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Aim: To investigate potential DNA methylation in methylcytosine dioxygenases and correlation of TET genes with vitamin B12/ferritin levels in cancer patients. Materials & methods: 200 blood samples were obtained from both cancer patients and healthy individuals. Results: The expression of DNMT1, DNMT3a and DNMT3b was increased in patients with low vitamin B12 and ferritin levels, while the expression of MTR, TET1 and TET3 significantly decreased. DNA methylation analysis in patients with deficient vitamin B12/ferritin levels showed methylomic changes within the location 318/CG and 385/CG in the promoter region of TET1 and TET3, respectively. Conclusion: Vitamin B12/ferritin deficiency contributes to DNA methylation progress in cancer patients.

Prognosis in certain types of cancers still poor like in glioblastoma, some types of leukemia & lung cancer. Royal Jelly (RJ) chemical investigations started in 1960s and Major Royal Jelly proteins (MRJPs)were first reported in 1992. Later on, in 2006 after bee genome publication, nine different types of MRJPs were confirmed. Apisimin a new peptide found in RJ was discovered in 2002, and in 2004 Jelleines peptides group were also reported in RJ. While Apisimin and Jellein 4 of not known biological activities recorded, Jellein 1, 2 &3 peptides showed antibacterial effect, antifungal effects, mast cell degranulation activity and hemolysis. However, nobody used Jelleins, Apisimin derivatives or both in a trial to treat cancer. Here we show new significant cancer inhibitions for a combination of Apisimin derivatives and modified Jelleins (with a change of few amino acids to d-form). In vivo studies, using a combination of peptide J1d (modified Jellein 1)and Ap3d( peptide contains 8 amino acids from c-terminal of Apisimin) in one group and a peptide K2( synthetic peptide consists of Ap3d + J1d) in another group in U-87 nude mice, we got significant inhibitions in both groups. In another studies, using K2 peptide in one group and K3 peptide( synthetic peptide consists of Ap4d+ J2d) in another group versus C1498 and LLC syngeneic models, we also got significant inhibitions. We got no effect when using any Jelleins as well as with any Apisimin derivatives. Our results demonstrate the effectiveness of using Apisimin derivatives peptides and modified Jelleins simultaneously in cancers.

Background: Cancer is the second-leading cause of death worldwide, caused by several mutations in DNA within the cells including epigenetic alteration. The epigenetic changes are external modifications to the DNA that switch “on” or “off” gene expression. The present study was conducted to investigate the epigenetic modifications and its correlation with the levels of vitamin B12 and ferritin in cancer patients with hepatocellular carcinoma (HCC), breast cancer (BC), lung cancer (LC), or colon cancer (CC). Methods and Results: A total of 200 blood samples were obtained from cancer patients and healthy individuals. The relative expression of DNA methyltransferases (DNMTs), Ten-Eleven translocation (TET), and methionine synthase (MS) was evaluated in patients with the normal level of vitamin B12/ferritin and patients with the deficient levels of them. DNA methylation within the promoter regions was investigated of each indicated genes using the methylation-sensitive restriction enzyme HpaII and bisulfite PCR. Interestingly, the expression of DNMT1, DNMT3a, and DNMT3b was increased in patients with low levels of vitamin B12 and ferritin, while the expression of MS, TET1, and TET3 was significantly decreased. DNA methylation analysis in patients with deficient levels of vitamin B12/ferritin showed a methylated-cytosine within the location 318/CG and 385/CG in the promoter region of TET1 and TET3, respectively. Moreover, the bisulfite PCR assay further confirmed the methylation changes in the promoter region of TET1 and TET3 at the indicated locations. Conclusion: These data indicate that the deficiency in vitamin B12 and ferritin in cancer patients plays a key role in the epigenetic exchanges during cancer development.

