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Nov 2019 DOI 10.14302/issn.2642-3146.jec-19-3072
Mendelevium nanoparticles absorb energy of descendent light and generate some heat in the particle. The generated heat transferred to the surrounding environment and leads to increase in temperature of adjacent points to nanoparticles. Heat variations can be obtained by heat transfer equation. In the current study, thermoplasmonic characteristics of Mendelevium nanoparticles with spherical, core–shell and rod shapes are investigated. In order to investigate these characteristics, interaction of synchrotron radiation emission as a function of the beam energy and Mendelevium nanoparticles were simulated using 3D finite element method. Firstly, absorption and extinction cross sections were calculated. Then, increases in temperature due to synchrotron radiation emission as a function of the beam energy absorption were calculated in Mendelevium nanoparticles by solving heat equation. The obtained results show that Mendelevium nanorods are more appropriate option for using in optothermal human cancer cells, tissues and tumors treatment method. When Mendelevium nanoparticles are subjected to descendent light, a part of light scattered (emission process) and the other part absorbed (non–emission process). The amount of energy dissipation in non–emission process mainly depends on material and volume of nanoparticles and it can be identified by absorption cross section. At the other hand, emission process which its characteristics are depend on volume, shape and surface characteristics of nanoparticles explains by scattering cross section. Sum of absorption and scattering processes which lead to light dissipation is called extinction cross section.
Apr 2019 DOI 10.14302/issn.2328-0182.japst-19-2759
Cancer is the leading cause of death worldwide, and there is a constant need for new treatment strategies. Sesquiterpene lactones containing a 3-methylenedihydrofuran-2(3H)-one (or α-methylene-γ-lactone) moiety, for example damsin (1), are Michael acceptors that affect biological processes such as cell proliferation, death/apoptosis, and cell migration, by interfering with cell signalling pathways. Although the reactivity of the α-methylene-γ-lactone moiety is important for these effects, the Michael addition is reversible and it can be assumed that also other parts of the molecules will moderate any given biological activity. In this investigation, the cytotoxicity of 23 -methylene--lactones towards normal breast epithelial MCF-10A cells as well as breast cancer JIMT-1 cells is compared. Most of the investigated compounds are semisynthetic derivatives prepared by the condensation of the natural product damsin (1) with aldehydes. The two cell lines were treated with various concentrations of the compounds in dose response assays, and the 50 % inhibitory concentration (IC50) was determined from dose response curves. The IC50 values were found to depend strongly on the overall structure. The ratio between the IC50 values for MCF-10A and JIMT-1 cells, as a measure for the selectivity of a compound to kill cancer cells, was calculated, and found to vary between just over 1 to more than 10. The most potent derivatives formed from the condensation of 1 with aromatic aldehydes towards JIMT-1 cells are 3a and 3i, both with ratios between the IC50 values for MCF-10A and JIMT-1 cells close to 5. Also some aldol condensation products with acyclic aldehydes, i.e. 3r and 3u, were equally potent, and the latter showed the highest selectivity (ratio > 10). Structure-activity relationships that may explain the observed differences in potency and selectivity are discussed.
Oct 2018 DOI 10.14302/issn.2372-6601.jhor-18-2396
Although surgery is the main treatment for solid tumors, it could enhance the growth and metastasis of minimal residual cancer. In this review article we have discussed the perioperative changes in cancer cells and surrounding environment as well as the alterations in the immune system. Several trials are ongoing to develop new diagnostic and therapeutic options for minimal residual cancer after surgery.
