Novel ectopic expression of zona pellucida 3 glycoprotein in lung cancer promotes tumor growth.

Zona pellucida 3 (ZP3) expression is classically found in the ZP-layer of the oocytes, lately shown in ovarian and prostate cancer. A successful ZP3 ovarian cancer immunotherapy in transgenic mice suggested its use as an attractive therapeutic target. The biological role of ZP3 in cancer growth and progression is still unknown. We found that ~88% of the analyzed adenocarcinoma, squamous and small cell lung carcinomas to express ZP3. Knockout of ZP3 in a ZP3-expressing lung adenocarcinoma cell line, significantly decreased cell viability, proliferation, and migration rates in vitro. Zona pellucida 3 knock out (ZP3-KO) cell tumors inoculated in vivo in immunodeficient non-obese diabetic, severe combined immunodeficient mice showed significant inhibition of tumor growth and mitigation of the malignant phenotype. RNA sequencing revealed the deregulation of cell migration/adhesion signaling pathways in ZP3-KO cells. This novel functional relevance of ZP3 in lung cancer emphasized the suitability of ZP3 as a target in cancer immunotherapy and as a potential cancer biomarker.

Current insight into the transient X-zone in the adrenal gland cortex.

Mouse models have been widely used in the study of adrenal gland development and diseases. The X-zone is a unique structure of the mouse adrenal gland and lineage-tracing studies show that the X-zone is a remnant of the fetal adrenal cortex. Although the X-zone is considered analogous to the fetal zone in the human adrenal cortex, the functional significance of the X-zone has remained comparatively more obscure. The X-zone forms during the early postnatal stages of adrenal development and regresses later in a remarkable sexually dimorphic fashion. The formation and regression of the X-zone can be different in mice with different genetic backgrounds. Mouse models with gene mutations, hormone/chemical treatments, and/or gonadectomy can also display an aberrant development of the X-zone or alternatively a dysregulated X-zone regression. These models have shed light on the molecular mechanisms regulating the development and regression of these unique adrenocortical cells. This review paper briefly describes the development of the adrenal gland including the formation and regression processes of the X-zone. It also summarizes and lists mouse models that demonstrate different X-zone phenotypes.

DHCR24, a Key Enzyme of Cholesterol Synthesis, Serves as a Marker Gene of the Mouse Adrenal Gland Inner Cortex.

Steroid hormones are synthesized through enzymatic reactions using cholesterol as the substrate. In steroidogenic cells, the required cholesterol for steroidogenesis can be obtained from blood circulation or synthesized de novo from acetate. One of the key enzymes that control cholesterol synthesis is 24-dehydrocholesterol reductase (encoded by DHCR24). In humans and rats, DHCR24 is highly expressed in the adrenal gland, especially in the zona fasciculata. We recently reported that DHCR24 was expressed in the mouse adrenal gland's inner cortex and also found that thyroid hormone treatment significantly upregulated the expression of Dhcr24 in the mouse adrenal gland. In the present study, we showed the cellular expression of DHCR24 in mouse adrenal glands in early postnatal stages. We found that the expression pattern of DHCR24 was similar to the X-zone marker gene 20αHSD in most developmental stages. This finding indicates that most steroidogenic adrenocortical cells in the mouse adrenal gland do not synthesize cholesterol locally. Unlike the 20αHSD-positive X-zone regresses during pregnancy, some DHCR24-positive cells remain present in parous females. Conditional knockout mice showed that the removal of Dhcr24 in steroidogenic cells did not affect the overall development of the adrenal gland or the secretion of corticosterone under acute stress. Whether DHCR24 plays a role in conditions where a continuous high amount of corticosterone production is needed requires further investigation.

Comparison on the consistency of Mindray and Siemens chemiluminescence analyzers for detecting FT3, FT4 and TSH in patients with hyper- and hypothyroidism.

