GBP5 Expression Predicted Prognosis of Immune Checkpoint Inhibitors in Small Cell Lung Cancer and Correlated with Tumor Immune Microenvironment.

Background: The discovery and development of immune checkpoint inhibitors (ICIs) has significantly enhanced the arsenal of immunotherapy treatments available for cancer patients. The identification of biomarkers that are indicative of an individual's sensitivity to treatment with ICIs is useful for screening SCLC patients prior to commencement of any ICIs based immunotherapy. However, the relationship between GBP5 and the prognosis of SCLC immunotherapy is still unclear and requires further study.

FOXD3 confers chemo-sensitivity in ovarian cancer through a miR-335/DAAM1/myosin II axis-dependent mechanism.

Background: Chemotherapy is among the most common treatment methods for ovarian cancer (OC). However, chemoresistance limits the effectiveness of chemotherapy and leads to treatment failure. We herein investigate the biological effect of forkhead box D3 (FOXD3) in the chemoresistance of OC cells.

The impact of low intensity ultrasound on cells: Underlying mechanisms and current status.

Low intensity ultrasound (LIUS) has been adopted for a variety of therapeutic purposes because of its bioeffects such as thermal, mechanical, and cavitation effects. The mechanism of impact and cellular responses of LIUS in cellular regulations have been revealed, which helps to understand the role of LIUS in tumor treatment, stem cell therapy, and nervous system regulation. The review summarizes the bioeffects of LIUS at the cellular level and its related mechanisms, detailing the corresponding theoretical basis and latest research in the study of LIUS in the regulation of cells.

Noninvasive prenatal testing for β-thalassemia by targeted nanopore sequencing combined with relative haplotype dosage (RHDO): a feasibility study.

Noninvasive prenatal testing (NIPT) for single gene disorders remains challenging. One approach that allows for accurate detection of the slight increase of the maternally inherited allele is the relative haplotype dosage (RHDO) analysis, which requires the construction of parental haplotypes. Recently, the nanopore sequencing technologies have become available and may be an ideal tool for direct construction of haplotypes.

The safety and effectiveness of genetically corrected iPSCs derived from β-thalassaemia patients in nonmyeloablative β-thalassaemic mice.

Background: β-Thalassaemia is a clinically common cause of hereditary haemolytic anaemia stemming from mutations in important functional regions of the β-globin gene. The rapid development of gene editing technology and induced pluripotent stem cell (iPSC)-derived haematopoietic stem cell (HSC) transplantation has provided new methods for curing this disease.

Methods: Genetically corrected β-thalassaemia (homozygous 41/42 deletion) iPSCs that were previously established in our laboratory were induced to differentiate into HSCs, which were transplanted into a mouse model of IVS2-654 β-thalassaemia (B6;129P2-Hbb/J mice) after administration of an appropriate nonmyeloablative conditioning regimen.

MYCN-mediated regulation of the HES1 promoter enhances the chemoresistance of small-cell lung cancer by modulating apoptosis.

MYCN, a member of the MYC family, is correlated with tumorigenesis, metastasis and therapy in many malignancies; however, its role in small-cell lung cancer (SCLC) remains unclear. In this study, we sought to identify the function of MYCN in SCLC chemoresistance and found that MYCN is overexpressed in chemoresistant SCLC cells. We used MYCN gain- and loss-of- function experiments to demonstrate that MYCN promotes in vitro and in vivo chemoresistance in SCLC by inhibiting apoptosis.

Noninvasive prenatal diagnosis of β-thalassemia by relative haplotype dosage without analyzing proband.

Background: β-thalassemia is one of the most common monogenic diseases in the world. Southeast China is a highly infected area affected by four β-thalassemia mutation types (HBB:c.-78A>G, HBB:c.

Salvage radiotherapy improves survival in patients with locoregionally relapsed stage IE-IIE extranodal natural killer/T-cell lymphoma, nasal type.

Background: This study aims to retrospectively analyze the salvage treatment outcomes and prognostic factors of patients with early stage locoregionally recurrent (LRR) extranodal natural killer (NK)/T-cell lymphoma, nasal type (ENKTCL).

Methods: Between January 1995 and December 2014, 540 patients with stage IE-IIE ENKTCL received chemotherapy (ChT) and/or radiotherapy (RT) in our hospital, and among these, 56 patients who experienced LRR were included in this study. Salvage treatments included RT alone in 4 patients (7.

Antioxidants retard the ageing of mouse oocytes.

The aim of the present study was to verify the effects of heavy metal coupling agents (sodium citrate and EDTA) and antioxidants (acetyl carnitine and lipoic acid) on the number of oocytes, as well as the ageing of mitochondria, chromosomes and spindles in mice. C57BL/6 female mice were randomly classified into four groups (n=12 per group): i) Heavy metal coupling agent; ii) antioxidant; iii) mixed group; and iv) the normal control group. For the treatments, heavy metal coupling agents and antioxidants were added to the drinking water provided to the mice.

CRISPR/Cas9-Targeted Deletion of Polyglutamine in Spinocerebellar Ataxia Type 3-Derived Induced Pluripotent Stem Cells.

Spinocerebellar ataxia type 3 (SCA3) is caused by an abnormal expansion of the cytosine-adenine-guanine (CAG) triplet in ATXN3, which translates into a polyglutamine (polyQ) tract within ataxin-3 (ATXN3) protein. Although the pathogenic mechanisms remain unclear, it is well established that expression of mutant forms of ATXN3 carrying an expanded polyQ domain are involved in SCA3 pathogenesis, and several strategies to suppress mutant ATXN3 have shown promising potential for SCA3 treatment. In this study, we described successful clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-mediated deletion of the expanded polyQ-encoding region of ATXN3 in induced pluripotent stem cells (iPSCs) derived from a SCA3 patient, and these patient-specific iPSCs retained pluripotency and neural differentiation following expanded polyQ deletion.

Generation of GZKHQi001-A and GZWWTi001-A, two induced pluripotent stem cell lines derived from peripheral blood mononuclear cells of Duchenne muscular dystrophy patients.

Duchenne muscular dystrophy (DMD) is an X-linked disease caused by mutations in the DMD gene, which spans ~2.4Mb of genomic sequence at locus Xp21. This mutation results in the loss of the protein dystrophin.

Generation of integration-free induced pluripotent stem cells (GZHMUi001-A) by reprogramming peripheral blood mononuclear cells from a 47, XXX syndrome patient.

47, XXX syndrome is one of several sex-chromosomal aneuploidies, and it has an incidence of approximately 1/1000 in newborn females. Because of heterogeneity in X-inactivation, these patients may exhibit a variety of clinical symptoms. Here, we report the generation of an integration-free human induced pluripotent stem cell line (GZHMUi001-A) by using Sendai virus to reprogram peripheral blood mononuclear cells from a 47, XXX syndrome patient with premature ovarian failure.

Autophagy Promoted the Degradation of Mutant ATXN3 in Neurally Differentiated Spinocerebellar Ataxia-3 Human Induced Pluripotent Stem Cells.

Spinocerebellar ataxia-3 (SCA3) is the most common dominant inherited ataxia worldwide and is caused by an unstable CAG trinucleotide expansion mutation within the gene, resulting in an expanded polyglutamine tract within the ATXN3 protein. Many studies have examined the role of autophagy in neurodegenerative disorders, including SCA3, using transfection models with expression of pathogenic proteins in normal cells. In the current study, we aimed to develop an improved model for studying SCA3 using patient-derived cells.