Tumor is a complex systemic disease, involving abnormalities at multiple levels, such as DNA, RNA, protein and metabolite. According to the central rule, the derived omics methods are genomics, transcriptomics, proteomics and metabonomics. In the past few decades, there have been remarkable achievements in the single omics study of tumor, but the exact mechanism of tumor development is still unclear. In order to reveal the process of tumorigenesis and development in a more systematic way, the research of multiomics came into being, which promoted the transformation of tumor research paradigm from single parameter model to multi parameter system model. The integration of multi-omics methods is expected to clarify the mechanism of tumor occurrence and development, find biomarkers with diagnostic, prognostic and predictive performance, explore new treatment targets, and finally achieve predictive, preventive, and personalized medicine (PPPM). This paper reviews the research methods and progress of different omics techniques in tumor research, especially emphasizes the importance and scientific value of the integration of multiple omics techniques in tumor research and clinical related results.

Proteomics research has been performed for more than 20 years. Early research was based on simple Western blot technology, and later, mass spectrometry was used to identify proteins. However, the limited sequencing depth and the number of identified proteins in initial mass spectrometry technology have caused bottlenecks in proteomics research. In recent years, with the rapid development of mass spectrometry technology, high-throughput proteomics identification has been achieved, and proteomics research has entered a new era. At present, the application of high-throughput proteomics technology in the field of cancer mainly includes revealing the mechanism of tumorigenesis and development, searching for specific biomarkers, elucidating the mechanism of drug resistance, and identifying new therapeutic targets. Early detection and diagnosis of tumors are helpful for timely medical intervention, greatly improving the survival rate and quality of life. Recently, several candidate tumor biomarkers have been identified, but only a few have been used clinically. Here, aiming to explore tumor-specific biomarkers, we selected four high morbidity/mortality rate tumors with extensive application of high- throughput proteomics technology, such as lung, breast, colorectal, and liver cancer. We screened recently published studies from journals with high impact factors, evaluated by their expanded sample size or functional verification, and strong evidence in different tumor types. This article first briefly introduces mass spectrometry-based high-throughput proteomics technology and commonly used specimen types, and then focuses on reviewing the protein markers that may be used for early diagnosis, prognosis, and targeted therapy in the above four high-incidence cancers, aiming to provide a new theoretical basis for accurate diagnosis and treatment of tumors.

OBJECTIVE: To detect pathogenic variant of the FGD1 gene in a boy with Aarskog-Scott syndrome. METHODS: Genetic variant was detected by high-throughput sequencing. Suspected variant was verified by Sanger sequencing. The nature and impact of the candidate variant were predicted by bioinformatic analysis. RESULTS: The child was found to harbor a novel c.1906C>T hemizygous variant of the FGD1 gene, which has led to conversion of Arginine to Tryptophane at codon 636(p.Arg636Trp). The same variant was found in his mother but not father. Based on the American College of Medical Genetics and Genomics guidelines, the c.1906C>T variant of FGD1 gene was predicted to be likely pathogenic(PM1+PM2+PM5+PP2+PP3+PP4). CONCLUSION The novel c.1906C>T variant of the FGD1 gene may underlay the Aarskog-Scott syndrome in this child. Above finding has enabled diagnosis for the boy.
Child ; Dwarfism ; Face/abnormalities* ; Genetic Diseases, X-Linked ; Genitalia, Male/abnormalities* ; Guanine Nucleotide Exchange Factors/genetics* ; Hand Deformities, Congenital/genetics* ; Heart Defects, Congenital ; Humans ; Male ; Mutation

甲状腺癌是常见的内分泌恶性肿瘤，发病率逐年增加。深入了解甲状腺癌发生发展机制对提高诊断准确性、进行精准风险分层和实现个性化治疗至关重要。近年来，随着质谱相关技术的不断发展，基于不同标本类型（细胞、组织、血清和尿液）的多种蛋白质组学分析方法已被广泛应用于甲状腺癌的研究中，从阐明发病机制、诊断分型、预测预后和靶向治疗等方面积极地推动了甲状腺癌精准诊疗的发展。

Objective:To investigate the effect of mannose on the radiosensitivity of six human non-small cell lung cancer cell lines and its possible mechanism.Methods:The expression of mannose phosphate isomerase in six lung cancer cell lines were detected by Western blot. The inhibitory effect of mannose on the proliferation of lung cancer cell lines were observed by MTT assay. When irradiated with 0, 2, 4, 6, 8 and 10 Gy, the effect of mannose on the radiosensitivity of six lung cancer cell lines was detected by plate clone formation assay, respectively; and the apoptosis rates of normal control, mannose, irradiation and combined groups were detected by flow cytometry.Results:The expression levels of mannose phosphate isomerase were different among six lung cancer cell lines. Among them, A549 cells had the highest expression level and H460 cells showed the lowest expression level. When aD ministrated with 11.1 mmol/L mannose, the same inhibitory effect was observed on both A549 and H460 cell lines. Moreover, the inhibitory effect on H460 cell line was significantly increased with the increase of mannose concentration. In addition, aD ministration of 11.1 mmol/L mannose could significantly increase the radiosensitivity and apoptosis rate of H460 cell line. However, it exerted limited effect upon the radiosensitivity and apoptosis rate of A549 cell line. Conclusion:In six lung cancer cell lines with high expression of mannose phosphate isomerase, the aD ministration of mannose can enhance the radiosensitivity of partial tumors cells.