Objective:To analyze the situation of articles published in Journal of Leukemia & Lymphoma and provide reference for the development of the journal and better service to readers and authors. Methods:All articles published in Journal of Leukemia & Lymphoma from January 2019 to December 2021 were searched on the official website of the journal (www.bxblbl.com.cn) and the full-text database of Chinese medical journals (www.yiigle.com), and the statistical analysis of the articles published in the journal was performed using bibliometric methods and Excel software. Website readings and downloads were recorded based on data from the Chinese medical journal network publishing platform (https://app.yiigle.com/cmaapp/). Results:From January 2019 to December 2021, 36 issues of Journal of Leukemia & Lymphoma were published, containing a total of 578 articles, with an average of about 16 articles per issue. There were 222 (38.4%) original articles, 173 (29.9%) brief communications, 11 (1.9%) guidelines and consensus articles, 58 (10.0%) topic reviews, and 94 (16.3%) reviews; the degree of authorship cooperation was 5.10 (2 946/578). The first author's affiliation included 28 provinces, cities and autonomous regions. The top 10 regions were Jiangsu, Henan, Beijing, Fujian, Shanxi, Guangdong, Tianjin, Shanghai, Hebei, and Shandong, with a total of 425 (73.5%) articles. There were 257 (44.5%) funded articles, including 105 (18.2%) articles funded by national funds. The average number of citations per article was 18.6 (10 751/578). The average annual number of reads was 104 630, and the top 20 most-read articles in 2021 were mostly in the category of guidelines and consensus and topical reviews. Conclusions:Journal of Leukemia & Lymphoma has developed well in recent years, and its influence in the field of hematology-oncology has steadily increased. In the future, according to the purpose of the journal, the special columns should be further created, and the academic quality should be improved to better serve the readers and authors.

Objective:To analyze the articles and literature indicators of Cancer Research and Clinic, in order to provide reference for the development of the journal. Methods:All articles published in Cancer Research and Clinic from January 2017 to December 2021 were searched on the official website of the journal (www.zlyjylc.com.cn), and the core literature indicators of Cancer Research and Clinic published in the Citation Report of Chinese Science and Technology Journals (Core Edition) from 2018 to 2022 were searched, and the statistical analysis of the articles and literature indicators was performed using bibliometric method and Excel software. Results:From 2017 to 2021, a total of 60 issues of Cancer Research and Clinic were published, containing a total of 1 065 articles, with an average of 17.8 articles per issue; a total of 4 416 pages of articles were published, with an average of 4.1 pages per article. There were 609 original articles (57.2%), 193 brief communications (18.1%) and 224 reviews (21.0%) in the main sections. The degree of authorship cooperation was 3.84 (4 086/1 065). The first author affiliation of the article was located in 31 regions, of which the top 10 regions in terms of the number of articles published were Shanxi, Jiangsu, Beijing, Shandong, Hubei, Shaanxi, Liaoning, Guangdong, Henan, and Hebei, with a total of 822 articles (77.2%). A total of 487 articles (45.7%) were funded by the foundation, including 134 articles (12.6%) funded by the national foundations. The average number of citations per article was 19.3 (20 557/1 065); the total number of marked keywords was 4 412, with an average of 4.1 per article. The impact factor and total citation frequency in 2018 were the highest (0.680 and 775), and the rate cited, open factor and overall evaluation total score in 2021 were the highest (0.94, 42 and 29.8). Conclusions:Cancer Research and Clinic has adhered to its own purpose and formed its own characteristics, and its academic quality and influence have steadily improved in the field of oncology in China in recent years. It should continue to improve the quality and strive to be a first-class oncology journal in the future.