Background: To examine the consistency of the Mindray and Siemens full-automatic chemiluminescence analyzers in detecting serum free triiodothyronine (FT3), free thyroxine (FT4) and thyroid stimulating hormone (TSH) in patients with hyper- or hypothyroidism. Methods: Included in this study were 164 new patients with abnormal thyroid function assessed at Nan Fang Hospital of Southern Medical University in 2021: 107 patients with hyperthyroidism and 57 with hypothyroidism. Additional 100 healthy individuals comprised the control group. Consistency of the FT3, FT4 and TSH results from the two systems in the different groups was analyzed by Kappa, linear correlation, regression, Bland-Altman and area under the receiver operating characteristic curve (AUC). Results: Compared with the control group, FT3 and FT4 levels were increased and TSH level was decreased in the hyperthyroid group (both P<0.05), whereas FT3 and FT4 levels were decreased and TSH level was increased in the hypothyroidism group (both P<0.05), suggesting that both test systems could provide references for relevant clinical evaluation. Kappa analysis showed high consistency of the two systems in detecting FT3, FT4 and TSH in both hyper- and hypothyroidism patients (mean Kappa value >0.7). In addition, there was a good linear correlation between the test results of the two systems (R2>0.90). Bland-Altman consistency analysis showed that most mean difference values were within the consistency limit (x±1.96s), indicating that the difference between the two systems was acceptable. AUC of FT3, FT4 and TSH detected by the two systems was higher than 0.80 in each group, showing no significant difference between them (both P>0.05), and the difference in sensitivity and specificity was within the acceptable range. Conclusions: Mindray and Siemens chemiluminescence analyzers are highly consistent in detecting FT3, FT4 and TSH in both hyper- and hypothyroidism patients.

Early transcriptomic response of mouse adrenal gland and Y-1 cells to dexamethasone.

Glucocorticoids have short- and long-term effects on adrenal gland function and development. RNA sequencing (RNA-seq) was performed to identify early transcriptomic responses to the synthetic glucocorticoid, dexamethasone (Dex), in vitro and in vivo. In total, 1711 genes were differentially expressed in the adrenal glands of the 1-h Dex-treated mice. Among them, only 113 were also considered differentially expressed genes (DEGs) in murine adrenocortical Y-1 cells treated with Dex for 1 h. Gene ontology analysis showed that the upregulated DEGs in the adrenal gland of the 1-h Dex-treated mice were highly associated with the development of neuronal cells, suggesting the adrenal medulla had a rapid response to Dex. Interestingly, only 4.3% of Dex-responsive genes in the Y-1 cell line under Dex treatment for 1 h were differentially expressed under Dex treatment for 24 h. The heatmaps revealed that most early responsive DEGs in Y-1 cells during 1 h of treatment exhibited a transient response. The expression of these genes under treatment for 24 h returned to basal levels similar to that during control treatment. In summary, this research compared the rapid transcriptomic effects of Dex stimulation in vivo and in vitro. Notably, adrenocortical Y-1 cells had a transient early response to Dex treatment. Furthermore, the DEGs had a minimal overlap in the 1-h Dex-treated group in vivo and in vitro.

Congenital Hypothyroidism and Hyperthyroidism Alters Adrenal Gene Expression, Development, and Function.

Background: The human adrenal cortex undergoes several rapid remodeling steps during its lifetime. In rodents, similar remodeling occurs postnatally in the "X-zone" layer through unknown mechanisms. Furthermore, little is known regarding the impact of thyroid hormone (TH) on adrenal glands in humans. Methods: To investigate the impact of TH on adrenal pathophysiology, we created two genetic murine models mimicking human nonautoimmune hypothyroidism and hyperthyroidism. Moreover, we analyzed serum thyrotropin (TSH) and steroid hormone concentrations in patients diagnosed with congenital hypothyroidism and premature adrenarche (PA). Results: We found that TH receptor beta-mediated hypertrophy of the X-zone significantly elevated the adrenal weights of hyperthyroid women. In the hypothyroid model, the X-zone was poorly developed in both sexes. Moreover, large reciprocal changes in the expression levels of genes that regulate adrenal cortical function were observed with both models. Unexpectedly, up- and downregulation of several genes involved in catecholamine synthesis were detected in the adrenal glands of the hypothyroid and hyperthyroid models, respectively. Furthermore, TSH and adrenal steroid concentrations correlated positively in pediatric patients with congenital hypothyroidism and PA. Conclusions: Our results revealed that congenital hypothyroidism and hyperthyroidism functionally affect adrenal gland development and related steroidogenic activity, as well as the adrenal medulla.

Isolate Cell-Type-Specific RNAs from Snap-Frozen Heterogeneous Tissue Samples without Cell Sorting.

Cellular heterogeneity poses challenges to understanding the function of complex tissues at a transcriptome level. Using cell-type-specific RNAs avoids potential pitfalls caused by the heterogeneity of tissues and unleashes the powerful transcriptome analysis. The protocol described here demonstrates how to use the Translating Ribosome Affinity Purification (TRAP) method to isolate ribosome-bound RNAs from a small amount of EGFP-expressing cells in a complex tissue without cell sorting. This protocol is suitable for isolating cell-type-specific RNAs using the recently available NuTRAP mouse model and could also be used to isolate RNAs from any EGFP-expressing cells.

