The occurrence and development of tumors are determined by both intrinsic and microenvironmental factors. The components of the tumor microenvironment exhibit great heterogeneity resulting in either pro-tumor or anti-tumor effects. The deep exploration of tumor immune microenvironment gave birth to the hypothesis of cancer immunoediting, which is supported by more and more evidence. Cancer immunoediting is accomplished through the interactions among various cells and factors in the microenvironment. While many molecular mechanisms have been studied, the cellular mechanisms of cancer immunoediting have been paid attention. This article explores the roles of cellular mechanisms in the cancer immunoediting, including immunogenic cell death, cellular senescence and neutrophil extracellular trap. The elucidation of these mechanisms not only reveals the complexity of the pathogenesis and progression of tumors, but also provides new targets and prognostic indicators for the diagnosis and treatment of tumors.

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.

Objective To analyze the correlation between detection of influenza pathogenic subtypes and epidemic situation in Hefei City during the surveillance years of 2015-2021, and to provide references for developing influenza prevention and control strategies. Methods The relevant data of influenza-like illness (ILI) surveillance, influenza etiology, and outbreak/cluster outbreaks reported from influenza surveillance sentinel hospitals in Hefei City from 2015 to 2021 in the China Influenza Surveillance Information System were analyzed. The statistical analysis was carried out. Results A total of 3 332 553 outpatient and emergency visits in 2 sentinel hospitals were reported in Hefei City from 2015 to 2021, of which 139,082 were ILI cases, accounting for 4.17%. The monthly proportion ranged from 1.60% to 7.15%. A total of 14 663 ILI specimens were submitted for detection, the submission rate was 10.54%, and the positive rate of influenza virus detection was 11.30%. There was no correlation between the proportion of monthly influenza like cases and the detection rate (r_s=0.176, P=0.107). The composition ratio of each subtype of influenza virus varied greatly, showing diversified seasonality, and the epidemic strains changed constantly. The Victoria subtype (BV subtype) was dominant (40.21%). There was a moderate correlation between the positive rate of ILI in sentinel hospitals and the number of outbreaks per month (r_s=0.696, P=0.000). There was a strong correlation between the monthly number of outbreaks and the detection rate (r_ss=0.696, P=0.000). There was a strong correlation between influenza A virus H3 subtype and BV subtype (r_{s -H3}=0.686, P=0.030; r_{s -BV}=0.632, P=0.000). There was a moderate correlation between the new A1 subtype and B Yamagata subtype (r_{s -new A H1}=0.481, P=0.000 0; r_{s -BY}=0.515, P=0.000). Conclusion There are two epidemic peaks in spring and winter in Hefei. Influenza subtypes are diverse. The results of ILI etiology can predict the outbreaks of different subtypes of influenza. Prediction and surveillance should be used for influenza control and outbreak management in a timely manner.

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.

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.

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.

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.

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.

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.

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.