Objective: To explore the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection who received entecavir alone or in combination with anluohuaxianwan for 78 weeks. Methods: Patients with chronic HBV infection were randomly treated with entecavir alone or in combination with anluohuaxian for 78 weeks. Ishak fibrosis score was used for blind interpretation of liver biopsy specimens. The improvement in liver fibrosis condition before and after the treatment was compared. Student's t test and non-parametric test (Mann-Whitney U-Test and Kruskal-Wallis test) were used to analyze the measurement data. The categorical variables were analyzed by Chi-square test method and Spearman’s rank correlation coefficient was used to test bivariate associations. Results: Liver fibrosis improvement rate after 78 weeks of treatment was 36.53% (80/219) and the progression rate was 23.29% (51/219). The improvement of liver fibrosis was associated to the degree of baseline fibrosis and treatment methods (P < 0.05). The improvement rate of hepatic fibrosis in patients treated with anluohuaxianwan combined with entecavir at baseline F < 3 (54.74%, 52/95) was significantly higher than that in patients treated only with entecavir (33.33%, 16/48), P = 0.016 and the progression rate of hepatic fibrosis (13.68%, 13/95) was lower than that in patients treated alone (18.75%, 9/48), P = 0.466. In patients with baseline F < 3, the proportion of patients with improved and stable liver fibrosis in the combined treatment group (68.1%, 32/47) was higher than that in the treatment group alone (51.7%, 15/29). Conclusion Combined anluohuaxianwan and entecavir treatment can significantly improve the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection. Furthermore, it has the tendency to improve the stability rate and reduce the rate of progression of liver fibrosis.

Objective To investigate the application of statistical methods in clinical research articles of oncology in China. Methods The core journals in Chinese oncology journals were retrieved in "Wanfang Data", and the application of statistical methods in the clinical research articles published in the first issue of 2017 were analyzed,including the selection of statistical indicators,the selection of statistical methods and the interpretation of statistical results. Results A total of 176 clinical research articles from 24 journals were taken into the study.In the selection of statistical indicators, 12.6 %(16 articles) used the description method of normal distribution data for the skewness distribution measurement data; 37.9 % (47 articles) described the count data with samples<20 as a percentage; 14.5 % (9 articles) replaced the constituent percentages with composition ratios. In the selection of statistical methods, 10.3 % (12 articles) did not perform analysis of variance when comparing among multiple groups, and the t test was used to compare each other directly. 15.1 % (8 articles) disregarded the preconditions of the use of the χ 2test. In the interpretation of statistical results, 18.4 % (27 articles) confused the statistical significance with biological significance. Conclusions The statistical problems are widespread in Chinese oncology clinical research articles,involving the entire process from study design to interpretation of results. Scientific research management departments, clinical researchers, and journal editorial board need to work together to improve the scientificity of clinical scientific research results of oncology in China.

Objective: To detect differentially expressed microRNAs in chronic hepatitis B (CHB) before being treated with pegylated interferon (PegIFN) and the relationship between their target genes and HBsAg loss. Methods: Pretreatment differentially expressed microRNAs between different response groups were screened using high throughput microarrays and validated by quantitative reverse-transcription polymerase chain reaction (RT-qPCR). Bioinformatics analysis was performed to determine their target genes potential mechanistic roles. Results: A total of 417 microRNA were differentially expressed between different response groups, among which 342 were up-regulated and 75 were down-regulated. miR-3960, miR-126-3p, miR-23 a-3p and miR-335-5p were verified to be down-regulated by RT-qPCR result in HBsAg loss group. Bioinformatic analysis result show that the relevant pathways of microRNAs include AMPK signal pathway, NOD-like signal pathway, NF-kappa B signal pathway and mTOR signal pathway. Conclusions HBsAg loss is probably achieved as the result of genes expression regulated in association with immune response, further enhance the immune response of HBV elimination and acquire HBsAg loss.

