BACKGROUND:Hematopoietic microenvironment regulates hematopoietic stem cel s mainly through the cel-cel , cel-soluble regulator and cel-extracel uar matrix modes. OBJECTIVE:To review the molecular mechanism underlying regulation of hematopoietic stem cel s under the cel-cel , cel-soluble factors and cel-extracel ular matrix modes. METHODS:A computer-based online search of PubMed database was performed to search related articles with the key words of“Niche, HSC, VCAM-1, VLA-4, TPO, MPL, ECM, Integrin, N-cadherin, ANG-1, Tie2, VLA-5, Jagged-1, Notch, CXCL12, CXCR4, SCF, Kit, BMPs/TGF-β, TGF-βR, IFNα, IFNαR”in English. Irrelevant or repetitive studies as wel as old literature were excluded, and final y 80 articles were included in result analysis. RESULTS AND CONCLUSION:Cel s on the endosteal surface, vascular endothelial cel s, perivascular cel s, and some unknown or certain cel s or smal molecules in the bone marrow cavity constitute the specialized microenvironment for hematopoietic stem cel s. Hematopoietic stem cel s in the hematopoietic microenvironment remain a relatively steady state, which is the result of mutual contact of hematopoietic stem cel s and hematopoietic microenvironment under the regulation of some important molecules, such as Pten and osteopontin, via the pathway between cel-intercel ular adhesions, intercel ular soluble factors, and cel s and extracel ular matrix.

BACKGROUND:It has been observed recently that tumor recurrence is closely related to cancer stem cel s. Cancer stem cel theory provides a new avenue for the study of gastric cancer pathogenesis, diagnosis and treatment. To determine the cel phenotype is helpful to target gastric cancer stem cel s, and contributes to exploring the self-renewal and differentiation of gastric cancer stem cel s, further providing new ideas for the treatment of gastric cancer. However, the phenotype of gastric cancer stem cel s remains controversial.
OBJECTIVE:To review the research progress in gastric cancer stem cel phenotype.
METHODS:A computer-based online search of PubMed database was performed to search related articles published between January 1965 and October 2015 with the key words of“Gastric Cancer Stem Cel s”in English. Sixty-eight articles were included for final analysis.
RESULTS AND CONCLUSION:Traditional cancer stem cel phenotypes are unsuitable for marking
gastric cancer stem cel s. Studies have found that CD90 expresses in primary gastric cancers, and cancer stem cel spheres would be required via serum-free culture by CD90 maker. CD24 expression can improve the adhesion, invasion and migration of gastric cancer cel s. Further studies have confirmed that a lot of cel s positive for both CD44 and CD54 can be found in patients with early recurrence of gastric cancer rather than those with advanced recurrence, and CD44 and CD54 expression in tumor cel s is likely to be an important cause of gastric cancer occurrence and recurrence. By analyzing the sorting, CD44+CD24+CD90+CD54+is likely to be the gastric cancer stem cel phenotype.

BACKGROUND: Telomere-associated proteins wil directly affect the function of telomeres, adjust the length of telomeric DNA, which are closely related with cellsenescence and carcinogenesis. OBJECTIVE: To find the key regulatory molecules in the cellsenescence process through observing the telomere-associated factor expression in normal cel replicative senescence process. METHODS: Based on established cel replicative senescence model, reverse transcription-PCR and western blot were used to detect the telomere-associated factor expression on the molecular and protein levels, including the telomere-associated factor human telomere binding protein 1, tankyrase 1, telomerase RNA, telomere protection protein 1 and P53 expressions in the human embryonic lung fibroblast replicative senescence. RESULTS AND CONCLUSION: The results showed that with the cellsenescence, transcription of human telomere binding protein 1 did not changed, while the protein expression of human telomere binding protein 1 was increased gradual y and then decreased rapidly; mRNA and protein expressions of telomere protection protein 1 did not changed; with the human embryonic lung fibroblast replicative senescence, expression of telomere protection protein 1 was decreased gradual y; with cellsenescence, telomerase RNA component showed an increasing trend; protein expression of P53 did not changed. Human telomere binding protein 1, telomere protection protein 1 and telomerase RNA play an important role in cellsenescence.