Exosomal miR-3180-3p inhibits proliferation and metastasis of non-small cell lung cancer by downregulating FOXP4.

BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the most malignant cancers worldwide and its pathogenesis is not completely clear. In this study, we explored the functions and mechanisms of exosomes transferring miR-3180-3p in NSCLC progression. METHODS: The expression levels of miR-3180-3p in NSCLC tissues and paracarcinoma tissues was obtained from the GEO database (GEO: GSE53882). Exosomes derived from A549 cells were identified. Proliferation, migration and invasion were measured after treatment with exosomal miR-3180-3p or transfection using miR-3180-3p mimics. The relationship between miR-3180-3p and forkhead box P4 (FOXP4) was predicted using a bioinformatic tool and measured using a dual-luciferase reporter gene assay and western blotting. Finally, a mouse xenograft model of NSCLC cells was established to verify the function of exosomal miR-3180-3p in vivo. RESULTS: We found that miR-3180-3p decreased in both NSCLC cell lines and patient tissues. Overexpression of miR-3180-3p or treatment with exosomal miR-3180-3p significantly suppressed cell proliferation and metastasis in NSCLC cell lines. Subsequently, we found miR-3180-3p downregulated FOXP4 protein expression levels. Furthermore, the volumes and weights of nude mouse tumors expressing exosomal miR-3180-3p were significantly reduced. CONCLUSIONS: Exosomal miR-3180-3p suppresses NSCLC progression by downregulating FOXP4 expression. KEY POINTS: SIGNIFICANT FINDINGS OF THE STUDY: We found that exosomal miR-3180-3p suppressed NSCLC progression and also identified a miR-3180-3p target gene. These findings provide a foundation to determine innovative therapeutic strategies. WHAT THIS STUDY ADDS: This study contributes to research investigating exosomal containing miRNAs.

Performance verification of a new domestic chemiluminescence detection system.

BACKGROUND: Procalcitonin (PCT) is an acute phase response protein, which can be used as an indicator for early diagnosis of infection. At present, the main detection methods for PCT are electrochemiluminescence and enzyme-linked immunofluorescence. We aimed to explore the accuracy of PCT determination in a domestic chemiluminescence detection system and its correlation with other systems. METHODS: Clinical specimens were collected, and the precision, linearity, biological reference interval, contamination rate, Clinical reportable scope, and methodological comparison of the determination of PCT in a Chinese chemiluminescence detection system were evaluated and preliminarily verified by referring to Clinical and Laboratory Standards Institute (CLSI) documents or industry standards. RESULTS: The results of precision verification showed that the coefficient of variation (CV) values of the variation coefficient of precision in the samples of low and high values were 2.07% and 0.83% respectively, while the CV values of the total variation coefficient of precision were 3.05% and 1.81% respectively; these findings all met the experimental requirements. The results of linear verification test showed that the linear range was 0.006-96.96 ng/mL, and the linear relationship was well within the detection range (R2 =0.9891). The biological reference interval and the carrying contamination rate were also verified. The clinical reportable range was 0.02-369.585 ng/mL. The results showed that the correlation coefficient between the Mindray CL900I and the Roche E602 was 0.9986, and that between the Mindray CL900I and the Snibe 2000 was 0.983. Meanwhile, when the PCT was higher than 0.1 ng/mL, the correlation coefficient was 100%. CONCLUSIONS: The domestic chemiluminescence detection system has a good performance in the determination of calcitonin, as indicated by the measures of precision, linearity, biological reference interval, carrying contamination rate, and Clinical reportable scope, and can thus be used for clinical specimen detection. The results of methodological comparison showed that the correlation coefficient between the Mindray CL900I and Roche E602 was 0.9986, while the correlation coefficient between the Mindray CL900I and the Snibe 2000 was 0.983. The test results were consistent with the experimental requirements.

Autophagy and Tumour Radiotherapy.

Radiotherapy is an important component of cancer treatment modalities. With the rapid development of three-dimensional conformal, intensity-modulated, image-guided radiotherapy and the efficacy of radiotherapy continues to improve. Autophagy, as a catabolic process, is characterized by the formation of a double-membrane vesicle. Radiotherapy is known to induce autophagy in both cancer and normal cells. Here, we reviewed the interaction of radiotherapy and autophagy in the process of cancer treatment. The potential role of autophagy modification in enhancing radiotherapy treatment will also be reviewed.

