Dysregulated cell cycle-mediated cell transformation and uncontrolled cell growth are some of the fundamental biolog-ical features of malignant tumors. Thus, understanding the mechanism(s) involved in the cell cycle will facilitate the discovery of the na-ture of tumor initiation and progression as well as the molecular mechanism of tumor malignancy. Consequently, biomarkers and drug targets for early diagnosis and treatment would be obtained. This study was designed to analyze in detail the key regulators of cell cycle and their importance in carcinogenesis and clinical prevention, diagnosis and treatment, and anti-cancer drug discovery. The biological impact of the dysregulated cell cycle on tumor occurrence and malignancy development is systematically described. The theoretical and practical significance of the cell cycle regulation in tumor diagnosis and therapy are also provided.

Precision medicine is a new developing area of medical research and clinical practice, which is stemmed from the urgent need for high-profile medical health care and fast emergence of exquisite biological and medical technologies.Precision medicine, mainly based on the individualized molecular medicine and sophisticated medical techniques, offers multiple dimensional imaging examinations and biological molecular assays to make subsequent therapeutic strategies much more optimized to the personal disease characteristics than the traditional regimes, hence pursuing maximized efficacy and minimized side effects.The precision medicine in China is stepping into a vigorously developing stage after its first official initiation.This review summarized the development and program design of precision medicine in China to shed light on this growingly progressing area.

Gadd45a, a p53 and BRCA1-regulated growth arrest and DNA damage gene, plays important roles in suppressing cell transformation and tumor malignancy. Gadd45a maintains the genomic stability through inhibiting the cell growth and promoting the DNA repair etc, by which it suppresses the tumor development. Additionally, Gadd45a is involved in some important signaling pathway, contributing to its function in tumor suppressing.

Objective To indentify the gene expression on different fractionated radiation regimens with the same total radiation dose in xenografts with human lung adenocareinoma. Methods Forty-eight BALB/c-nu mice, implanted with human lung adenocarcinoma (Anip973), were randomized into 4 groups: normal control greup,60 Gy in 30 fractions conventional radiation group (2 Gy group) ,60 Gy in 10 fractions hypofractionated radiation group (6 Gy group) ,60 Gy in 6 fractions hypofractionaed radiation group (10 Gy group). Gene alterations were investigated with the microchip analytical procedures covering the entire genome. Genes with significantly different expression were further validated by the quantitative real-time polymerase chain reaction (RT-PCR). Results Compared to the 2 Gy group, the expression of the genes related with the cell growth inhibition and apoptesis was increased, while the genes related with the cell proliferation, anti-apoptosis and DNA damage repair were decreased in the 6 Gy and 10 Gy groups. Confirmed by RT-PCR, c-myc gene was distinctly suppressed in the 6 Gy group (2. 9%) comparing with 2 Gy (5.6%) group and 10 Gy (4.8%) group (P=0. 000,P=0. 002) , and was slightly suppressed in the 10 Gy group comparing with 2 Gy group (P = 0. 069). Conclusions In the BALB/c-nu mice implanted with human lung adenocarcinoma, the hypofractionated radiation regimens clearly inhibit the tumor growth more than conventional fractionation group, though with the same total dose. The 6 Gy group seem to be more effective than 10 Gy group in the inhibition of tumor growth.

Objective To screen the genes most relevant to lymph node metastasis of cervical cancer and identify the genes at the key knots of the regulatory network to provide the potential targets for cervical cancer intervention.Methods The transcriptional profiling database of TCGA was used, and random forests algorithm was adopted to rank the genes related to lymph node metastasis extracted from GeneCards database.STRING and Cytospace tolls were used to build the interactive regulatory network and identify the most weighted genes localized in the central of the network.DAVID platform was used to perform a functional annotation for the whole geneset.Results We ranked 2784 genes in respect to their potential contributions to lymph node metastasis of cervical cancer and identified the genes at the key knob.The genes related to cancer metastasis were enriched to cytokines pathway, MAPK pathway, wnt pathway, intercellular interaction, adhesive conjunction, cellular skeleton regulation, etc.Some of the identified key genes, like EGFR, NOTCH1, RHOA, etc. have been verified to be closely related cervical cancer metastasis in the basic and clinical research. Conclusion Random forests algorithm is useful, taking advantages of TCGA database, in enriching the genes playing significant role in cervical cancer metastasis.A majority of the genes in the analyzed geneset were indicated to be significantly correlated with lymph node metastasis.