Objective To screen mutations in genes including ASXL1, TET2, IDH1, IDH2, SETBP1, MPL515, JAK2 exon 12 and JAK2V617 in 135 polycythemia vera (PV) patients. To assess progreasson and genomics characteristics post polycythemic myelofibrosis. Methods DNA sequencing of ASXL1(Exon12),TET2 (Exons 3-11),IDH1(Exon4),IDH2(Ex-on4),SEPBP1(Exon4),JAK2 exon 12 and MPL515 (Exon 10) genes were carried out using Sanger method. JAK2V617 muta-tion was detected by allele-specific PCR in patients with PV. In the mean time, the mutation load of JAK2V617F allele (V617F%) was evaluated by real-time PCR using Tagman MGB probe. Then, the significant of gene mutations and clinical outcomes of post-PV Myelofibrosis(PPMF)was analyzed. To study risk factors of PPMF, logistic regression were employed. Results ASXL1, TET2, IDH1, IDH2 were mutated in 7.69%(8/104), 5.26%(1/19) , 0.08%(1/120) and 0.08%(1/121) of all PV patient respectively. JAK2 was mutated in 82.22%(111/135) of PV patients with mutation rate of exon12 of 2.96%(4/135) and there were no mutation of MPL515 and SETBP1 in PV patients. ASXL1 mutation was found in 31.82%(7/22) PPMF patients. Spearman analysis showed that ASXL1 is correlated with JAK2V617F (V617F%) (rs=0.298,P=0.002). The hemo-globin was lower in patients with ASXL1 mutation than patient without mutation (wild type). Leukocyte count, V617F%>50%rate, thrombosis and PPMF were higher in patients with ASXL1 mutation than that of ASXL1 wild type(P＜0.05). ASXL1 mu-tation, V617F%>50% rate and splenomegaly were all risk factors of PPMF. Conclusion ASXL1 mutation is the risk-fac-tor of PPMF and may promote V617F%by some mechanism.

Drug resistance is a major challenge in the treatment of breast cancer. Many causes and mechanisms lead to the occurrence of drug resistance in breast cancer. Exosomes and their contents (DNA, mRNA, protein, and non-coding RNA) are important mediators of intercellular communication and play a role in tumor progression, metastasis, and recurrence. Among them, non-coding RNA carried by exosomes plays a crucial role in limiting drug efficacy. This article reviews the latest research progress on the relationship between exosomal non-coding RNA and drug resistance of breast cancer at home and abroad.

OBJECTIVETo study the clinical manifestation, pathologic features and immunophenotype of histiocytic necrotizing lymphadenitis (HNL).

METHODSThe clinicopathologic data of 84 patients with HNL from 2005 to 2014 were retrospectively studied. Immunohistochemical staining using EliVision method for CD20, PAX5, CD3, CD45RO, CD4, CD8, CD56, CD68, CD123, granzyme-B, TIA1 and MPO was carried out. In-situ hybridization for Epstein-Barr virus RNA was performed on archival lymph node biopsy tissue.

RESULTSImmunohistochemical study showed that the lesional cells were predominantly histiocytes (CD68+), plasmacytoid dendritic cells (CD123+) and T lymphocytes (CD3+ and CD45RO+). Clusters of CD68-positive cells with strong and diffuse MPO expression were identified. T lymphocytes with CD4 and CD8 positivity were noted. CD56+ natural killer cells and CD20+/PAX5 B cells were rare. Apoptosis-related markers, including TIA1 and granzyme B were expressed by T lymphocytes and histiocytes in lymph nodes of HNL. In-situ hybridization for Epstein-Barr virus RNA was positive in only 10.0% of the cases.

CONCLUSIONSHNL shows no specific clinical and laboratory findings. Recognition of the characteristic histopathologic changes in lymph node biopsy of HNL is the key to correct diagnosis. Immunohistochemical study using a panel of markers, including CD3, CD4, CD8, MPO, CD123, granzyme-B and TIA1, is helpful in the differential diagnosis of HNL.

Antigens, CD ; analysis ; Biomarkers ; Dendritic Cells ; pathology ; Diagnosis, Differential ; Granzymes ; analysis ; Herpesvirus 4, Human ; genetics ; Histiocytes ; pathology ; Histiocytic Necrotizing Lymphadenitis ; complications ; immunology ; pathology ; virology ; Humans ; Immunohistochemistry ; Immunophenotyping ; In Situ Hybridization ; methods ; Lymph Nodes ; RNA, Viral ; analysis ; Retrospective Studies ; T-Lymphocytes ; immunology ; pathology