BackgroundColorectal carcinoma (CRC) is the seventh-most common malignancy and is the main cause of death in Iraq. The incidence of this cancer has increased sharply after the invasion of Iraq in 2003.AimTo estimate immunohistochemical expression of vascular endothelial growth factor (VEGF) in CRC in relation to other parameters, such as grade and stage of tumour.MethodsFormalin fixed, paraffin-embedded blocks from 52 patients (27 male and 25 female) with CRC were included in this study. A group of 22 patients with non-cancerous colonic tissues were included as a control group. Avidin–biotin complex method was employed for immunohistochemical detection of VEGF.Results VEGF immuno-expression was positive in 51.9% of CRC, while it was 18.2% in the normal colonic tissue (p <0.05). VEGF immunostaining was positively correlated with grade of colonic malignancy (p <0.05).ConclusionThese findings provide further evidence for the role of VEGF in the carcinogenesis of CRC. However, VEGF could not be well correlated with stage of tumour and hence may be a poor prognostic parameter of state of malignancy of colonic carcinoma.
ObjectiveInvestigate PTEN gene expression and tumor aggressiveness in endometrial carcinoma specimens from patients living in either areas of depleted uranium [DU] pollution or unpolluted regions to determine any evidence for the effect of war pollution on the rising trends of cancer incidence in Iraq.ResultsTumor PTEN gene expression was significantly increased in patients living in the areas of high risk DU exposure, in comparison to patient tumors from low risk areas [P = 0.001]. The age distribution between the potentially DU exposed (55.09 ± 1.24) and unexposed subjects 56.38 ± 1.18) was not significant [P = 0.45]. Endometrial carcinoma aggressiveness was equivalent in both subject groups, with no significant differences in either tumour grade and [P = 0.286] stage distribution [P = 0.98]. Finally, there were no significant differences between the potentially exposed and unexposed subjects with regard to cervical [P = 0.532] or to ovarian involvement [P = 0.518]. The results linked environmental war pollutants [DU] to alterations in PTEN gene expression in endometrial carcinoma. Furthermore, this finding may explain the overall increasing cancer trends observed in Iraq. Strategies should be considered for the therapeutic targeting of cancers with elevated PTEN gene expression to improve patient outlook.
Patients with absent thymic CD20 expression had significantly more postoperative complications and cardiac obstructive defects than those with positive CD20 expression.
Background: Colonic polyps are slow-growing overgrowth that projects above the surrounding mucosa's of the colon that carry a small risk (< 1%) of becoming malignant. However, because colonic polyps are highly prevalent in the general population (especially with increasing age), they confer an important predisposition to colon cancer and are therefore removed when detected. The distribution of Ki67 and p53 as markers of cell proliferation is very studied in Colorectal Carcinoma. In Iraq, IHC studies to detect p53 & ki-67 expression in GIT malignancy has been conducted. Aims of the study: To detect the expression of p53 & ki-67 in colonic polyps patient by immunohistochemistry. To assess the possible correlation between p53 &ki-67 in colonic polyps patient. To detect the possibility of conversion of pre-malignant colonic polyps to malignant form. Methodology: Fifty cases (27 male and 23 female ) were selected randomly with different types of colonic polyps were included in this study and using descriptive study. The age of patients were ranging from 4 up to 80 years, with mean age of [ 46.3 ] years. Cases were collected from the laboratory of histopathology in Al-sadder Medical city in Al-Najaf and from some private laboratories in the same governorate(Al-Najaf). the data analyzed by qi squared. Result: There is a significant correlation between P53 & age ,p53 & type of polyp also there is a significant correlation between Ki-67& age, Ki-67 & type of colonic polyp .There is a correlation between ki67 & p53. Conclusion: The study represent a trial to understand the probable conversion of polyps to colorectal carcinomaand the role of P53 & KI-67 in genesis of colorectal carcinoma. Recommendation: Screen and follow up to all patient with colonic polyps specially to patient with multiplepolyps. All type of polyps should be removed ,because polypectomy currently constitutes the best strategy forpreventing colorectal cancer
Chronic myeloid leukemia (CML) is a hematopoietic stem cell disease, associated with a reciprocal translocation between chromosomes 9 and chromosome 22, lead to the formation of the BCR-ABL fusion gene (Philadelphia chromosome). This fusion gene is believed to play golden role in the initial development of CML with constitutive tyrosine kinase activation. Successful use of tyrosine kinase inhibiters (TKIs) play a role in improve survival and increase prevalence of CML, but un fortunately mutations in the BCR-ABL kinase domain may cause, or contribute to increase, resistance to TKIs in CML patients. This study was designed to assess the association of five most common BCR-ABL kinase domain mutations (T315I, M351T, E255K, M244V and E255V) with resistance state of CML patients on TKIs in Iraqi Middle Euphrates region. A retrospective case-control study in which 85 patients with chronic myeloid leukemia in chronic phase (45 patients as cases group and 40 patient as control group) were selected from three hemato-oncology centers in middle Euphrates in Iraq during the period from January 2016 till October 2016 out of a total of 240 CML patients ( 108 male and 132 female) who were registered during this period in these three centers and all patients on TKI (Imatinib and Nilotinib). Venous blood sampling done for BCR-ABL kinase domain mutations screening. four patients from cases group (4/45) were carriers of one of five selected ABL kinase domain mutations and no one of control group. T315I mutation was detected in 3/45 (6.6 %) of resistant patients, with a significant risk association to develop resistance to TKI therapy (odd ratio and C. I. ) (6.67, 0.3340 -133.2255). E255V was detected in 1/45 ( 2.2 %) and also had significant risk association to develop resistance to TKIs( odd ratio, C.I.) (2.73, 0.1081 -68.9424). No one of these mutation had significance correlation with demographic or hematological features. M351T, E255K and M244V were not detected in any one of our study groups CML patients. T315I and E255V among five ABL kinas domain mutations were detected in our CML patients with resistance to TKIs. All of them may play a role in development variable degree of resistance to first and second generation TKIs weather primary or secondary.T315I mutation is most common mutation within BCR-ABL domain kinase gene.
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