RNA-Seq Reveals Sub-Zones in Mouse Adrenal Zona Fasciculata and the Sexually Dimorphic Responses to Thyroid Hormone.

The sex-specific prevalence of adrenal diseases has been known for a long time. However, the reason for the high prevalence of these diseases in females is not completely understood. Mouse studies have shown that the adult adrenal gland is sexually dimorphic at different levels such as transcriptome, histology, and cell renewal. Here we used RNA-seq to show that in prepubertal mice, male and female adrenal glands were not only sexually dimorphic but also responded differently to the same external stimulus. We previously reported that thyroid hormone receptor ß1 (TRß1) in the adrenal gland is mainly expressed in the inner cortex and the fate of this TRß1-expressing cell population can be changed by thyroid hormone (triiodothyronine; T3) treatment. In the present study, we found that adrenal glands in prepubertal mice were sexually dimorphic at the level of the transcriptome. Under T3 treatment, prepubertal females had 1162 genes differentially expressed between the saline and T3 groups, whereas in males of the same age, only 512 genes were T3-responsive. Immunostaining demonstrated that several top sexually dimorphic T3-responsive genes, including Cyp2f2 and Dhcr24, were specifically expressed in the adrenal inner cortex, precisely in an area partially overlapping with the X-zone. Under T3 treatment, a unique cortical layer that surrounds the adrenal X-zone expanded significantly, forming a distinct layer peculiar to females. Our findings identified novel marker genes for the inner adrenal cortex, indicating there are different sub-zones in the zona fasciculata. The results also highlight the sex-specific response to thyroid hormone in the mouse adrenal gland.

Microwaving and Fluorophore-Tyramide for Multiplex Immunostaining on Mouse Adrenals - Using Unconjugated Primary Antibodies from the Same Host Species.

Immunostaining is widely used in biomedical research to show the cellular expression pattern of a given protein. Multiplex immunostaining allows labeling using multiple primary antibodies. To minimize antibody cross-reactivity, multiplex immunostaining using indirect staining requires unlabeled primary antibodies from different host species. However, the appropriate combination of different species antibodies is not always available. Here, we describe a method of using unlabeled primary antibodies from the same host species (e.g., in this case both antibodies are from rabbit) for multiplex immunofluorescence on formalin-fixed paraffin-embedded (FFPE) mouse adrenal sections. This method uses the same procedure and reagents used in the antigen retrieval step to strip the activity of the previously stained primary antibody complex. Slides were stained with the first primary antibody using a general immunostaining protocol followed by a binding step with a biotinylated secondary antibody. Then, an avidin-biotin-peroxidase signal development method was used with fluorophore-tyramide as the substrate. The immunoactivity of the first primary antibody complex was stripped through immersion in a microwaved boiling sodium citrate solution for 8 min. The insoluble fluorophore-tyramide deposition remained on the sample, which allowed the slide to be stained with other primary antibodies. Although this method eliminates most false positive signals, some background from antibody cross-reactivity may remain. If the samples are enriched with endogenous biotin, a peroxidase-conjugated secondary antibody may be used to replace the biotinylated secondary antibody to avoid the false positive from recovered endogenous biotin.

Plasma levels of Interleukin 18 but not amyloid-ß or Tau are elevated in female depressive patients.

BACKGROUND: Depression is associated with inflammation and Alzheimer's disease (AD). However, detailed molecular mechanisms linking mood, neuroinflammation and AD remain unclear. Although changes in peripheral inflammatory factors such as Interleukin 18 (IL18), and AD-associated amyloid-ß (Aß) peptides have been linked to depression, a solid relationship between these factors in depressive disorder has yet to be established. This study aims to further determine whether plasma IL18, Aß40, Aß42, and the AD-associated tangle component Tau, as well as IL18 single nucleotide polymorphisms (SNPs) may be biomarkers for depression. METHODS: We measured plasma IL18, Aß40, Aß42, and Tau in 64 depressive patients and 75 healthy controls, and characterized genotypes of three IL18 SNPs (rs187238, rs1946518 and rs1946519) in these subjects. Comparisons between depressive patients and controls were carried out in males, in females or in combination. Regression analyses were conducted to examine the correlation between these parameters. RESULTS: We found that none of the plasma levels of IL18, Aß40, Aß42, and Tau, the ratio of Aß42/Aß40, and the genotypes of IL18 SNPs were significantly different between combined depressive patients and combined healthy controls, or between male depressive patients and male controls. However, IL18 levels were less in females than in males in healthy people and were significantly increased in female depressive patients compared to female controls. Moreover, IL18 and standardized IL18 were correlated with standardized Aß42/Aß40 ratio and standardized Tau in depressive patients. CONCLUSIONS: Plasma IL18 may be a potential biomarker for depression in women.