Objective To investigate the diagnostic criteria for HBV-related acute-on-chronic pre-liver failure (pre-ACLF) which can effectively predict the risk of liver failure.Methods A total of 1279 patients with severe icteric chronic hepatitis B (CHB) and/or severe acute exacerbation of CHB were enrolled.The influence of serum levels of alanine aminotransferase (ALT),aspartate aminotransferase (AST),and total bilirubin (TBil),international normalized ratio (INR) of prothrombin time,sex,and age on the incidence rate of acute-on-chronic liver failure (ACLF) was analyzed,the diagnostic criteria for pre-ACLF and predictive model for ACLF were developed.The chi-square test was used for comparison of categorical variables,and the independent samples t-test was used for continuous data;multivariate logistic regression analysis was performed to evaluate the risk of liver failure.Results The baseline serum levels ofALT,AST,and TBil,and INR were independent risk factors for liver failure (P ＜ 0.05).The diagnostic criteria for pre-ACLF were as follows:(1) INR ≥ 1.30;(2) AST ≥ 10×upper limit of normal (ULN) and obvious jaundice (TBil ≥ 51.3 μmol/L),or TBil ≥ 342.0 μmol/L.These criteria had a positive predictive value of 45.9％,a negative predictive value of 89.8％,a sensitivity of 69.1％,and a specificity of 76.9％.The predictive model for the risk of ACLF was PY =1=eX/(1+ex) (PY represented positive results of logistic regression analysis),X =-10.245+0.026×AST(ULN)-0.025×AST(ULN)+0.046×TBil(mg/d1) + 4.642×INR+0.049×age(years).The patients with higher PY values tended to have a higher incidence rate of ACLE The incidence rate of ACLF was 75.3％ in patients with PY ≥ 0.60,more than 50％ in patients with a PY value of 0.40-0.59,and 1.8％ in patients with PY ＜ 0.10 (P ＜ 0.01).Conclusion The diagnostic criteria for pre-ACLF and predictive model can effectively evaluate the risk of HBV-related ACLF.

OBJECTIVEThe aim of this study was to explore the effect of SPARC on the anti-cancer effect of gemcitabine and underlying mechanism in pancreatic cancer.

METHODSAfter treating with gemcitabine, the proliferation rate of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells was detected by MTT assay. The cell cycle distribution and cell apoptosis in each group were examined by flow cytometry, and the capability of clone formation was tested by adhesion-dependent clone formation assay. The apoptosis-related proteins were analyzed by Western blot.

RESULTSThe growth of pancreatic cancer cells was inhibited by gemcitabine in a time-dependent and dose-dependent manner. Its IC50 at 24, 48, and 72-h was (40.1 ± 2.5) µmol/L, (15.0 ± 0.5) µmol/L and (6.6 ± 0.1) µmol/L, respectively. The overexpression of SPARC increased the inhibitory effect of gemcitabine on growth of pancreatic cancer MIA PaCa2/SPARC69 cells, presenting a dose- and time- dependent manner. Its IC50 at 24, 48, 72 h was (24.3 ± 1.5) µmol/L, (7.7 ± 0.3) µmol/L and (4.8 ± 0.2) µmol/L, respectively. The clone formation assay showed that before gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (2350 ± 125), (2130 ± 120) and (1567 ± 11), respectively. After gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 1674 ± 79) , (1587 ± 94) and (557 ± 61), respectively. The overexpression of SPARC enhanced the chemosensitivity of MIA PaCa2 cells to gemcitabine chemotherapy. After treating with 10 µmol/L gemcitabine for 48 h, the ratio of G0/G1 cells in MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (56.0 ± 5.5)%, (55.0 ± 4.5)% and (68.0 ± 7.0)%, respectively. The cells arrested at G0/G1 phase were significantly increased in the MIA PaCa2/SPARC69 cells. The apoptosis rates of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (22.4 ± 2.5)%, (19.9 ± 2.0)% and (37.7 ± 3.9)%, respectively, indicating that overexpression of SPARC enhanced the gemcitabine-induced apoptosis in MIA PaCa2 cells. The Western blot analysis showed that, compared with MIA PaCa2 and MIA PaCa2/V cells, the expression of caspase-2, -8, -9 and cleaved PARP protein was significantly increased, while the expression of Bcl-2 was not changed significantly in the MIA PaCa2/SPARC69 cells.

CONCLUSIONSPARC can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine via regulating the expression of apoptosis-related proteins.

