Tunneling nanotubes(TNT) are cellular communication and transport mechanism discovered recently. TNTs play important role in immunological response and viral spread, also may involve embryonic development, regulation of gene expression and carcinogenesis. However, it was not easy to study TNT for clinical samples since intricate assay method for TNT. We suggested using histochemical assay PAS staining in cell drip to show TNT in leukemia and lymphoma samples.

Objective To observe the effect of extracorporeal shock waves (ESW) therapy on avascular necrosis of femoral head (ANFH) of stage IV. Methods 72 hips of 44 patients with ANFH of stage IV, according to Association Research Circulation Osseous, were randomly divided into treatment group (n=37) and control group (n=35). The control group received routine therapy, while the treatment group received ESW in addition, 2.0-4.0 bar, 10 Hz, 6000 times. They were evaluated with Harris Hip Score, Manual Muscle Test (MMT) and Short Form of health survey (SF-36) before and 1 month after treatment. Results The scores of Harris Hip Score and MMT improved more in the treatment group than in the control group (P<0.05) after treatment, as well as the scores of SF-36 except physical health and vitality (P<0.05). Conclusion The ESW can obviously improve the motor function and quality of life of patients with ANFH of stage IV.

Viral etiology of tumor has been studied for a century.Seven human tumor viruses were identified over the past half century.The complexity and regularity of the pathogenic mechanisms of human tumor viruses have been elucidated preliminarily.Human genome sequencing indicated that 8 ％ of human genes were composed of human endogenous retroviruses (HERVs).Owing to the findings that adult T-cell leukemia virus (HTLV) can cause human adult T-cell leukemia and animal exogenous and HERVs can induce tumors and malignant diseases,the relationship between HERVs and human tumors has attracted much attention receutly.Here this article discusses the association of the expression of HERVs with leukemia and solid tumors progression,which may be an important aspect of tumor virology.

As novel organisms,tumors undergo microevolution in limited time and space in vivo.Due to genetic mutations and epigenetic mechanisms,tumor cell clones undergo linear or branching evolution.In most clinic patients,tumors develop through branching evolution pathways,causing tumor heterogeneity and affecting tumor progression.Microevolution is the biological basis for the refractoriness and recurrence of tumors and has been paid attention in research and clinic recently.In this paper,acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are used as examples to demonstrate tumor microevolution and the concept of linear and branching evolution.Questions and perspective in the field of tumor microevolution research are also discussed.

Cell death as the partner of cell proliferation is one of the basic mechanism in cell biology. Recently, it became obscure since more and more patterns of cell death were reported. However, the classification of cell death, which was recommended by the Nomenclature Committee on Cell Death (NCCD) in 2009, clarified the criteria. The theme of the recommendation and recent data from the literature were discussed in this review. The significance of studies on cell death was discussed.

The disturbance of life rhythm exerts negative influence on modem life.The relationship between the disruption of circadian rhythms and tumor growth has attracted much attention.It has been studied in breast cancer and prostate cancer,and chronotherapeutics has been used for treatment of some cancers in clinic.Researchers have begun to investigate the association of circadian rhythms with leukemia/lymphoma outside China.The literatures were reviewed and the launch of research on this field was appealed.

Objective To investigate the effects and possible mechanisms of decitabine on heat-shock protein 22 (HSP22) expression in hematopoietic tumor cell lines and bone marrow samples from patients with hematopoietic tumor.Methods The expression of HSP22 in 13 hematopoietic tumor cell lines,20 primary patients' samples and 10 normal donor' samples were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).After HSP22 induction with a demethylating agent decitabine (2 μmol/L),the methylation of the HSP22 promoters in hematopoietic tumor cell lines,healthy donors and bone marrow samples from patients with hematopoietic tumor were detected by methylation specific PCR (MSP).Results Expression of HSP22 was not detected in 13 hematopoietic tumor cell lines,20 primary patients' samples or 10 healthy donors' samples.Decitabine can induce the expression of HSP22 in hematopoietic tumor cell lines and bone marrow samples from patients with hematopoietic tumor.Decitabine can maintain partially demethylation of HSP22 promoters in hematopoietic tumor cell lines.HSP22 promoters were highly methylated in BMMC of the healthy donors and patients with hcmatopoictic tumor.Conclusion Decitabine can induce the expression of HSP22 in hematopoietic tumor cells partly by demethylation of HSP22 promoters.