BabaoDan attenuates high-fat diet-induced non-alcoholic fatty liver disease via activation of AMPK signaling.

BACKGROUND: Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD. METHODS: C57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin-eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis. RESULTS: We found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway. CONCLUSION: In summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling.

A circular RNA hsa_circ_0079929 inhibits tumor growth in hepatocellular carcinoma.

PURPOSE: Most recently, circular RNAs (circRNAs) were considered playing regulatory roles in tumor initiation and development. The specific function of circRNAs in hepatocellular carcinoma (HCC) remains unknown. This study was designed to detect specific roles of a circRNA hsa_circ_0079299 in HCC. METHODS: The expression of hsa_circ_0079299 in HCC and tumor cell lines was detected using quantitative PCR (qPCR). Cell proliferation, migration, cell cycle and apoptosis after overexpression of the circRNA were measured using cell counting kit-8 (CCK8) assay, colony formation, 5-ethynyl-2'-deoxyuridine (EdU) assay, wound healing assay, transwell culture system and flow cytometry. Western blotting assay detected the protein expression of PI3K/AKT/mTOR signaling pathway and cyclin B1 (CCNB1). Overexpression of the circRNA in vivo was measured by nude mice tumorigenesis. RESULTS: The expression of hsa_circ_0079299 was lower in HCC tissues. Overexpression of hsa_circ_0079299 suppressed tumor growth in vitro and in vivo, retarded cell cycle progression while had no effect on cell migration and apoptosis. The inhibitory effect of hsa_circ_0079299 was partly mediated by PI3K/AKT/mTOR signaling pathway. CONCLUSION: Our study shows that tumor suppressive role of hsa_circ_0079299 in HCC provides new recognition of circRNAs in cancers.

Chronic administration of quetiapine attenuates the phencyclidine-induced recognition memory impairment and hippocampal oxidative stress in rats.

The underlying mechanism of atypical antipsychotics in treating cognitive impairment in schizophrenia is unclear. The aim of the present study was to evaluate the effects of quetiapine, an atypical antipsychotic drug, on object recognition memory and hippocampal oxidative stress in a phencyclidine (PCP) rat model of schizophrenia. Rats were treated with chronic quetiapine (10 mg/kg/day, intraperitoneally) for 16 days or acute quetiapine (10 mg/kg/day, intraperitoneally) on day 16. On day 16, 1 h after the administration of quetiapine, the rats were administered PCP (50 mg/kg, subcutaneously). After the last object recognition behavioral test on day 18, the rats were killed for the measurement of hippocampal protein expression of nitrotyrosine, a protein marker of oxidative stress. The results showed that chronic quetiapine significantly attenuated object recognition memory impairment and hippocampal oxidative stress in the PCP-injected rats. These suggest that the attenuating effect of chronic quetiapine on hippocampal oxidative stress may be related to quetiapine's beneficial effects on object recognition memory in PCP rats, and further suggest that neuroprotective mechanisms are involved in chronic quetiapine treatment.

Body fluid levels of neuroactive amino acids in autism spectrum disorders: a review of the literature.

A review of studies on the body fluid levels of neuroactive amino acids, including glutamate, glutamine, taurine, gamma-aminobutyric acid (GABA), glycine, tryptophan, D-serine, and others, in autism spectrum disorders (ASD) is given. The results reported in the literature are generally inconclusive and contradictory, but there has been considerable variation among the previous studies in terms of factors such as age, gender, number of subjects, intelligence quotient, and psychoactive medication being taken. Future studies should include simultaneous analyses of a large number of amino acids [including D-serine and branched-chain amino acids (BCAAs)] and standardization of the factors mentioned above. It may also be appropriate to use saliva sampling to detect amino acids in ASD patients in the future-this is noninvasive testing that can be done easily more frequently than other sampling, thus providing more dynamic monitoring.

[CD20 Expression in Adult Patients with B-lineage Acute Lymphoblastic Leukemia and Its Prognostic Significance].