Background: Cancer is the second-leading cause of death worldwide, caused by several mutations in DNA within the cells including epigenetic alteration. The epigenetic changes are external modifications to the DNA that switch “on” or “off” gene expression. The present study was conducted to investigate the epigenetic modifications and its correlation with the levels of vitamin B12 and ferritin in cancer patients with hepatocellular carcinoma (HCC), breast cancer (BC), lung cancer (LC), or colon cancer (CC). Methods and Results: A total of 200 blood samples were obtained from cancer patients and healthy individuals. The relative expression of DNA methyltransferases (DNMTs), Ten-Eleven translocation (TET), and methionine synthase (MS) was evaluated in patients with the normal level of vitamin B12/ferritin and patients with the deficient levels of them. DNA methylation within the promoter regions was investigated of each indicated genes using the methylation-sensitive restriction enzyme HpaII and bisulfite PCR. Interestingly, the expression of DNMT1, DNMT3a, and DNMT3b was increased in patients with low levels of vitamin B12 and ferritin, while the expression of MS, TET1, and TET3 was significantly decreased. DNA methylation analysis in patients with deficient levels of vitamin B12/ferritin showed a methylated-cytosine within the location 318/CG and 385/CG in the promoter region of TET1 and TET3, respectively. Moreover, the bisulfite PCR assay further confirmed the methylation changes in the promoter region of TET1 and TET3 at the indicated locations. Conclusion: These data indicate that the deficiency in vitamin B12 and ferritin in cancer patients plays a key role in the epigenetic exchanges during cancer development.

Autophagy is a cellular housekeeping process that incorporates lysosomal-degradation to maintain cell survival and energy sources. In recent decades, the role of autophagy has implicated in the initiation and development of many diseases that affect humanity. Among these diseases are autoimmune diseases and neurodegenerative diseases, which connected with the lacking autophagy. Other diseases are connected with the increasing levels of autophagy such as cancers and infectious diseases. Therefore, controlling autophagy with sufficient regulators could represent an effective strategy to overcome such diseases. Interestingly, targeting autophagy can also provide a sufficient method to combat the current epidemic caused by the ongoing coronavirus. In this review, we aim to highlight the physiological function of the autophagic process to understand the circumstances surrounding its role in the cellular immunity associated with the development of human diseases.

Backgound: The challenge with malignancy control approaches, although of all traditional methods of treatment like surgery, chemotherapy, radiotherapy, immunotherapy etc. makes more stress upon the scientific community to look for a solution for this challenge even far from the traditional ways. Methods: A growth inhibitory assay was performed. Samples of peptide A and peptide F, 5 mg each, were dissolved in 500 μL Dulbecco’s Phosphate-Buffered Saline to prepare the stock solution, which was added into the wells directly. A 1% trifluoroacetic acid (TFA) solution was used as the control. (a) Cells were placed into a 96-well assay plate at a density of 5000 and 10000 cells/well for adherent and suspension cell lines, respectively, with a 50 μL complete cell culture medium. (b) Stock solutions (10 μL) of the compounds were added into the wells. (c) For data analysis, 10 μL 1% TFA solution was used as control. (d) Complete medium of 40 μL was added into the wells to reach a total volume of 100 μL. (e) The plate was incubated at 37℃ for 72 hours. (f) CellTiter-Glo assay mix solution (50 μL) was added to each well and mixed gently at room temperature for 10 minutes; subsequently, the luminescence was read using PHERAstar Plus (Molecular Devices). Results: Apparent inhibitory effects of those peptides were noticed in 17 of 18 tumour cell lines. Similar effects were noted in an in vivo study using the U87MG tumour mouse model. Conclusion: This study has introduced new synthetic peptides derived from honey proteins, which may help in cancer control through direct apoptotic action not limited to only a certain tumour cell line. Patent: WO/2014/040605A1, US/2015/0291663A1, and CN105283198A.

Objective: Changes in DNA sequence are usually caused by viruses, certain chemicals and radiation as well as by transposons, somatic hyper mutation and errors during meiosis. We can consider gene therapy as an induced DNA sequence changes by inserting certain gene or genes, through viral vectors mainly. Anyhow, many problems met gene therapy like short-lived nature, need for multiple rounds of that therapy, immune response for gene or vector as foreigners, problems with viral vectors and malignancy induction. Wet nurse or foster suckling mother means breastfeeding an infant that is not one's biological offspring which was a job from ancient Egyptians times till the present. Results: Here we show a significant change in DNA sequence in babies after foster mothers suckling compared to their DNA before suckling foster mother suggesting presence of potential factors in foster mother milk which can change DNA sequence in babies before weaning. This may open the door to study milk as a new potential method for gene transmission and therapy. A method, that probably overcome many of problems meeting gene therapy as well as a possible cause for evolution in mammalians if we consider cross nursing during milk feeding from other species before weaning.