Open Access Short Research Article
Girardi heart cells are cell culture of right atrial cells contaminated with HeLa cervical adenocarcinoma cells. The combined cells have genotypic characteristics of cervical cancer. In this study, was investigated influence of complex of DDMC vector with small non-coding RNAs (sncRNAs) on Girardi Heart cells. As the result, the genotypic and phenotypic characteristics of Girardi heart cells were changed. Micro-RNAs (miRs) and pi-RNAs (piRs) are sncRNAs, a class of small epigenetic regulatory molecules that control normal development and differentiation of different cell types. For transfection, the cells were treated with a complex of non-viral DDMC vector with piR-30074 and antago-miR-155, followed by the addition of a complex of DDMC vector with miR-125b. I observed OCT4 gene and protein expression in the cells after treatment using the complexes of DDMC vector with piR-30074 and antago-miR-155. The expression of KIR2DL1, GITR1, DICER1, PIWIL1, RISC1, FLT3, NOS2, MAFB, LIN28 genes was detected and the expression of CD4+ and CD117+ protein markers was observed. The expression of these genes and proteins was not observed in control cells.
Open Access Original Research Article
Aims: To evaluate the Activated Partial Thromboplastin Time (APTT) and fibrinogen levels in patients with Polycythemia vera (PV).
Study Design: Analytical, laboratory, hospital-based, cross sectional study.
Place and Duration of Study: Hematology clinic at Fedail hospital Khartoum State, Sudan. From April to August 2016.
Methodology: Research protocol was approved by SUMASRI International Review Board (SIRB) at University of Medical Sciences And Technology (UMST), Sudan. A total of 19 patients (14 male, 5 female; mean age of 59 ±4 years ) were selected from PV patients who came to the hospital during study period and who met inclusion criteria and 29 samples were collected from healthy subjects as control. APTT and fibrinogen level were assayed. Statistical evaluation was performed by SPSS (version 20) using Student's t test and Pearson correlation tests.
Results: Patients with Polycythemia vera had shortened APTT (26.9±1.3s vs. 35.4±4.4 s); P <0.05) and higher fibrinogen (569±79 mg/dl vs. 290±96 mg/dl; P <0.05) values when compared with to normal control. Strong negative correlation between the Fibrinogen level and shortened APTT in PV was seen (R -0.766, p<0.05).
Conclusion: This study indicates that, the patients with PV were prone to develop hypercoagulable state. Therefore, routine examinations of APTT and fibrinogen are significant to assess coagulation abnormality in order to prevent PV-associated thrombosis.
Open Access Review Article
Recently there has been a renewed interest on the signaling pathways and metabolic changes in cancer cells. It is well known that there are several oncogenes and tumor suppressors that affect cancer metabolism and re-engineer it for better growth and survival. The best description of tumor metabolism is the Warburg effect, which shifts from ATP production through oxidative phosphorylation to ATP production through glycolysis, even in the presence of oxygen. The Warburg effect is controlled by oncogenes—c-Myc, Kras, P1K/AKT/mTOR pathway—and tumor suppressors—p53, LKB1/AMPK, PTEN, and RB. Studies on oncogenes and tumor suppressors suggest potential therapeutic strategies. The oncogene Kras promotes increased glucose uptake, glycolytic flux and ribose biogenesis, and mediates reprogramming of glutamine metabolism by changes in gene expression. The tumor suppressor p53 promotes the expression of antioxidant proteins that regulate oxidative stress and glucose metabolism. The LKB1/AMPK agonists have potential to be anticancer drugs, as patients treated by metformin for diabetes had a lower incidence of cancer. Discovering the mechanism by which oncogenes and tumor suppressors regulate metabolism will allow for designing treatment strategies. This review discusses how several oncogenes and tumor suppressors regulate cellular metabolism, and the current therapeutic findings.
Open Access Review Article
This review is intended to take us through a journey on how cancer had been treated and highlight the paradigm shift in understanding its treatment since adoption of evolution concept and hope to point to a possible future breakthrough in cancer management. Researchers estimate there will be 26 million or more new cases a year by 2030, and some 17 million cancer deaths yearly. The US president in 1971 Richard Nixon proposed the war on cancer in a bid to find lasting cure to cancer in the space of 25 years. An evaluation was carried out after 25 years, which, showed that although there had been major breakthrough in the battle against cancer yet the war continues and we are not yet close to a definite victory with local invasion, and distant metastasis that is resistant to conventional therapy being the major causes of death. This attitude of cancer cells had been more understood in the light of ecology and evolution in recent years as the Darwinian theory of evolution by natural selection now becomes a theoretical framework for the study of cancer behaviour. However, the implication of this eye opener to the cure of cancer had to be more highlighted if the moon shot war against cancer as declared by President Obama in 2016 would be successful. Early diagnosis taking into cognizance polyploidy parameters, more specific choice and scheduling of cancer treatment; selective toxicity, Inhibiting other chemicals or factors that initiate and sustains angiogenesis in cancer cells (tumour or human specific), supporting the immune system, boosting normal cell fitness and Restoring a more normal ecological niche may be the answer we have long sorted for as we strive to find a lasting cure to cancer.