Feb 2016 DOI 10.14302/issn.2574-4496.jtc-15-838
Thyroid transcription factor-1 (TTF-1) is known to play key roles in thyroid organogenesis, in thyroid cell proliferation and in the expression of genes involved in thyroid differentiated function. Many human thyroid cancer cell lines keep producing TTF-1 despite the loss of differentiated gene expression, raising a question about the role of the factor in these cells. In order to investigate this point, we used a chimeric protein acting as a functional antagonist of TTF-1 transcriptional activity that was expressed conditionally in 8505C cells originating from an anaplastic thyroid carcinoma. We observed a growth arrest of 8505C thyroid cancer cells when the endogenous TTF-1 transcriptional activity was inhibited. It correlated with decreased levels of several mRNAs encoding positive effectors of cell proliferation like CDK1 and cyclinB1, and increased levels of various mRNAs encoding negative regulators of cell division like CDKN2B and DUSP6. In conclusion, the persistence of TTF-1 expression observed in the dedifferentiated human thyroid cancer cell line 8505C reflects the need of TTF-1 activity for the proliferation of these tumor cells.
May 2015 DOI 10.14302/issn.2471-7061.jcrc-14-574
Colon cancer has a five-year survival of 64.7%, and about 50,000 people are expected to die from colon cancer this year. Patients with metastatic colorectal cancer have a significantly worse prognosis, a 12.9% five-year survival. This emphasizes the need for strategies to inhibit the growth and metastases of colorectal cancer. Prostate apoptosis response protein 4 (Par-4) is a pro-apoptotic protein that has been shown to mediate apoptosis in response to stimuli, such as chemotherapeutics and radiation. Recombinant Par-4 protein has been shown to reduce the occurrence of Lewis lung carcinoma metastases in-vivo; however, the mechanism by which Par-4 can inhibit metastasis has not been elucidated. In this study, human colon cancer cell lines - SW480 and SW620 - were transfected with Par-4 plasmid or anti-Par-4 shRNA, and the effect on metastasis was examined. Par-4 overexpression inhibited cell migration and invasion, while Par-4 knockdown promoted it. Moreover, the morphology of SW620 cells was altered when Par-4 levels were increased. The change was characteristic of a mesenchymal-to-epithelial transition (MET) in these cells. MET can be induced by upregulation of E-cadherin expression, and RT-PCR and Western blot analyses showed that E-cadherin mRNA and protein levels, respectively, were increased in the Par-4 overexpressing cells concomitant with a decrease in vimentin. The results of this study demonstrate the potential of Par-4 in colon cancer therapy, not only in primary tumors but also in metastatic cells.
Dec 2014 DOI 10.14302/issn.2326-0793.jpgr-14-598
Colorectal cancer is one of the most commonly diagnosed cancers worldwide and its prevalence can be reduced by changes to lifestyle and diet. Fermentation of dietary fibre by the gut microbiota and formation of short chain fatty acids, in particular butyrate, is widely thought to play a role in preventing development of the disease. Despite butyrate’s known pro-apoptotic effects, a subpopulation of cancer cells is able to overcome these anti-neoplastic effects of colonic luminal butyrate to proliferate and establish tumours in vivo. In this study, a time course analysis of HT29 and HT29-BR cells treated with butyrate was conducted and global gene expression analysis was used to identify novel mechanisms associated with butyrate-induced apoptosis and in the acquisition of butyrate resistance. Bioinformatic analysis of the data identified deregulated O-GlcNAcylation activity and disruption to gene transcription by BRD4 as possible factors involved with butyrate-induced apoptosis. EGF signalling was identified as being potentially involved in the acquisition of butyrate resistance. Furthermore, the expression of the minichromosome maintenance protein family was significantly reduced in the HT29-BR cell line reflecting disruptions to the DNA replication process. Together, this may confer a unique survival advantage for cells with acquired butyrate resistance.
Mar 2014 DOI 10.14302/issn.2372-6601.jhor-13-362
A narrative review summarizes how fenofibrate influences cancer cell metabolism and proliferation. It reviews PPAR‑α–dependent and independent mechanisms, context‑specific effects, and implications for repurposing studies.
