the remaining 14 (17%) cases harbored either the GSTM1wt/wt or the GSTM1wt/*0 genotype. In contrast, among the control cases, 23 (65%) had the null genotype (GSTM1*0/*0) and 12 (35%) had either the GSTM1wt/wt or the GSTM1wt/*0 genotype. The current report emphasizes the impact of the GSTM1 null genotype on the increased risk of colorectal carcinoma in Saudi Arabia.

Polymorphism of the glutathione S-transferase P1 gene (GST-pi) in breast carcinoma.

Breast carcinoma is the most common cancer and cause of death among females worldwide, including Jordan. The risk factors for breast carcinoma are linked to DNA mutation and failure of DNA repair or detoxification systems. Identification of susceptibility factors that predispose individuals to breast carcinoma if they are exposed to particular environmental agents might give further insight into the etiology of this malignancy. The glutathione S-transferase (GST) enzyme family detoxifies carcinogenic compounds. Several genes that code for these enzymes are polymorphic, with particular genotypes previously shown to confer an increased carcinoma risk. The present study investigates GST-pi polymorphism in 100-tissue samples previously diagnosed as breast carcinoma, and in 48 non-cancer age-matched breast tissues, using the restriction fragment length polymorphism (RFLP) method for the polymerase chain reaction (PCR) product. Among breast cancer cases, 58%, 40% and 2% were homozygous (Ile/Ile), heterozygous (Ile/Val) and homozygous (Val/Val) respectively. In the control group, 58%, 37.5% and 4.2% were homozygous (Ile/Ile), heterozygous (Ile/Val), and homozygous (Val/Val) respectively. Our results did not support the involvement of GST-pi gene polymorphism in susceptibility to breast carcinoma in the tested North Jordanian female population.

Emergency decompressive craniectomy for trauma patients with Glasgow Coma Scale of 3 and bilateral fixed dilated pupils.

BACKGROUND: Trauma patients with Glasgow Coma Scale (GCS) of 3 and bilateral fixed dilated pupils (BFDP) usually have dismal outcome, and neurosurgeons are less likely to treat such patients aggressively. In this work, the authors assessed whether emergency decompressive craniectomy (EDC) can change the poor outcome of these patients. METHODS: We reviewed all patients with GCS of 3 and BFDP admitted to our neurosurgical unit from January 2004 to January 2008. Injury data, prehospital times, findings on brain computed tomography (CT) scan, procedures, and outcomes were recorded. RESULTS: During this period, 21 patients were admitted with GCS of 3 and BFDP following traumatic brain injury (TBI). Brain CT scan showed diffuse brain edema in 17 patients (81%), and in 13 patients (62%) it showed different types of intracranial hemorrhage. All patients received conservative medical treatment. Urgent decompressive bifrontal craniectomy was performed in five patients at a mean of 4.6 h (range 2-6 h) from time of injury. Intracranial pressure (ICP) was recorded hourly by intraparenchymal sensor (Codman, Johnson & Johnson). Although decompressive craniectomy was effective in controlling ICP, all patients with GCS of 3 and BFDP died within 30 days of trauma. CONCLUSIONS: Despite control of ICP following emergency decompressive craniectomy in patients with severe TBI, GCS of 3, and BFDP, this did not change the dismal outcome of these patients; on the contrary, it may increase the suffering for patients and their families and add unnecessary medical burden. We propose that these patients have irreversible severe brain insult.

Glycophenotype of prostatic carcinomas.

The factors that affect the progression of prostatic carcinoma are poorly understood, but it is known that carbohydrate antigens on the tumour cell surface play a role in the transforming and metastatic processes. The present report aimed to perform a comparative, lectin-histochemical study of benign and carcinomatous prostates, using a battery of lectins, in combination with monoclonal antibodies against Lewis antigens, and a semi quantitative study, to investigate the changes in glycosylation patterns that occur in prostatic carcinoma. Blocks from 27 necropsy cases of prostatic carcinoma were sectioned and stained with H+E, fifteen biotinylated lectins chosen to probe for a wide range of oligosaccharide sequences within several categories of glycoprotein glycans, using a lectin-biotin avidin-peroxidase method, and monoclonal antibodies against Lewisa, sialyl Lewisa and sialyl Lewisx antigens. The glycophenotype of prostatic carcinoma differed from that of the noncancerous prostate in revealing more intense staining with the following lectins (AAA, UEA-1, DBA, WFA, VVA, HPA, BSA-1B4, MPA, ECA, AHA, and CTA), while the binding patterns of (GNA and NPA) were almost similar in both prostatic carcinoma and the noncancerous prostate. Lewis antigens are found to be expressed in prostatic carcinomas but not in the noncancerous prostate. The observations of this study suggest that the gylcophenotype of transformed prostatic cells was modified. It showed a moderate increase in, and changing patterns of, fucosylation and galactosylation, increased branching of side chains and sharp rise in 2 deoxy, 2 acetamido galactosylation and masking process by sialylation, especially by α2-3 and α2-6 linkages. All these changes in the glycosylation pattern of the transformed prostatic cells were observed on O-glycans, no changes were observed on N-glycans.