OBJECTIVE: To explore the relationship between the expression of CD20 antigen and clinical characteristics in adult patients with B-acute lymphoblastic leukemia(B-ALL). METHODS: The CD20 expression of 126 acute lympho-blastic leukemia patients in our hospital from July 2009 to July 2012 were determined by flow cytometry. The characteristics, examination results and outcome were analyzed retrospectively. The complete remission rate (CR rate), relape rate, 2-year survival rate and 2-year event-free survival (EFS) of patients with CD20 positive and negative after the first cycle of chemstherapy were compared. RESULTS: Positive rate of CD20 antigen expression in 126 patients was 24.4% (31 cases), negative rate of CD20 antigen expression in 126 patients was 75.6% (95 cases). No significant relationship was found between CD20 antigen expression and sex, age, peripheral blood leucocytes count and chromosomal changes. The relapse rate, 2-year survival rate (OS) and 2-year event-free survival (EFS) of adult patients with B-ALL in CD20 positive and negative groups were 53.3% and 38.0%, 52.1% and 92.3%, 33.7% and 70.8% respectively. CONCLUSION: Expression of CD20 in adult patients with B-ALL did not related with clinical features, but related with poor prognosis.

[Therapeutic efficacies of decitabine application prior to hematopoietic cell transplantation in patients with myelodysplastic syndrome and acute myeloid leukemia].

OBJECTIVE: To explore the therapeutic efficacies of decitabine application prior to hematopoietic cell transplantation (HSCY) in patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). METHODS: Retrospective reviews were conducted for 46 patients with MDS (n = 14) and AML (n = 32) on a therapy of decitabine prior to allo-HSCT between September 2009 and February 2013. RESULTS: In MDS patients, complete remission (CR, n = 10), partial remission (PR, n = 2) and stable disease (SD, n = 1) were achieved prior to HSCT. And the remission rate of one course was 10/14. After decitabine dosing, 17/32 patients achieved CR in 32 with AML and the remission rate of one course was 53.1％ (17/32) and effective rate of one course (CR+PR) achieves 78.1％ (25/32). Successful engraftment was attained in all MDS patients and 12/14 patients survived disease-free and one died of pneumonia after relapse. And 28 patients with AML attained successful engraftment after using decitabine prior to allo-HSCT and there were 20 disease-free survivors. Ten patients died and another lived with tumor. The incidences of acute and chronic graft-versus-host disease (GVHD) among evaluable patients were 4.3% (2/26) and 23.9% (11/46) respectively. After a median follow-up of 8 months for survivors, the treatment-related mortality was 23.9% (11/46). The 30-month disease-free survival (DFS) rate was 53.1% and 30-month overall survival rate after decitabine dosing 61.9%. CONCLUSION: Thus decitabine is an effective therapy during bridge time to HSCT in patients with MDS and AML.

[Retrospective efficacy analysis of decitabine bridging allogeneic hematopoietic stem cell transplantation on the treatment of myelodysplastic syndrome].

OBJECTIVE: To evaluate the efficacy of decitabine (DAC) bridging therapy followed by allogeneic hematopoietic stem cell transplantation (allo-HSCT) in patients with myelodysplastic syndrome (MDS). METHODS: The clinical characteristics and curative effect of MDS patients who received allo-HSCT from 2010 July to 2013 December were retrospectively analyzed. Of them, 25 MDS patients who received decitabine bridging allo-HSCT were randomly selected (referred to as the bridging group),while at the same time another 33 MDS patients who did not receive decitabine for allo-HSCT in MDS were also randomly selected as control group. The effect of decitabine bridging allo-HSCT on the patients' survival and occurrence of graft versus host disease (GVHD) was analyzed. RESULTS: With decitabine bridge therapy, 64.0% patients (16/25) achieved marrow complete remission before allo-HSCT, while the control group was only 15.1% (5/33, P<0.05). Decitabine bridging group of early transplant-related mortality was lower than that of the control group (4.0% vs 18.2%), but the difference was not statistically significant (P=0.106). Up to follow-up deadline, the mortality of decitabine bridging group was 12.0%, while that of the control group was 30.3% (P<0.05). The 2-year OS of decitabine bridging group was 83.0%, while that of the control group was 59.0% (P<0.05). Of the 14 patients in decitabine bridging group with aGVHD, 7 was grade IaGVHD, 3 grade II and 4 grade III. Of the 16 patients in control group with aGVHD, 7 was grade IaGVHD, 8 grade II and 1 grade III. CONCLUSION: Decitabine bridging therapy followed by allo-HSCT in the treatment of MDS is safe and effective.