Objective To investigate the biological effects of exosomes secreted by KYSE410 cells on migration and invasion of KYSE410,KYSE510,YES2 cells and the possible mechanisms underlying the phenotype change.Methods The exosomes were isolated from the conditional supernatant of esophageal cancer cell line KYSE410 by ultracentrifugation.The morphology of exosomes was observed by transmission electron microscopy (TEM).Western blotting was used to detect the protein markers of exosomes.The uptaken of fluorescence-labeled KYSE410 exosomes by KYSE410,KYSE510 and YES2 was also recorded under confocal microscopy.Migration and invasion ability of the three esophageal carcinoma cell lines and the effects of exosomes from KYSE410 on migration and invasion of KYSE410,KYSE510 and YES2 cells were analyzed by Transwell chamber,respectively.The alteration of Wnt/β-catenin and PI3K/Akt pathway-related proteins were detected by Western blotting.Results The membrane structure of KYSE410 derived exosomes could be observed with its diameter ranged between 30-100nm.The invasion and migration ability of three esophageal cancer cells are KYSE410＞ KYSE510＞ YES2.KYSE410 exosomes promoted the migration and invasion of KYSE410,KYSE510 and YES2 cells.Conclusions Concentrated exosomes derived from the highly migratory and invasive esophageal cancer cell line KYSE410 promoted the migration and invasion potentials of itself and esophageal cancer cell lines KYSE510 and YES2,which possibly exerted the effects by activating Wnt/β-catenin and PI3K/Akt signaling pathways.

Objective Mitotic spindle and midbody are both microtubule-based temporary structures during cell growth and play essential roles in mitosis.The purpose of this study was to establish a mature and efficient method to extract mitotic spindle and midbody.Methods Through the cell cycle synchronization method,mitotic spindle or midbody was made appear inside cells.Low permeability swelling and glycerol gradient centrifugation principles were then used to extract spindle and midbody.Results By Western Blot and immunofluorescence staining,the extracts were identified as mitotic spindle and midbody.Conclusions The successful extraction of mitotic spindle and midbody from synchronized Hela cells will provide foundation for identifying the proteins located in cell during mitosis,and be of great significance to the study of molecular regulation mechanisms of mitosis and tumorigenesis.

长链非编码RNA（long non-coding RNA，lncRNA）最初被认为是不具有功能的“转录噪声”，但越来越多的研究发现， lncRNA的失调在很多肿瘤中起着癌基因或抑癌基因的作用，是癌症发展的关键分子。PANDAR作为一种重要的lncRNA受到了 诸多关注。有研究证明，PANDAR在许多肿瘤中特异性表达，在大多数肿瘤中上调，但在非小细胞肺癌中显著下调，PANDAR的 特异性表达与肿瘤大小、TNM分期和总生存率显著相关。本文通过对lncRNAPANDAR在恶性肿瘤细胞中的主要作用模式、 表 达情况、作用机制及对各类肿瘤发生发展的影响进行综述，旨在为临床恶性肿瘤生物学诊治疗提供新的靶标。

外泌体是一种纳米级别的生物膜结构，由机体的多种细胞分泌，广泛分布于唾液、血浆、乳汁等体液中。外泌体中含 有蛋白质、mRNA、miRNA、lncRNA、细胞因子、转录因子受体等多种生物活性物质。肿瘤细胞或肿瘤旁细胞分泌的外泌体可将 一些肿瘤特有的生物信息转移到邻近细胞，甚至远处细胞，并且通过这种细胞间通信传递肿瘤的特性，从而促进肿瘤的发生发 展。本综述旨在着重讨论肿瘤细胞及癌旁细胞分泌的含lncRNA的外泌体对肿瘤微环境，肿瘤的生物学特性的影响，为肿瘤的基 础研究及临床诊断治疗提出新的思路。

肺癌的发病机制非常复杂，目前仍未明确。研究发现miRNA是肿瘤中的一组重要的调节因子，与肺癌的发生发展密 切相关，异常表达后可作为致癌miRNA或抑癌miRNA参与调控信号通路基因的表达，影响肺癌细胞的增殖、迁移、侵袭、转移等 过程。本文就miRNA作为抑癌或致癌基因在肺癌发生发展中机制的最新研究进展进行综述。