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Macrophages have plastic and diverse phenotypes and functions, and they play different roles in host defense, tissue homeostasis and repair, development, and various pathologic processes. Although the classically activated macrophage (M1) and alternatively activated macrophage (M2) phenotypes are widely accepted, most macrophages under physiologic and pathologic conditions are polarized to a continuum of states between the M1 and M2 extreme phenotype poles. In recent years, research on the regulatory mechanisms of M1 and M2 macrophages has made great progress, preliminarily elucidating the role of cellular metabolic reprogramming in macrophage polarization and the role of glycolytic enzymes in controlling inflammatory macrophages. The knowledge lays the foundation for elucidating the mechanisms in the regulation of macrophage functional phenotypes. Tumor-associated macrophages play important roles in the development of tumors. The macrophages in the microenvironment of hematologic malignancies have unique features, and a deep study on them will provide new thoughts and clues for clinical diagnosis and therapeutics.
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The purpose of this study was to clone and characterize the ZFP36L1 (zinc finger protein 36-like 1) gene, clarify its expression characteristics, and elucidate its expression patterns in different tissues of goats. Samples of 15 tissues from Jianzhou big-eared goats, including heart, liver, spleen, lung and kidney were collected. Goat ZFP36L1 gene was amplified by reverse transcription-polymerase chain reaction (RT-PCR), then the gene and protein sequence were analyzed by online tools. Quantitative real-time polymerase chain reaction (qPCR) was used to detect the expression level of ZFP36L1 in intramuscular preadipocytes in different tissues and adipocytes of goat at different differentiation stages. The results showed that the length of ZFR36L1 gene was 1 224 bp, and the coding sequence (CDS) region was 1 017 bp, encoding 338 amino acids, which was a non-secretory unstable protein mainly located in nucleus and cytoplasm. Tissue expression profile showed that ZFP36L1 gene was expressed in all selected tissues. In visceral tissues, the small intestine showed the highest expression level (P < 0.01). In muscle tissue, the highest expression level was presented in longissimus dorsi muscle (P < 0.01), whereas the expression level in subcutaneous adipose tissue was significantly higher than that in other tissues (P < 0.01). The results of induced differentiation showed that the expression of this gene was up-regulated during adipogenic differentiation of intramuscular precursor adipocytes (P < 0.01). These data may help to clarify the biological function of the ZFP36L1 gene in goat.
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Animais , Cabras/genética , Sequência de Aminoácidos , Fígado , Clonagem MolecularRESUMO
The tumors originate from transformation cells caused by gene mutations. These cells are frequently kept at dormant state or detected and cleared by the immune surveillance. The research data show that the hallmarks of tumors and aging share many similarities, which is the biological basis for tumors as aging-related diseases. With the increase of tumor initiation cells and the decline of immune function in the elderly, the morbidity and mortality of tumors steadily increase. The core mechanisms are inflammaging and immunosenescence in the elderly. This article reviews recent advances in the field of tumorigenesis, inflammaging and immunosenescence, which elucidates the hypothesis and possible mechanism that tumors are aging-related diseases.
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B-cell lymphomas are a group of highly heterogeneous malignancies. The phenotypes of different subtypes depend on the differentiation stage and genetic changes of B-cell, which reflects in the immunophenotype, karyotype and tumor microenvironment changes, especially the differences in the cellular composition of microenvironment. This article reviews the characteristics of B-cell lymphoma cells and the cellular composition of microenvironment, discusses the role of tumor microenvironment cells in the occurrence and development of B-cell lymphoma, which provides new ideas for clinical diagnosis and treatment.
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Half a century ago,it was confirmed that leukemia could be induced by retroviruses in some animals.There are numerous en-dogenous retroviruses in the human genome.However,retrovirus-related human adult T-cell leukemia is only endemic in some local areas. Recently,an extensive study on apolipoprotein B mRNA editing enzyme catalytic polypeptide 3(APOBEC3)family members has revealed the resistance mechanism in human to retrovirus-induced leukemia.The Epstein-Barr virus is widely spread in the human population and exists as a latent infection in the human body for a long time.It is closely associated with the occurrence and development of some lymphomas and solid tumors,indicating its tumorigenicity.The relationship between other viral infections and leukemia/lymphoma remains unclear. The interaction may be mediated by complex,multistep,and indirect networks,which need to be further illuminated.
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Human herpes virus (HHV) spreads widely in a latent-infected way. HHV is divided into 3 kinds and 8 types. Herpes simplex caused by HHV-1 and HHV-2, varicella-zoster caused by HHV-3 and Epstein-Barr virus (EBV) known as HHV-4 and recognized firstly as human tumor virus, are well known in the field of virology. With the application of hematopoietic stem cell transplantation , cytomegalovirus (HHV-5) and HHV-6 have gained an increasing attention. The biological characteristic of HHV is latent infection in a long time and HHV can be reactivated in some immunocompromised individuals. Clarification of latent infection mechanism will help provide targets for therapy and lay a foundation for clinical treatment. This paper summarizes the clinical significance of HHV infection. Taking the mechanism of EBV latent infection as an example, the pathway and significance as well as strategy of co-evolution of organism and virus will be discussed in order to provide clues for prevention and therapy.
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Soft tissue sarcomas (STSs) are malignant tumors originating from mesenchymal tissues. They have lower morbidity rates than other cancers, which is only about 1% among adult malignancies. STSs consist of several subtypes and many of them are highly malignant. The 5-year survival rate is approximately 50%-60%. Investigation of STS pathogenesis demonstrated that epigenetic chang-es were closely related to the occurrence and development of STSs. Different from genetics changes, epigenetic changes are heritable and occur mainly through DNA methylation, histone modification, non-coding RNA regulation, and chromatin remodeling, all of which occur without changing the DNA sequence. Elucidation of the epigenetic mechanisms involved in STSs can help develop new clinical di-agnosis and treatment methods, and this article aims to review the recent advances in epigenetic research on STS.
