Increased CD14(+) monocytes with loss of HLA expression were seen in patients with higher stage disease, more aggressive pathology, and in relapse or refractoriness to treatment. Identifying therapeutic strategies to overcome the suppressive properties of these monocytes could be of value.

. We also found a significantly higher frequency of the XRCC1 399Gln allele in patients with ESRD than in controls (OR: 2.22; 95% CI: 1.16-4.25; p ¼ 0.02). Combination of the Arg/Gln or Gln/Gln genotypes of XRCC1 Arg399Gln polymorphism with Asp/Asn or Asn/Asn genotypes of XPDAsp312Asn or with the Lys/Gln or Gln/Gln genotypes of XPD Lys751Gln was significantly associated with the development of ESRD. Haplotypes association showed that association of Gln allele of XRCC1 Arg399Gln polymorphism with the Asn allele of XPDAsp312Asn polymorphism (p ¼ 0.004) or Gln allele of XRCC1 Arg399Gln polymorphism with the Gln allele of XPD Lys751Gln polymorphism (p ¼ 0.003) was highly significantly associated with the development of ESRD. This study revealed that XRCC1 Arg399Gln polymorphism may confer increased risk for the development of ESRD. Furthermore, larger studies should be conducted to confirm these results.

Aim:  To evaluate the value of peripheral blood mammaglobin (MG) gene expression for diagnosis and prediction of metastasis in breast cancer patients. Methods:  MG expression was detected by nested reverse‐transcription polymerase chain reaction in the peripheral blood of 46 females (32 breast cancer, 12 benign breast lesions, 2 no breast abnormalities). In total 28 breast cancer patients were followed up through a period of 34 months for the development of metastasis. Results:  MG expression was detected in 16/32 (50%) breast cancer patients but not in patients with benign lesions or healthy participants. Five patients had metastasis at diagnosis. During the 34 months of follow up, five more MG‐positive patients showed metastatic lesions and none of the MG negative patients who were followed up developed metastasis. Conclusion:  The study suggests blood MG expression is a specific molecular marker for detection of occult mammary carcinoma cells of patients with operable breast cancer. It might be of value as a predictor of subsequent metastasis. Large‐scale studies and longer follow‐up periods are needed.

Background and study aim: Hepatocellular carcinoma (HCC) is a hypervascular tumor and its progression is known to be closely related to angiogenesis. Angiopoietin-2 (Ang-2) is one of the angiogenic factors that may have a diagnostic value in HCC. Alpha-fetoprotein (AFP) serum levels are used for screening for HCC with limited success. This study aimed to evaluate diagnostic value in using angiopoietin-2 as a serum marker in HCC patients. Patients and Methods: 50 patients with HCC (G1), 20 patients with liver cirrhosis (G2), and 20 healthy control persons (G3) were included in this study. Serum AFP and Ang-2 levels were measured by enzyme-linked immunosorbent assay. Results: Serum Ang-2 levels in the HCC group (1523.54±886.46 pg/ml) was highly significantly elevated as compared to those with cirrhotic liver (222.55±153.60 pg/ml) and controls (138.35±54.09 pg/ml). The Ang-2 levels were significantly different between patients with liver cirrhosis and controls. In HCC patients, the serum Ang-2 levels in patients with portal vein (PV) thrombosis (n=7, 2164.0±960.85 pg/ml) and with large HCC (>5cm in diameter) (n=17, 2017.70±903.06 pg/ml) were significantly higher than those without PV thrombosis (n=43, 1274.47±727.56 pg/ml) and with small HCC (≤5cm in diameter) (n=33, 1268.97±773.93 pg/ml), while the serum AFP levels in patients with portal vein (PV) thrombosis (961.05±1007.70 ng/ml) and with large HCC (>5cm in diameter) (1000.81±1079.57 ng/ml) were not significantly higher than those without PV thrombosis (500.24±733.07 ng/ml) and with small HCC (437.87±611.02 ng/ml). Conclusion: Combined measurement of serum AFP and Ang-2 significantly increases the sensitivity and specificity of HCC detection rather than using of AFP or Ang-2 separately.

Objective. To detect biomarkers that can be used to predict COVID-19 severity to identify patients with high probability of disease progression and poor prognosis. Methods. Of the 102 patients with confirmed COVID-19 who were admitted to King Fahd General Hospital, Jeddah City, Saudi Arabia, from July 1, 2021 to August 5, 2021, 50 were included in this cross-sectional study to investigate the influence of serum amyloid A (SAA) on disease severity and survival outcomes of COVID-19 patients. Dynamic shifts in SAA, C-reactive protein (CRP), white blood cell (WBC), lymphocytes, neutrophils, biochemical markers, and disease progression were examined. At admission, and at three, five, and seven days after treatment, at least four data samples were collected from all patients, and they underwent clinical status assessments. Results. Critically ill patients showed higher SAA and CRP levels and WBC and neutrophil counts and significantly lower lymphocyte and eosinophil counts compared to the moderately/severely ill patients, especially with regard to disease progression. Similarly, nonsurvivors had higher SAA levels than survivors. The moderately/severely ill patients and the survivors had significantly higher dynamic changes in SAA compared to the critically ill patients and nonsurvivors, respectively, with differences clearly noticed on the fifth and seventh day of treatment. ROC curve analysis revealed that the combination of SAA and CRP was valuable in evaluating the disease progression and prognosis of COVID-19 patients at different time points; however, a combination of SAA and lymphocyte counts was more sensitive for disease severity prediction on admission. The most sensitive parameters for predicting survival on admission were the combination of SAA/WBC and SAA/neutrophil count. Conclusions. The study findings indicate that SAA can be used as a sensitive indicator to assess the degree of disease severity and survival outcomes of COVID-19 patients.

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Background: P53 polymorphism involves the substitution of an arginine for a proline at codon position 72. Many studies have investigated a genetic link between this variation and response to treatment in cancer. This study aimed to study p53 codon72 polymorphism in relation to cytogenetic response to imatinib treatment in patients with chronic myeloid leukemia (CML). Methods: This study was conducted on 54 CML patients presented to Clinical Oncology Department, Menoufia University during the period from June 2013 and April 2015. They were classified according to their cytogenetic response to imatinib therapy into 40 CML patients cytogenetic responder to imatinib and 14 CML patients cytogenetic non responder to imatinib. Patients were genotyped for P53codon72 polymorphism using Polymerase Chain Reaction (PCR). Follow up of the patients should be done after 3, 6, 9, 12 and 18 months after diagnosis. And was done by CBC, conventional cytogenetic and FISH. Results: Age, gender, hematologic and cytogenetic response to imatinib in CML patients did not differ significantly among P53 codon72 genotypes (arg /arg, arg /pro and pro /pro) (P ¼ 0.44, p ¼ 0.45 and p ¼ 0.11 respectively). P53 codon72 polymorphism did not significantly alter the risk to imatinib cytogenetic unresponsiveness (P ¼ 0.9221). Conclusions: It could be concluded that P53 codon72 polymorphism is not associated with imatinib unresponsiveness in CML.