Facuty of Medicine

The mechanisms of obesity-induced breast carcinogenesis are not clear. One hypothesis is that high levels of adipokines could promote breast cancer (BC) development. The aim of this study was to investigate the correlation of resistin, visfatin, adiponectin, and leptin with BC risk in pre- and postmenopausal females. A total of 82 BC newly diagnosed and histologically confirmed patients and 68 age and BMI matched healthy controls were enrolled. Both groups were subdivided into post- and premenopausal subgroups. Resistin, visfatin, adiponectin, and leptin were measured by ELISA. There were significantly higher levels of leptin, resistin, and visfatin in postmenopausal BC patients than their respective controls. Only in postmenopausal subgroups, leptin, resistin, and visfatin levels were positively correlated with TNM staging, tumor size, lymph node (LN) metastasis, and histological grading. In postmenopausal females, multivariate logistic regression analysis revealed that adiponectin...

Objectives: The role of various adipokines as a link between obesity and diabetes mellitus has recently been better elucidated. The aim of this study was to investigate the correlation of the leptin/adiponectin ratio (LAR) with insulin resistance in obese and diabetic Saudi females. Methods: This study included 373 Saudi females divided into two groups: type 2 diabetic (n=196) and normal control (n=177).The groups were further divided according to BMI into normal obese (n=85), normal non-obese (n=92), diabetic obese (n=118) and diabetic nonobese (n=78) subgroups. For all studied groups, levels of leptin, adiponectin, insulin and C-reactive protein were measured using (ELISAs).The glucose, triglyceride, cholesterol, LDL and HDL levels were determined using colorimetric assays, and the homeostasis model assessment ratio (HOMA-IR) was determined using a formula derived from fasting insulin and glucose levels. Results: The leptin levels were significantly higher and the adiponectin levels were significantly lower in the diabetic group compared to the normal control group (P value < 0.05).

Polymorphisms in the promoter region of CD14 gene have been associated with asthma and atopy although the findings between cohorts have not been uniform. We aimed at investigating the association between CD14 gene (-1145G/ A) polymorphism and bronchial asthma in Egyptian children. Genotyping of CD14 gene (-1145G/A) polymorphism was done by real-time PCR in 192 asthmatic children (atopic, n = 100 and non-atopic, n = 92) and 181 age- and gender-matched healthy children. Serum levels of total IgE were measured by ELISA. Skin prick test was performed on all patients. We found that the frequency of AA genotype was significantly higher in asthmatic children compared to healthy controls. Asthmatic children carrying GG genotype had a significantly lower prevalence of atopic asthma. Meanwhile, the ‘‘A’’ allele was significantly higher in atopic asthmatic children compared to healthy and non-atopic children. Moreover, atopic children carrying the ‘‘G’’ allele showed better asthma control. In conclusion, our findings represent an evidence for the role of CD14 gene (-1145G/A) polymorphism in childhood asthma and asthma control.

Lung cancer is the leading cause of cancer-related death in industrialized countries. CXCL8 is a cytokine that has been shown to exert effects relevant to cancer growth and progression. There are few reports on the clinical roles of CXCL8 in lung cancer progression. The aim of our study was to evaluate the serum levels of CXCL8 and the tissue expression of Bcl-2 and p53 in squamous cell lung cancer patients in order to explore the possible diagnostic role of CXCL8 in squamous cell lung cancer and to clarify the relationship of these markers to each other and with classical clinicopathological factors. Serum and tissue samples were obtained from 50 patients who underwent fibreoptic bronchoscopy for squamous cell lung carcinoma. The tissue expression of both Bcl-2 and p53 proteins in the malignant and control groups were evaluated by ELISA and Western blot. Serum levels of CXCL8 were measured by ELISA. They showed significant increase in the malignant group versus the control group. Regarding the different clinicopathological factors, serum CXCL8 showed significant increase with the histological grades and stages. While no statistical difference was found in the median levels of Bcl-2, p53 as regards the different stages and only p53 showed statistical difference as regards the different histological grades. Concerning the levels of the three investigated biomarkers to each other, p53 and CXCL8 were the only biomarkers that demonstrated a significant correlation. CXCL8 also showed higher sensitivity and specificity in comparison to the other parameters.

Lung cancer is the leading cause of cancer-related death in industrialized countries. CXCL8 is a cytokine that has been shown to exert effects relevant to cancer growth and progression. There are few reports on the clinical roles of CXCL8 in lung cancer progression. The aim of our study was to evaluate the serum levels of CXCL8 and the tissue expression of Bcl-2 and p53 in squamous cell lung cancer patients in order to explore the possible diagnostic role of CXCL8 in squamous cell lung cancer and to clarify the relationship of these markers to each other and with classical clinicopathological factors. Serum and tissue samples were obtained from 50 patients who underwent fibreoptic bronchoscopy for squamous cell lung carcinoma. The tissue expression of both Bcl-2 and p53 proteins in the malignant and control groups were evaluated by ELISA and Western blot. Serum levels of CXCL8 were measured by ELISA. They showed significant increase in the malignant group versus the control group. Regarding the different clinicopathological factors, serum CXCL8 showed significant increase with the histological grades and stages. While no statistical difference was found in the median levels of Bcl-2, p53 as regards the different stages and only p53 showed statistical difference as regards the different histological grades. Concerning the levels of the three investigated biomarkers to each other, p53 and CXCL8 were the only biomarkers that demonstrated a significant correlation. CXCL8 also showed higher sensitivity and specificity in comparison to the other parameters.