Antimetabolites, Antineoplastic ; administration & dosage ; pharmacology ; Apoptosis ; drug effects ; Caspase 2 ; metabolism ; Caspase 8 ; metabolism ; Caspase 9 ; metabolism ; Cell Cycle ; drug effects ; Cell Cycle Checkpoints ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cysteine Endopeptidases ; metabolism ; Deoxycytidine ; administration & dosage ; analogs & derivatives ; pharmacology ; Dose-Response Relationship, Drug ; Drug Resistance, Neoplasm ; Humans ; Osteonectin ; metabolism ; Pancreatic Neoplasms ; metabolism ; pathology ; Poly(ADP-ribose) Polymerases ; metabolism ; Time Factors

OBJECTIVETo explore the clinical effect of L-ornithine L-aspartate (LOLA) granules in treating chronic liver disease in patients with high-level serum gamma-glutamyltransferase (G-GT) using a 24-week treatment course.

METHODSTwo-hundred patients with chronic liver disease and above normal G-GT were given a 12-week course of LOLA granules (9 g/d) and then classified into the following three groups according to the change in serum Gamma-GT:group I:patients with Gamma-GT level returned to normal;group II:patients with serum Gamma-GT level that was reduced during the treatment; group III:patients with serum Gamma-GT level that did not decrease or that increased to a higher level than at start of treatment.After the 12-week treatment course, the patients in group I were divided into three subgroups for receipt of a control drug (compound glycyrrhizin, 50mg/d) or an additional 12-week course of Gamma-GT at a reduced dose (LOLA granules 3 g/d) or at the original dose; groups II and III were maintained on the initial dose for an additional 12 weeks.The groups were reassessed at the end of the second 12-week course (at the end of week 24 of the study's observation period).Count data were compared using the x2 test and measurement data were compared using the t-test.

RESULTSIn group I, the serum Gamma-GT level was 90.9% at the end of the first 12-week course and dropped to a mean level of 52.2% for both of the subgroups that received the reduced and original dose after the additional 12 weeks of LOLA granules treatment; the difference from week 12 to week 24 was significant (x2=8.213, P less than 0.05).The 24-week change in serum Gamma-GT levels for the group I reduced and original dose subgroups vs.the control subgroup were also significantly different from those seen in groups II and III (P less than 0.05).The percentage of patients in group I who achieved normal level serum Gamma-GT after 24 weeks of treatment (78.6%) was significantly higher than that for the control group (vs.55.0%, x2=11.452, P less than 0.05).When the patients in group 1 who had received the 12 additional weeks of LOLA granules treatment were measured again at two weeks after the treatments had been discontinued (end of week 26), the percentage of patients with normal serum Gamma-GT level was 92.7%, with only three cases showing obviously abnormal levels; in contrast, the group I patients in the control group of the second 12-week study period had on 66.7% of patients with normal-level serum Gamma-GT.The difference in change between the treated groups (both reduced and original dose) and the control group was significant (x2=14.964, P less than 0.05).

CONCLUSIONPatients whose serumGamma-GT levels returned to normal after receipt of LOLA granules for 12 weeks benefitted from an additional 12 weeks of consolidation treatment, and those given the treatment at the original dose benefitted most.Compared with the compound glycyrrhizin, LOLA granules provided a better maintenance of resolved Gamma-GT level.Therefore, the effect of LOLA appears to be reliable and stable as well as safe for clinical use.

Chronic Disease ; Dipeptides ; therapeutic use ; Humans ; Liver Diseases ; drug therapy ; Liver Function Tests ; gamma-Glutamyltransferase ; blood