Apr 2023
Through T-cell engineering, researchers at the California South University (CSU) Cancer Research Institute (CRI) have shown that tumor growth can be stopped in a variety of cancers and prevented from spreading to other tissues. Findings from this study are the result of decades of research by Professor Ph.D. A. Heidari and our team of CSU, who discovered a protein called AH that can inhibit the growth and spread of cancer cells in several different ways. They become in the tissues of the body. The T cells were armed with MDA-7/AH to target cancer more widely. The engineering of T cells to produce MDA-7/AH causes cancer cells to be destroyed regardless of the expression of the target molecules. The tumor site is often very hostile to immune cells. It was found in the research that MDA-7/AH can help T cells proliferate and increase the number of cancer cells. The T cells were armed with MDA-7/ AH to target cancer more widely. The engineering of T cells to produce MDA-7/AH causes cancer cells to be destroyed regardless of the expression of the target molecules. The tumor site is often very hostile to immune cells. We discovered that MDA-7/AH can help T cells proliferate and increase the number of cancer cells.
Oct 2022 DOI 10.14302/issn.2572-3030.jcgb-22-4284
Upon considering the anticancer effects of larger oligomeric proanthocyanidins and observing various papers reporting the high resolution mass spectroscopy of the oligomeric proanthocyanidins, it is determined that the unusual 13C enrichment in some plant oligomeric proanthocyanidins may be responsible for the anticancer activities of these food products. Such correlation of the 13C in the oligomeric proanthocyanidins also correlate with their scavenging of free-radicals, anti-virial and anti-bacterial properties. Proanthocyanidins in grape seeds are observed to have high enrichment in heavy isotopes of 2H, 13C, 15N and/or 17O. Mass analysis of DNA from human cancer cells are compared to normal human cells and cancer cells show bond specific enrichment of heavy isotopes in nucleotides G, A, T and C. On such basis, this study suggests possible stronger interactions of proanthocyanidins with DNA in cancer verses DNA in normal cells due to heavy isotope bond specific enrichments in both proanthocyanidins and the cancer DNA. Such 13C interactions from oligomeric proanthocyanidins with nucleic acids and proteins involved in replications, transcriptions and translations in cancer cells for interacting and chemically altering anabolism and cell division of the cancer cells are consistent with the author’s mechanism for normal cell to cancer cell transformations via possible replacements of primordial 1H, 12C, 14N, 16O, and 24Mg isotopes by nonprimordial 2H, 13C, 15N, and 17O and 25Mg isotopes in the proteins and nucleic acids. Such is also consistent with the proposed treatment for cancer by the author by use of foods containing proteins, nucleic acids, carbohydrates and/or drug molecules enriched with the nonprimordial isotopes of 2H, 13C, 15N, and 17O and 25Mg.
Mar 2022 DOI 10.14302/issn.2471-7061.jcrc-22-4139
We examined special roles of the Central Nervous System (CNS) in an attempt to resolve the puzzle that chronic diseases cannot be cured in medicine. By exploring a skill-learning model, we found that the CNS is able to remember certain information reflecting biochemical and cellular (B&C) processes in the body. From the skill-using ability, we found that the CNS is able to control basic B&C processes that drive and power the skill. From the ability to adjust forces and moving direction of body parts, we infer that the CNS is able to adjust B&C processes that control physical acts. From this controlling capability, we inferred that the CNS must also store certain information on the baseline B&C processes, is able to up-regulate or down-regulate the B&C processes, and make comparisons in performing its regulatory functions. We found that chronic diseases are the results of deviated baseline B&C processes, the CNS plays a role in maintaining deviated baseline B&C processes, and protects the body state of a fully developed disease. The three CNS roles can explain that cancer progresses with increasing malignancy, cancer quickly returns after a surgery, cancer cells repopulate after chemotherapy and radiotherapy, cancer patients develop drug resistance inevitably, immune cells rebound after suppression, etc. We further showed that long-term exercises generally can correct part of the departures in B&C processes and thus help to reverse chronic diseases. Finally, we propose strategies for resetting the CNS’ state memory as an essential condition for curing chronic diseases and cancer.
