Molecular Characteristics of T Cell-Mediated Tumor Killing in Hepatocellular Carcinoma.

Background: Although checkpoint blockade is a promising approach for the treatment of hepatocellular carcinoma (HCC), subsets of patients expected to show a response have not been established. As T cell-mediated tumor killing (TTK) is the fundamental principle of immune checkpoint inhibitor therapy, we established subtypes based on genes related to the sensitivity to TKK and evaluated their prognostic value for HCC immunotherapies.

Methods: Genes regulating the sensitivity of tumor cells to T cell-mediated killing (referred to as GSTTKs) showing differential expression in HCC and correlations with prognosis were identified by high-throughput screening assays.

Modelled Economic Analysis for Dacomitinib-A Cost Effectiveness Analysis in Treating Patients With EGFR-Mutation-Positive Non-Small Cell Lung Cancer in China.

Objectives: To establish the cost-effectiveness of dacomitinib compared to gefitinib from the Chinese healthcare system perspective.

Patients: Advanced non-small cell lung cancer (NSCLC) harbouring epidermal growth factor receptor (EGFR) mutations.

Methods: Partitioned survival analysis was undertaken to examine the cost-effectiveness of dacomitinib utilising individual patient data (IPD) from the pivotal randomised controlled trial (RCT) (ARCHER 1050).

eena Promotes myeloid proliferation through stimulating ERK1/2 phosphorylation in zebrafish.

The EEN (extra eleven nineteen) gene is one of the fusion partners of mixed-lineage leukemia, located on chromosome 19p13. Here we cloned two een genes (designated as eena and eenb) in zebrafish, which are assigned to linkage groups 8 and 2, respectively. Whole-mount in situ hybridization assay showed that eena and eenb have overlapping but distinct expression patterns during embryogenesis.

[Effects of arsenic trioxide and ATRA on PLZF-RARalpha-positive U937 leukemic cells].

Aim: To investigate effects of arsenic trioxide (As(2)O(3)) and alltrans retinoic acid (ATRA) on PLZF-RARalpha-positive cells.

Methods: PLZF-RARalpha-positive U937 cells (U937/PLZF) were used as an in vitro model. The change of cell morphology was observed by Wright-Giemsa staining.

Aberrant transcriptional regulation of the MLL fusion partner EEN by AML1-ETO and its implication in leukemogenesis.

The EEN (extra eleven nineteen) gene, located on chromosome 19p13, was cloned as a fusion with MLL from a patient with acute myeloid leukemia (AML) with translocation t(11;19)(q23;p13). In this study, we characterized the genomic structure of the EEN gene, including its 5' regulatory region and transcription start site (TSS). We found that Sp1 could bind to the guanine-cytosine (GC)-stretch of the EEN promoter and was critical for the normal EEN expression, whereas the leukemia-associated fusion protein AML1-ETO could aberrantly transactivate the EEN gene through an AML1 binding site.

[Molecular cloning, purification, and serological characterization of four specific antigens of Mycobacterium tuberculosis].

Objective: To express the 14,000, 37,000, and 6,000 early secretory antigenic target (ESAT-6) and mtb81 antigen genes in bacteria, and to purify the product and determine their activity.

Methods: The 14,000, 37,000 , ESAT-6, and mtb81 antigen genes were amplified from Mycobacterium tuberculosis genomic DNA by polymerase chain reactions and cloned into pGEX 4T-1 expression vector. BL21 strain of Escherichia coli was transformed with the recombinant vectors and induced to express recombinant proteins.