Objective The aim of this study was to explore the effect of SPARC on the anti-cancer effect of gemcitabine and underlying mechanism in pancreatic cancer . Methods After treating with gemcitabine, the proliferation rate of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells was detected by MTT assay .The cell cycle distribution and cell apoptosis in each group were examined by flow cytometry, and the capability of clone formation was tested by adhesion-dependent clone formation assay . The apoptosis-related proteins were analyzed by Western blot .Results The growth of pancreatic cancer cells was inhibited by gemcitabine in a time-dependent and dose-dependent manner .Its IC50 at 24, 48, and 72-h was (40.1 ±2.5) μmol/L, (15.0 ±0.5) μmol/L and (6.6 ±0.1) μmol/L, respectively.The overexpression of SPARC increased the inhibitory effect of gemcitabine on growth of pancreatic cancer MIA PaCa2/SPARC69 cells, presenting a dose-and time-dependent manner .Its IC50 at 24, 48, 72 h was (24.3 ±1.5) μmol/L, (7.7 ±0.3) μmol/L and (4.8 ±0.2) μmol/L, respectively.The clone formation assay showed that before gemcitabine treatment , the clone numbers of MIA PaCa 2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 2350 ±125 ) , ( 2130 ±120 ) and ( 1567 ±11 ) , respectively . After gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 1674 ±79) , (1587 ±94) and (557 ±61), respectively.The overexpression of SPARC enhanced the chemosensitivity of MIA PaCa 2 cells to gemcitabine chemotherapy .After treating with 10 μmol/L gemcitabine for 48 h, the ratio of G0/G1 cells in MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (56.0 ±5.5)%, (55.0 ±4.5)% and (68.0 ±7.0)%, respectively.The cells arrested at G0/G1 phase were significantly increased in the MIA PaCa 2/SPARC69 cells.The apoptosis rates of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (22.4 ±2.5)%, (19.9 ±2.0)% and (37.7 ± 3.9)%, respectively, indicating that overexpression of SPARC enhanced the gemcitabine-induced apoptosis in MIA PaCa2 cells.The Western blot analysis showed that , compared with MIA PaCa2 and MIA PaCa2/V cells, the expression of caspase-2,-8,-9 and cleaved PARP protein was significantly increased , while the expression of Bcl-2 was not changed significantly in the MIA PaCa 2/SPARC69 cells.Conclusion SPARC can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine via regulating the expression of apoptosis-related proteins .

Objective The aim of this study was to explore the effect of SPARC on the anti-cancer effect of gemcitabine and underlying mechanism in pancreatic cancer . Methods After treating with gemcitabine, the proliferation rate of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells was detected by MTT assay .The cell cycle distribution and cell apoptosis in each group were examined by flow cytometry, and the capability of clone formation was tested by adhesion-dependent clone formation assay . The apoptosis-related proteins were analyzed by Western blot .Results The growth of pancreatic cancer cells was inhibited by gemcitabine in a time-dependent and dose-dependent manner .Its IC50 at 24, 48, and 72-h was (40.1 ±2.5) μmol/L, (15.0 ±0.5) μmol/L and (6.6 ±0.1) μmol/L, respectively.The overexpression of SPARC increased the inhibitory effect of gemcitabine on growth of pancreatic cancer MIA PaCa2/SPARC69 cells, presenting a dose-and time-dependent manner .Its IC50 at 24, 48, 72 h was (24.3 ±1.5) μmol/L, (7.7 ±0.3) μmol/L and (4.8 ±0.2) μmol/L, respectively.The clone formation assay showed that before gemcitabine treatment , the clone numbers of MIA PaCa 2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 2350 ±125 ) , ( 2130 ±120 ) and ( 1567 ±11 ) , respectively . After gemcitabine treatment, the clone numbers of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were ( 1674 ±79) , (1587 ±94) and (557 ±61), respectively.The overexpression of SPARC enhanced the chemosensitivity of MIA PaCa 2 cells to gemcitabine chemotherapy .After treating with 10 μmol/L gemcitabine for 48 h, the ratio of G0/G1 cells in MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (56.0 ±5.5)%, (55.0 ±4.5)% and (68.0 ±7.0)%, respectively.The cells arrested at G0/G1 phase were significantly increased in the MIA PaCa 2/SPARC69 cells.The apoptosis rates of MIA PaCa2, MIA PaCa2/V and MIA PaCa2/SPARC69 cells were (22.4 ±2.5)%, (19.9 ±2.0)% and (37.7 ± 3.9)%, respectively, indicating that overexpression of SPARC enhanced the gemcitabine-induced apoptosis in MIA PaCa2 cells.The Western blot analysis showed that , compared with MIA PaCa2 and MIA PaCa2/V cells, the expression of caspase-2,-8,-9 and cleaved PARP protein was significantly increased , while the expression of Bcl-2 was not changed significantly in the MIA PaCa 2/SPARC69 cells.Conclusion SPARC can enhance the chemosensitivity of pancreatic cancer cells to gemcitabine via regulating the expression of apoptosis-related proteins .