Feb 2022
Cancer cells need strong drug to be eliminated. Cancer lesions cure could achieve by topical application of crude bee venom. Bee venom medication used to prevent malignancies in groups most at risk (predisposing factors). Bee venom crosses the blood brain barriers because its components are very small. However, Bee venom contraindicated administered by intravenous injection because it’s hemolytic substance, mellitin which is powerful anticoagulant. However, the cationic peptides mellitin govern the mode of action of bee venom as anticancer and antiviral in vivo; 1 there is a negative charge on cancer cells, viral infected cells, diseased cells, and generally any cells that contain toxins or damage, and viruses are carrying negative charge even when it is outside the living body. 2Bee venom component (melittin) carries a positive charge, it destruct negatively charged cancer cells. 3 The role that the herpes virus is likely to play in increasing the severity of cancerous diseases, worsen the conditions: herpes viruses are opportunistic viruses that strike the body whose immunity is weakened for any reason. Therefore, the role of herpes virus must be neutralized when you planning to treat a cancer patient. Fortunately, bee venom is a powerful antiviral, and thus we hit three birds with one stone, that is, we kill cancer cells, kill opportunistic viruses, and improve tissue immunity to participate in the fight against cancer and get rid of toxic exudates more efficiently.
Feb 2022
Using samples of small cell lung tumors, a research team led by biologist Dr. Raymond discovered two new ways to induce tumor cell death. By activating ferroptosis, one of two subtypes of tumor cells can be targeted: first, iron-dependent cell death due to oxidative stress, and second, oxidative stress. Therefore, cell death can also be induced in a different way. Both types of cell death must be caused by drugs at the same time to eliminate the majority of the tumor mass. It is currently in clinical trials for cancer treatment. Auranofin, which inhibits the production of protective antioxidants in cancer cells, has been used to treat rheumatoid arthritis for decades. Future clinical trials using this combination therapy will determine the extent to which this targeted treatment option improves the prognosis of small cell lung cancer patients. It is currently in clinical trials for cancer treatment. Lung cancer is the leading cause of cancer death in the United States. Despite evidence of molecular abnormalities in biological specimens, progress in this disease is hampered by the lack of diagnostic markers useful for clinical practice. The majority of patients with lung cancer are still diagnosed at an advanced stage, when prognosis is poor. This article reviews new strategies being studied for the early detection of lung cancer. These strategies involve new methods of imaging (including low-dose computed tomography CT scanning), DNA analysis, and proteomic-based techniques. These strategies have not only improved our understanding of lung cancer but show promise in offering better survival to patients with this deadly disease. Of paramount importance in the search for methods of early detection is the need for the identification of the ideal population to screen, a multidisciplinary approach, and validation of promising techniques.
Dec 2020
This article has been retracted on March 01, 2021. VIEW THE RETRACTION NOTICE (https://openaccesspub.org/jsce/article/2243) Background Apis Mellifera L venom (Honeybees) is potent and safe anticancer drug. The present case is Basal Cell Carcinoma (SBCC), recurrent and invasde the skin of head (upper right, in front of the right ear). The patient was 65 years old in time of first intervention and the origin of BCC was primarily seen as abnormal growths and changes in birth mole on right side of head. Materials & Methods Preparation Bee Venom solution: Bee venom powder (crude) of dose 1gm was dissolved in 1000 ml of sterile distilled water then filtered by 0.22 micron syring filter. That final concentration of the stock bee venom become 1 ug /ml (i.e. 1ul=1 ug), and kept at -20◦C. (1mg (dried BV) + 1ml (water) = Final concentration (1ug/1 ul)). Before this novel intervention, allergy test performed by subcutaneous injection of small dose of bee venom (0.1 ml) and wait for at least one hour. The patient was not hypersensitive to honeybees’ venom. First stage of treatment: 1- Syringe of 1ml volume was used for direct local injection of cancer area by 0.3 ml from prepared Honeybees venom (0.1 % conc.). 2- At the same time, subcutaneous injection of 0.5 ml of bee venom solution infiltrated around the affected ear. 3- Topical application of the bee venom ointment 2% (bee venom in Vaseline) inside affected ear to protect the ear drum. This process repeated daily with cleaning of the ear every time by suitable safe and sterile saline solutions. 2nd stage: daily S/C injection in axillary area upper lymph nodes of 0.3 ml / bee venom ‘total doses 0.6 ml BV’ (left & right). 3rd stage: bee venom dissolved in sterile Clove oil was applied on inner ear above the drum. 4th stage: Management of healing process was enhanced by ascorbic acid solution as topical application on dead cancer cells and to help in removal of exudates and debris. Results The complete removal of malignant growths in affected ear achieved after 1 month from first bee venom injections. However; the cancerous areas under the second surgical intervention were treated during the next month. Conclusions Apis Mellifera L venom as anticancer drug is totally different from using direct stings as a method of Apitherapy, that because collection of bee venom lead to evaporating of most allergic substance that present in bees stings, also it can be used per os in people who exhibit different degrees of allergy against the drug safely.
