Mesenchymal stem cells (MSCs), a kind of multipotent stem cells with self-renewal ability and multi-differentiation ability, have become the "practical stem cells" for the treatment of diseases. MSCs have immunomodulatory properties and can be used to treat autoimmune diseases, such as systemic lupus erythematosus (SLE) and Crohn's disease. MSCs also can be used in cancer and aging. At present, many clinical experiments are using MSCs. MSCs can reduce the occurrence of inflammation and apoptosis of tissue cells, and promote the proliferation of endogenous tissue and organ cells, so as to achieve the effect of repairing tissue and organs. MSCs presumably also play an important role in Corona Virus Disease 2019 (COVID-19) infection. Keywords Mesenchymal stem cells • Autoimmune diseases • Aging • Inflammation • Cancer • COVID-19 Abbreviations AA Alginate ARDS Acute respiratory distress syndrome BM-MSCs Bone marrow mesenchymal stem cells BMP-2 Bone morphogenetic protein 2 CBX4 Chromobox protein homologue 4 CRISPR Clustered Regularly Interspaced Short Palindromic Repeats Cas9 CRISPR-associated protein-9 nuclease Col Collagen COPD Chronic obstructive pulmonary disease COVID-19 Corona Virus Disease 2019 CRC Colorectal cancer CXCR7 C-X-C chemokine receptor type 7 CXCL12 C-X-C motif chemokine ligand 12

IntroductionThis study developed a prognostic nomogram of Hodgkin lymphoma (HL) for purpose of discussing independent risk factors for HL patients with Surveillance, Epidemiology and End Results (SEER) database.MethodsWe collected data of HL patients from 2010 to 2015 from the SEER database and divided it into two cohorts: the training and the verification cohort. Then the univariate and the multivariate Cox regression analyses were conducted in the training, the verification as well as the total cohort, after which the intersection of variables with statistical significance was taken as independent risk factors to establish the nomogram. The predictive ability of the nomogram was validated by the Concordance Index. Additionally, the calibration curve and receiver operating characteristic curve were implemented to evaluate the accuracy and discrimination. Finally, we obtained 1-year, 3-year and 5-year survival rates of HL patients.Results10 912 patients were eligible for the study. We discovered that Derived American Joint Committee on Cancer (AJCC) Stage Group, lymphoma subtype, radiotherapy and chemotherapy were four independent risk factors affecting the prognosis of HL patients. The 1-year, 3-year and 5-year survival rates for high-risk patients were 85.4%, 79.9% and 76.0%, respectively. It was confirmed that patients with stage I or II had a better prognosis. Radiotherapy and chemotherapy had a positive impact on HL outcomes. However, patients with lymphocyte-depleted HL were of poor prognosis.ConclusionsThe nomogram we constructed could better predict the prognosis of patients with HL. Patients with HL had good long-term outcomes but novel therapies are still in need for fewer complications.

Background. Histone deacetylase 3 (HDAC3) plays an important role in the development and progression of a variety of cancers, but its regulatory mechanism in acute myeloid leukemia (LAML) is not entirely understood. Methods. We analyzed the expression of HDAC3 in normal and cancerous tissues using Oncomine, UALCAN, and GEO databases. Changes of the HDAC3 gene were analyzed by cBioPortal. The genes coexpressed with HDAC3 were analyzed by WebGestalt, and the predicted signaling pathways in KEGG were discussed. Results. We discovered that the expression of HDAC3 was elevated in some types of acute myeloid leukemia. The HDAC3 gene has a strong positive correlation with SLC25A5, NDUFA2, Cox4I1, and EIF3K, which regulate cell growth and development. HDAC3 transcription is higher in patients with FLT3 mutation than in healthy people. HDAC3 can be directly involved in regulating the thyroid hormone signaling pathway. MEF2D is directly involved in the cGMP-PKG signaling pathway, and the HDAC3 gene has a strong synergistic relationship with MEF2D. HDAC3 is indirectly involved in the cGMP-PKG signaling pathway, thereby indirectly regulating the expression levels of p53 and p21 genes in patients with LAML. Genomics of Drug Sensitivity in Cancer (GDSC) database analysis revealed that the application of the HDAC3 inhibitor can inhibit the proliferation of leukemia cells. Conclusions. Therefore, our data suggest that HDAC3 may be a possible therapeutic target for acute myeloid leukemia.

Background and Aims. Histone deacetylase 1 (HDAC1) codes a protein that is a component of the histone deacetylase complex. The abnormal expression of HDAC1 is strongly correlated with cell proliferation, differentiation, transcription, and translation. Through continuous screening of genes associated with changes in lung adenocarcinoma (LUAD), gene networks are formed to explore tumor pathogenesis and new therapeutic targets. Methods. We evaluated HDAC1 gene survival analysis and its expression of LUAD using relevant websites and databases (TCGA and GEO databases). Through data mining, we determined the frequency and type of HDAC1 mutation, obtained the relevant heat map of the gene interaction network, completed the analysis of gene ontology and function enrichment, and understood the pharmaceutic of HDAC1. Results. We found that HDAC1 expression was associated with the prognosis of patients with LUAD. In gene expression analysis, HDAC1 was highly expressed in LUAD, and the HDAC1 interaction gene network (MARCKSL, eIF3I) was closely related to cellular gene expression. Functional network analysis shows that the expression of HDAC1 is related to the monitoring point of the G1-S phase of the cell cycle and the activation of the Notch signaling pathway (CSL transcription factor), which is involved in the process of cell proliferation and differentiation and gene expression associated with new therapeutic targets. Conclusion. Our data revealed the expression and potential regulatory factors of HDAC1 in LUAD of data mining, which laid a foundation for the study of the occurrence, development, and treatment of HDAC1 in LUAD.

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