Human herpesviruses (HHV) are widespread all over the world,and persist in human in latent infection.When reactivated,HHV plays an important role in the pathogenesis and development of tumor and other diseases.Much attention has been paid on EB virus which can cause different tumors and other diseases.Studies within this half century have elucidated the mechanism of oncogenesis of γ-HHV.Recently it was reported that other HHV may have oncomodulation functions.

Objective:To screen the plasma microRNAs( miRNAs) of differential expression in a high fat diet-induced insulin resistance in mouse models;further investigations on the mice with insulin resistance treated by TLR4 inhibitors TAK-242,and to study the changes of plasma miRNAs expression profile and the relationship among TLR4, miRNAs and high fat diet-induced insulin resistance. Methods:The plasma samples were from 3 mouse groups of previous study,namely,the control group with general basic diet ( low fat diet,LFD) ,TLR4 inhibitors TAK-242 treatment group with a high fat diet ( HFD-T) and the high fat diet control group( HFD-C) . The differential expressed miRNAs was screened by expression profiling of plasma miRNAs, which was detected using mouse miRNA microarray. The quantitative Real-Time PCR ( qRT-PCR ) was used to verify the results of microarray. The target genes of differential expressed miRNAs were predicted in TLR4 signaling pathway using bioinformatics methods,and the GO and KEGG database molecular annotation system were used to investigate the main effects of the miRNAs targeted genes on the biological functions or signal pathway. Results:The screening results of miRNA microarray chip showed that,comparing miRNAs expression between HFD group and LFD control group,185 miRNAs were significant in the high fat diet group,including 6 up-regulated and 179 down-regulated miRANs. A significant difference of miRANs was also found between HFD-T group and LFD control group,the total number of differential expression miRNAs was 171,and all of them were down-regulated. Comparing miRNAs expression between HFD-C group and HFD-T group,13
miRNAs were significant in HFD-T group,all of them were down-regulated. Bioinformatics analysis results showed that a total of 10 in-teraction proteins with TLR4 were predicted;the difference of mmu-miR-3095-3p,mmu-miR-5113,mmu-miR-709 and mmu-miR-335-3p expression levels was more than 1 000 times between HFD-C group and HFD-T group,and their target genes can be found in TLR4-in-teraction protein or Toll like receptor signaling pathway;GO and KEGG analysis showed 74% of these target genes belonged to the biological processes genes, and the transcription factors accounted for 82%. The expression of mmu-miR-3095-3p, mmu-miR-5113, mmu-miR-709 and mmu-miR-335-3p detected by qRT-PCR exhibited the similar patterns of down regulation to those shown in microarray results. Conclusion:When insulin resistance occurs,there is a change in plasma miRNAs expression profile,this change is associated with TLR4 and its signaling pathways. The finding enrichs the possible mechanisms of insulin resistance and provides a basis for finding miRNAs diagnostic markers for early diagnosis of insulin resistance.

Cancer stem cells (CSCs) are units in cancer evolution.The elucidation the origin of CSCs has great significance on prevention and treatment of cancers.This paper discusses possible origins,genetic pathways and mechanisms of CSC on the basis of the literature and authors' research.Normal stem cells could be malignantly transformed to CSC through long term accumulation of gene mutations.Induction to pluripotent stem cells by reprogramming is a possible pathway for somatic cells to become CSCs.Dedifferentiation of cancer cells to CSCs is another pathway.Epithelial-mesenchymal transition (EMT),which is an important mechanism for cellular plasticity,plays important roles in cancer metastasis and stemness of cancer cells.Cell-fusion inducing EMT could be a mechanism for the genesis of CSCs.Infection of some virus is also related to the genesis of CSCs.The complexity of cancer biology was also discussed.