Mar 2020 DOI 10.14302/issn.2372-6601.jhor-20-3235
Introduction Acute leukaemia are the clonal and malignant proliferation of immature hematopoietic cells (blast), blocked in their differentiation process. There is an interaction between cancer cells and the clotting process. This could be the expression of Tissue Factor (TF) on the surface of tumor cells; or a lesion of the vascular endothelium and platelet activation. The result is an activation of clotting that can lead to disseminated Intravascular Coagulation (DIC). The objective of this study was to assess the risk of DIC occurring in patients with acute leukaemia. Methods This was a cross-sectional study for analytical purposes that took place on 40 frozen samples from the biobank of the haematology laboratory of Teaching Hospital Yopougon for which the diagnosis of acute leukaemia had been taken from myelogram. The myelogram results were accompanied by hemogram data. PTTa, QT, fibrinogen and D-Dimers were performed on these samples. The risk assessment of DIC occurred was determined on the recommendations of the International Society of Thrombosis and Hemostasis (ISTH). Results We noted a female predominance with a Sex Ratio (M / F) of 0.90. The average age of the patients was 38 years (± 23 years) with extremes ranging from 2 to 84 years. ALL represented 20 % of cases against 80 % for AMLs. Hemogram parameters were characterized by severe anaemia (Tx Hb < 6 g / dL) in 52.5 % of cases; hyperleukocytosis > 100.103 / mm3 in 35 % of cases; thrombocytopenia < 25.103 / mm3 in 40 % of case; and significant blood and spinal cord blastosis (> 80 %). The lengthening of the PTTa was observed in 50 % of cases, compared to 40% for the QT. Similarly, hyperfibrinemia was present in 65% of cases. D-Dimers were high in almost all subject (95 % of cases). According to the ISTH criteria, 17.5 % of subjects were at risk of developing a DIC. Conclusion The risk of occurrence of DIC is indeed present during acute leukaemia. The parameters of haemostasis are thus found to be crucial data in the follow-up assessment during the diagnosis of acute leukaemia.
Nov 2019 DOI 10.14302/issn.2689-5773.jcdp-19-3061
Novel cancer therapeutics are superior and prevalent in the current scenario although a subset may not be satisfactorily alleviated or undergo disease relapse with the adoption of conventional chemotherapeutic agents. Cancer cells can comfortably elude immune destruction as interaction of cancer cells with native immune cells within tissue microenvironment is a cogent factor in evasion of cancer cells from pertinent immune surveillance. Thus, cancer immunotherapy can be safely contemplated as an efficacious and contemporary treatment modality for managing various malignant disorders.
