BackgroundOur earlier work has shown that a unique stem cell-based vaccine that comprises of murine embryonic stem cells (ESCs) and murine fibroblasts expressing the immunostimulant granulocyte-macrophage colony stimulating factor (GM-CSF) successfully protects mice from the outgrowth of an implantable form of murine lung cancer. The use of live ESCs raises the potential risks of inducing teratomas and autoimmunity. We have attempted to improve the safety and utility of this prophylactic vaccine by employing exosomes derived from murine ESCs engineered to produce GM-CSF (ES-exo/GM-CSF vaccine).MethodsWe have previously reported that ES-exo/GM-CSF immunization does protect mice from the outgrowth of an implantable form of murine lung cancer. Here, we have investigated the cancer prevention efficacy of ES-exo/GM-CSF vaccine in an experimental metastasis model of murine lung cancer, in which Lewis lung carcinoma (LLC) cells were administered into female C57BL/6 mice (8 weeks of age) through tail vein injection and subsequently LLC tumors were established in lungs.ResultsOur objective is to test the anti-cancer efficacy of ES-exo/GM-CSF vaccine in a mouse model of metastatic lung cancer. Our studies indicate that vaccination of mice with ES-exo/GM-CSF vaccine inhibited the growth of metastatic lung tumors. ES-exo/GM-CSF vactionation reduced lung tumor burden from 1.86% in non-vaccinated, LLC-challenged mice to 0.036% in corresponding vacinnated mice. Importantly, control exosomes without GM-CSF failed to provide protection against metastasized pulmonary tumors. The efficacy of ES-exo/GM-CSF vaccination was associated with a decrease in the frequencies of tumor-infiltrating immunosuppressive immune cells, including T regulatory cells, myeloid derived suppressor cells (MDSCs) and tumor-associated macrophages, as well as an increase in effector cytokine production from intra-tumoral CD8+ T cells.ConclusionsOverall, our research provides a novel strategy for developing a cell-free prophylactic vaccine against lung tumors.

[This corrects the article DOI: 10.21037/sci-2020-021.].

Wound healing phases comprise of highly synchronized process that begins due to a damage and restores the integrity of the injured tissues. Wound healing reduces the damage in tissue and supply sufficient oxygen and tissue perfusion, provide proper nourishment and humid wound healing atmosphere to re-establish the essential status of exaggerated parts. The untreated wound becomes susceptible for pus development, bacterial infection and complications like sepsis. Traditional and modern approaches are in practice to treat acute, open and chronic injuries, however, present wound care management has met with challenges and minimal positive effects. Stem cells have possible wound healing capability to overwhelm restrictions of the current wound care practices as it produces faster tissue regeneration in wound repair. Stem cells are unspecialized cells derived from adult body tissues and embryos that differentiate into any cell of an organism and capable of self-regeneration. The understanding on molecular mechanisms of stem cells has become the central and promising field in scientific study. This review focuses on the pre-existing traditional and modern treatments for wound healing, and types and roles of stem cells in wound care management. This review also focuses on the fundamental molecular characterization and factors influencing the molecular mechanisms of stem cells in wound healing.

Platelet-rich plasma (PRP) contains pro-angiogenic growth factors including vascular endothelial growth factor (VEGF). Angiogenesis is a necessary component of wound healing in instances of diabetic foot ulcers (DFU). PRP composition varies depending on methods and donor health status. Our group has developed an improved PRP protocol for diabetes treatment. The aims of this study were to examine the levels of the pro-angiogenic factor VEGF in these patient populations with and without diabetes. PRP was prepared using 24 mL of whole blood from 13 diabetic and 10 non-diabetic patients registered at Klinik Hayandra. Whole blood in sodium citrate tubes were centrifuged at 1,000 rpm for 5 minutes followed by plasma separation. Plasma samples were centrifuged at 3,000 rpm for 5 minutes. Upper platelet-poor plasma layers were discarded, leaving 5 mL of concentrated platelet containing plasma (PRP). Concentrated plasma samples were mixed, aliquoted, stored at -86 °C, and pooled for platelet count, VEGF, and total protein analyses. Platelet counting was also performed using fresh whole blood and PRP to measure changes following PRP preparation. Diabetic donors had higher whole blood platelet counts than non-diabetic donors, but this difference was not statistically significant. An average increase of more than 250% in platelet number after PRP preparation using our method was noted in both groups. Freezing-thawing samples at -86 °C lysed more than 90% of PRP platelets regardless of diabetes status. Diabetic PRP had lower mean total protein and higher VEGF concentrations. Lysed platelets from diabetic donors released more VEGF than those from non-diabetic donors. PRP from diabetic donors had higher VEGF content making autologous PRP application a promising treatment for DFU. However, this should be investigated another appropriate clinical trial.

Hematopoietic stem cell transplantation has been applied to treat the hematologic malignancies since the 1980s. However, allogenic transplantation has inherent complications such as graft-versus-host disease and graft failure. Autologous transplantation has become more and more popular because of its lower transplant-related mortality. This study was performed to analyze the possible prognostic factors for myeloma patients post stem cell transplantation. Patients' information was collected by history review and follow-up through the phone call. Kaplan-Meier was used to exhibit overall survival (OS) and progression-free survival (PFS). Univariate and multivariate analyses were performed using Cox proportional hazards model. A P<0.05 is considered statistically significant. Thirty patients with multiple myeloma were included in this study, 7 of them died because of myeloma relapse and myeloma-associated complications. The average survival time was 29.8 months and the median follow-up was 25.1 months. The 1-year OS and PFS were 93.3% and 90.0%, respectively. Both the 3-year OS and PFS were 76.7%. In a variety of factors, improved renal function showed a good effect on the outcome of transplantation. To prevent cancer relapse after autologous transplantation, it is of great significance to achieve a complete remission prior to the transplantation.

It is still one of the most intriguing questions in biology, how the multitudes of cell types a single organism possesses, are adequately born during development. It is clear that there are transcription factors with sufficient activity to drive cells towards specific cell identities, however to date the known genes are limited to a handful of linages (e.g., pluripotency, neurogenesis, β-cell development, etc.) and even in these cases we are far from a comprehensive understanding of contributing factors and molecular mechanisms.

Cancer is a genetic disease which results in a functional imbalance between tumour-repressive and oncogenic signals. The WHO highlights the burden of this indomitable disease, listing it as the second leading cause of death globally. The major cause of cancer-related death is rarely the effect of the primary tumour itself, but rather, the devastating spread of cancer cells in metastases. Epithelial-mesenchymal plasticity (EMP)-termed as the ability of cells to maintain its plasticity and transit between epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) states-plays a fundamental role in cancer metastasis. These cell transitions allow them migrate from the primary tumour and invade the secondary site. EMP is associated with migration, invasion, colonisation, self-renewal and drug resistance. This review briefly elucidates the mechanism of EMP and the association between cancer stem cells (CSCs) and circulating tumour cells (CTCs), biomarkers and signalling pathways involved in EMP as well as drug resistance and therapeutic targeting.

Signaling pathways integrate extracellular cues into intracellular gene expression profiles. Cell proliferation and differentiation are governed by many different signaling pathways that relay the extracellular spatiotemporal signals into the appropriate pattern of gene regulation within cells. There is complex interconnection and cross-talk between the signaling pathways during the process of development and regeneration, including during skeletal muscle regeneration and development. Wnt signaling has been shown to play an essential role in the regulation of the myogenic regulatory factors (MRFs) during embryonic development and adult muscle regeneration (1-3). Any alteration in signaling pathway input can lead to diseased conditions, including cancer.