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Human herpesvirus 6 (HHV-6) is recognized as a ubiquitous dsDNA virus in human with widespread cell tropism in vivo, which could induce lifelong latent infection and be reactivated in some immunocompromised individuals leading to serious diseases. With the increasing application of hematopoietic stem cell transplantation (HSCT), it is obvious that HHV-6 reactivation has a close relationship with several complications including encephalitis after transplantation. On the other hand, among about 1 % infected people, HHV-6 and subtelomeric region of cell chromosomes in the state of endogenous persistent infection play a part in activated virus infection. As the detection methods make a great progress in HHV-6 detection, clinical data reveals the relationship between HHV-6 reactivation and lots of chronic diseases, especially lymphoma, leukemia as well as some chronic hematopoietic and immunological diseases.
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Allee effect is a phenomenon in ecology characterized by a correlation between population size or density and the mean individual fitness of population or species.It is consistent with density dependent phenomenon in biomedical field.Recently,Allee effect has been studied by theoretical biologist in detail for oncology biological research.Leukemia cells,which reside in organic microenvironment,show an obvious Allee effect.The authors compared Allee effect with density dependent growth of leukemia cells based on their work experience and literature data.No principle distinction was found between these two terms.In this paper,Allee effect in leukemia cell culture and leukemia,especially in minimal residual disease,will be discussed in the view of ecology.The association between Allee effect and leukemogenesis and relapse dynamics will also be explored in the future research.
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Dormant follicular lymphoma, prostate carcinoma and breast carcinoma are frequently detected by autopsy of non-tumor patients. Dormancy of malignant cells in hematopoietic malignancies is associated with genesis, development and treatment of these diseases. Dormancy is the universally applied strategy by living organism during survival competition. As the in vivo neoplasm, tumor cells keep this property. Recently, much attention has been paid to the mechanisms of tumor dormancy. These studies not only have theoretical significance, provide new ways for the prevention and treatment of tumors, but also help the understanding of over-diagnosis, over-treatment and provide clues for precise medicine. This paper reviewed cellular mechanism of tumor cell dormancy,immunological and vascular regulation of dormant tumors. The clinical significance,application of these mechanisms and direction of further study, which will provide new clues for the treatment of hematopoietic malignancies, were also discussed.
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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.
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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.
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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.
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Objective To investigate the effects of overexpression of heat shock protein 22(HSP22) in hematopoietic malignant tumor cell lines.Methods A lentiviral system was used to mediate transduction of HSP22 complementary DNA-containing expression vector or empty vector into K562 and Namalwa cells.The transduction effeciency was tested by fluorescence microscope scan and flow cytometry.Semi-quantitative RT-PCR and Western blot were used to identify the expression levels of HSP22 mRNA and protein.Growth curve analysis,cell cycle analysis,colony-forming assay,tumor growth in nude mice and apoptosis analysis were used to evaluate the role of HSP22 in K562 and Namalwa cells.Results Lentivector expression systemmediated delivery of HSP22 into K562 and Namalwa cells can inhibit colony forming of K562 and Namalwa cells,the average numbers of colonies per well were 108,72,125 and 80 for K562-V,K562-H,Namalwa-V and Namalwa-H respectively (P =0.000 16 and 0.000 37 for K562 and Namalwa respectively).HSP22 transduction can also inhibit proliferation of Namalwa cells in vitro (P =0.015,0.042 and 0.048 for day 5,6 and 7 respectively) and K562 cells in vivo (P =0.022 for day 21).No significant difference in cell cycle and apoptosis was found in K562 and Namalwa cells compared with controls (all P ＞ 0.05).Conclusion Overexpression of HSP22 could inhibit the growth of hematopoietic malignant tumor cell lines K562 and Namalwa.
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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.
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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.
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After near a century of research,the diverse and complicated relationship between viruses and tumors has been elucidated gradually.Last century it was demonstrated that some retroviruses and some herpes viruses could induce lymphoma and leukemia in some animals.However,it is more complicated in human.During the last two decades it has been confirmed that several types of hepatitis viruses could cause hepatocellular carcinoma and the relationship between human papillomaviruses and cervix carcinoma has been established.These viral vaccines became useful tools to prevent prevalence of these carcinomas.Because of the successful inoculation of live attenuated viral vaccines all around the world in recent 15 years,oncolytic virotherapy is revived,and provides a novel strategy for treatment of refractory tumors.
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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.
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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.
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Objective To explore the mechanism of the cell-cycle arrest induced by human melanoma differentiation associated gene-7 (mda-7/IL-24) in chronic myelocytic leukemia cell line K562. Methods Microarray analysis was performed to determine the genes that were differentially regulated by mda-7/IL-24 in K562 cells, and was validated by realtime PCR. The phosphorylated pRb were detected by Western blotting analysis. Results A microarray analysis showed that G_0/G_1 phase-associated genes p21~(WAF-1) and BCCIP were up-egulated, while cdk6 and Smurf2 were down-regulated. The directional change in the expression of the four genes was successfully validated with real-time quantitative RT-PCR. pRb Set~(795) phosphorylation was observed with no modification of the pRb protein level. Conclusion These results suggest that IL-24/mda-7 may inhibit K562 proliferation and induce G_0/G_1 cell cycle angst by up-regulating p21~(WAF-1) and BCCIP, down-regulating cdk6 and Smurf2.