The mechanisms of obesity-induced breast carcinogenesis are not clear. One hypothesis is that high levels of adipokines could promote breast cancer (BC) development. The aim of this study was to investigate the correlation of resistin, visfatin, adiponectin, and leptin with BC risk in pre-and postmenopausal females. A total of 82 BC newly diagnosed and histologically confirmed patients and 68 age and BMI matched healthy controls were enrolled. Both groups were subdivided into post-and premenopausal subgroups. Resistin, visfatin, adiponectin, and leptin were measured by ELISA. There were significantly higher levels of leptin, resistin, and visfatin in postmenopausal BC patients than their respective controls. Only in postmenopausal subgroups, leptin, resistin, and visfatin levels were positively correlated with TNM staging, tumor size, lymph node (LN) metastasis, and histological grading. In postmenopausal females, multivariate logistic regression analysis revealed that adiponectin, leptin, visfatin, and resistin were risk factors for BC. Our results suggested that serum resistin, leptin, adiponectin, and visfatin levels as risk factors for postmenopausal BC may provide a potential link with clinicopathological features and are promising to be novel biomarkers for postmenopausal BC.

Obesity is a major health problem tremendously increasing
worldwide, obesity has been accompanied by a state of metabolic
dysregulation, characterized by insulin resistance and may be
associated with many comorbidities such as metabolic syndrome,
type 2 diabetes and cardiovascular complications. Lately a great
attention has been gained toward the association of obesity with
certain cancers. Numerous studies and meta-analysis reported
that, obesity is associated with increased risk of esophageal
adenocarcinoma, postmenopausal breast cancer, and endometrial,
renal, pancreatic, prostate and colorectal cancers. In spite of, the
evidence of such association that link obesity with risk and recurrence
or death from cancer, however the linking mechanisms has not been
yet fully explained. Obesity may promote cancer by: 1) alteration
of adipocytokines: Leptin, adiponectin, resistin and visfatin with
promotion of angiogenesis and interactions with other mediators and
cytokines. 2) Hypoxia and angiogenesis due to expansion of adipose
tissue with release of certain mediators that stimulate angiogenesis.
3) Metaflammation state of low grade and chronic inflammation that
merely stimulate release of cytokines as (TNFα) and (IL-6) and the
activation of pro-inflammatory signaling. 4) Insulin resistance with
hyperinsulinemia and increased levels of insulin and growth factors
as IGFs and IGF binding proteins. 5) Increased levels of sex steroids,
including estradiol and Dehydroepiandrosterone (DHEA) particularly
in cases of endometrial and postmenopausal breast cancers. 6)
oxidative stress and reduction of antioxidants with possibility of
oxidative damage or mutation of DNA. 7) epigenetic mechanisms,
including DNA methylation , histones and chromatin remodeling
factors . In fact, it remains unclear how the convergence of these
mechanisms may drive obesity-associated cancer, considering the
complex and multi-factorial characterization of cancer as well as
the variation of genetics background of obese subjects. Prospective
studies is worth pursuing especially towards therapeutic implications
to prevent or treat obesity- associated cancer. Our aim is providing
updated and comprehensive review about postulated and prospective
links and molecular mechanisms between obesity and cancer, focusing
upon mechanistic mediators that may drive obesity- associated
cancers and may be targeted molecules for prospectives therapies.

Hematological abnormalities, especially thrombocytopenia (TCP), are highly prevalent among patients with systemic lupus erythematosus (SLE) and at the same time it has been reported as a significant prognostic factor of SLE course. We further investigate the correlation between platelet count and the clinical manifestations and disease activity of SLE, in a cohort of Saudi Arabian female patients. A retrospective analysis was done for the medical records of 100 SLE female patients, selected from all patients diagnosed and treated for SLE at the Rheumatology outpatient clinics in Hera’a General Hospital, Holly Makkah, Saudi Arabia. The data collected from every patient’s file included laboratory investigations (complete blood count, platelet
parameters, ESR, anti-double-stranded DNA antibody, ANA), clinical manifestations, as well as SLE disease activity index (SLEDAI-2k) scores throughout a period of six sequential follow-up visits. Patients were divided into three groups according to the SLEDAI-2k: mild, moderate, and high-activity group. We found that, out of 100 patients, TCP was the most prevalent hematological abnormality evident in 15%, more than leucopenia (14%) and anemia (2%). TCP was acute in onset and associated with arthritis, neurologic manifestations, and nephritis. Platelet count showed a significant negative correlation with disease activity, in all of the three groups of patients. We concluded that platelet count has a negative correlation with disease activity in SLE patients, whatever the associated manifestations, and it should be considered as a prognostic factor, identifying patients with aggressive disease course.