Myeloid sarcoma (MS) is a neoplasm of immature granulocytes, monocytes, or both involving any extramedullary site. Twenty one patients with MS at diagnosis who were treated at King Hussein Cancer Center in Jordan were included in this retrospective study with a male to female ratio of 2 : 1. The most common site was the reticuloendothelial system. The most common morphology subtype was M2 (38%) and the most frequent chromosomal abnormality was trisomy 8. Twenty patients received induction chemotherapy; only 14 (70%) achieved complete remission. Median survival time was 24.7 months for the whole group and 58.6 months for patients who underwent allogenic bone marrow transplant. This paper showed that MS has frequent M2 morphology, carries chromosomal aberrations other than t(8;21), and requires aggressive therapy as a front line approach.
Deletion of phosphatase and tensin homolog (PTEN) in prostate cancer has been associated with early biochemical recurrence, increased metastatic potential, and androgen independence. We evaluated the status of PTEN loss in a cohort of prostate cancer patients from Jordan. We investigated 71 patients with prostate cancer and 52 control subjects with benign prostatic hyperplasia (BPH). PTEN status was assessed by immunohistochemistry. PTEN mutations on exons 1, 2, 5, and 8 were also evaluated by polymerase chain reaction single-stranded conformation polymorphism (PCR-SSCP). We found PTEN loss in 42 of 71 (59.2%) evaluated prostate cancer cases by immunohistochemistry. In contrast, 51 of 52 BPH (98.1%) cases had an intact PTEN. In a subset of 24 prostate cancer cases evaluated by PCR-SSCP, we found PTEN mutations in 15 (62.5%) cases, whereas 22 (91.7%) of BPH controls lacked PTEN mutations. Exon 5 was the most frequently mutated exon (37.5%). Although the loss of PTEN was not significantly correlated with the Gleason Score (GS) or the World Health Organization (WHO)-International Society of Urological Pathology (ISUP) Grade Group (GG), we found higher frequency of PTEN loss (64%) in patients with GS≥4+3/GG≥3, compared with patients with GS≤3+4/GG≤2 (47.6%). In this first study to address the question of PTEN loss in a predominantly Arab population, we documented the frequency of PTEN loss in prostate cancer patients from Jordan, which was found to be higher than in comparable cohorts from East Asia, and was at the higher end of the range of reported frequency of PTEN loss in respective cohorts from North America and Western Europe. Although there was more frequent PTEN loss in cancers with higher GS/GG, this was not statistically significant.
Background Lung cancer is a major health burden in Jordan. With the failure of tobacco control policies and the evolution of new smoking methods like water pipes and e-cigarettes, lung cancer is projected to further increase. This study investigates the epidemiology and the different histopathological subtypes of lung cancer in correlation with age, sex and smoking. Material and methods 434 tumors diagnosed in the main tertiary hospital in Northern Jordan throughout the period of 2004–2017 were included. Specimens were tested by H&E and immunohistochemical stains. Clinical data were collected from patients' medical files. IRB approval number 310/2016 was granted by Jordan University of Science and Technology review board. Results 86.9% of cases were males compared to 13.1% in females obtaining a male:female ratio of 6.6:1. The mean age was 63.8 years with a range of 28–103 years. Prevalence of cases increased with increasing age and smoking. Histopathologically, adenocarcinoma accounted for over half of the cases followed by Squamous cell carcinoma (SCC) and neuroendocrine tumors (NET) in both sexes. Adenocarcinoma had the lowest mean age; 62.74 years, while SCC had the highest mean age with 65.42 years. All subtypes increased with age but in different degrees. The increase was more pronounced in SCC and NET and less with adenocarcinoma. Adenocarcinoma was more common in both smokers and non-smokers. However, smokers to non-smokers ratio differed; where it was the highest in NET (6:1) compared to 4:1 in SCC and 2:1 in adenocarcinoma. Conclusion Median age of our patients was slightly lower than that previously reported in Jordan. This study also showed an increase in the relative incidence of adenocarcinoma compared to SCC.
Introduction: Olanzapine (OLZ) is one of the second-generation antipsychotics drugs (APDs) used to treat several psychiatric illnesses. Olanzapine treatment is often associated with many metabolic side effects in a dose dependent manner such as obesity, dyslipidemia and insulin resistance, induction of type II diabetes and acute pancreatitis in some patients.Methods: Hyperbaric Oxygen therapy (HBOT) was investigated as a tool to mitigate olanzapine metabolic side effects in rats. Thirty-six female Sprague Dawley (SD) rats were divided into 4 groups; rats on olanzapine treatment either exposed to hyperbaric oxygen therapy (HBOOLZ) or left without exposure (OLZ) then non-treated rats that either exposed to hyperbaric oxygen therapy or left without exposure (control). Rats received Hyperbaric Oxygen therapy for 35 days at 2.4 atmospheres absolute (ATA) for 2.5 h daily followed by intraperitoneal injection of olanzapine at 10 mg/kg or placebo.Results: Rats on either hyperbaric oxygen therapy or olanzapine had a significant loss in body weight. Olanzapine treatment showed a decrease in serum insulin level, triglyceride, highdensity lipoprotein (HDL) cholesterol, and lipase level but an increase in fasting blood sugar (FBS), insulin resistance index (HOMA-IR) and amylase, while rats’ exposure to hyperbaric oxygen therapy reversed these effects. The Pancreatic Langerhans islets were up-regulated in both hyperbaric oxygen therapy and olanzapine treatments but the combination (HBOOLZ) doubled these islets number.Discussion: This study advocated that hyperbaric oxygen therapy can be an alternative approach to control or reverse many metabolic disorders (MDs) associatedwith olanzapine treatment. In addition, it seems that hyperbaric oxygen therapy positively affect the pancreatic Langerhans cells activity and architecture.
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