Aug 2018 DOI 10.14302/issn.2639-1716.jn-18-2208
Breast cancer (BC) is the leading cause of cancer-related deaths in young to middle-aged women worldwide. Moreover, the survival rate in BC-patients is only 20% when associated with metastatic disease. The high mortality rate observed in BC women with metastatic disease has precipitated a major challenge revealing an unmet need to develop new therapeutic strategies in treating metastatic cancer. One such approach has involved utilization of chemokines and their receptors as therapeutic targets for cancer metastasis. It has been established that a definitive correlation exists between overexpressed CXCR4 malignant cell receptors and cancer cell growth, invasion, and migration. It is also widely accepted that the CXCR4 receptor, complexed to its CXCL12 ligand, plays a major role in establishing migratory pathway gradients for cancer cells migrating to distant tissues/organ sites. It would follow that chemokine decoy ligands, such as peptide antagonists and inhibitors, could serve to induce receptor blockade and impede subsequent intracellular signaling. Such ligands, synthetic and natural, reportedly contribute to reducing cancer cell growth, invasion, adherence, and migration. The present commentary describes several existing synthetic CXCR4 receptor-ligand peptide antagonists and presents a strategy to develop naturally-occurring human protein-derived peptide candidates.
Mar 2018 DOI 10.14302/issn.2639-1716.jn-18-1993
Cardiovascular disease and lung cancer are two of the most common causes of death in the United States. The cardioprotective benefits of statin class drugs is predominantly mediated through the inhibition of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase, decreasing available mevalonate, and thus limiting in vivo cholesterol biosynthesis. Mevalonate and its metabolites have significant roles in cellular membrane synthesis, which is dysregulated during tumorigenesis, and is therefore a potential source for anti-tumor effects of statins. Similarly, dysregulation of cellular signaling is a hallmark of tumorigenesis. In vitro studies of EGFR, RAS, and AKT signaling pathways in cancer cells can all be reformed back to states more indicative of normally functioning cells when treated with statins. Statins have also been shown to exert beneficial properties in the presence of chemotherapeutic medications and radiation therapies by modulating the deleterious effects of reactive oxygen species, decreasing tumor cell resistance, and minimizing damage to surrounding native tissues. There is abundant of in vitro evidence to support the beneficial effects of statins on lung cancer patients. Prospective studies to determine the value of statin therapy on lung cancer prevention could lead to a significant change in lung cancer treatment.
Feb 2014 DOI 10.14302/issn.2372-6601.jhor-13-346
Targeting cell metabolism is a therapeutic approach which has been used for the treatment of cancers with high levels of proliferation. Inhibition of metabolic processes in cancer cells has shown synergy with current therapeutic options to reduce refractory disease and relapse. In contrast, chronic lymphocytic leukaemia (CLL) is a disease where expansion of the malignant clone results from a combination of enhanced cell survival coupled with low level proliferation. The purpose of this article is to highlight how further research is needed to determine whether targeting cell metabolism may be a viable therapeutic strategy in this disease. We discuss how lymphocyte doubling time (LDT) remains a robust prognostic indicator used in the current clinical management of CLL, and how recognition of CLL as a proliferative disease has led to a greater understanding of the importance of energy-generating processes in its pathobiology. We summarize what is currently known about normal B cell metabolism and consider whether there is evidence of the Warburg effect in CLL cells. Finally, we speculate on how CLL cells may exploit protective mechanisms such as autophagy during times of metabolic stress and how they might influence or be influenced by metabolic characteristics of the microenvironment.
Sep 2013 DOI 10.14302/issn.2326-0793.jpgr-13-257
Lapatinib, a small molecule tyrosine kinase inhibitor is currently used in the treatment of HER2-positive breast cancer. The aim of this study was to further understanding of lapatinib response for the development of novel treatment lapatinib-focussed treatment strategies. HER2-overexpressing SKBR3 breast cancer cells were treated with lapatinib for 12 hours and the resultant proteome analyzed by a comprehensive ion-current-based LC-MS strategy. Among the 1224 unique protein identified from SKBR3 cell lysates, 67 showed a significant change in protein abundance in response to lapatinib. Of these, CENPE a centromeric protein with increased abundance, was chosen for further validation. Knockdown and inhibition of CENPE demonstrated that CENPE enhances SKBR3 cell survival in the presence of lapatinib. Based on this study, CENPE inhibitors may warrant further investigation for use in combination with lapatinib.