Today, the comprehensive surgical treatment for gastrointestinal cancer is almost in the perfect stage. It is difficult to further improve the curative effect by surgery only. To improve the overall curative effect of gastrointestinal tumor, translational medicine research should be promoted in the fields of the early diagnosis, etiology and pathogenesis and comprehensive treatment. Researches of discovering the new tumor markers for early diagnosis of tumor, etiology and pathogenesis involve many aspects, including environmental factors, genetic susceptibility, variation and accumulation of genetics, and epigenetic changes, which should be transferred to new methods of treatment. This review summarizes the gastrointestinal tumor-associated hot topics in the field of basic research and its progress, and provides the clinical clues from their conversion.
Biomarkers, Tumor ; Gastrointestinal Neoplasms ; diagnosis ; genetics ; Humans

With the improvement of high-throughput genomic technology such as microarray and next-generation sequencing over the last ten to twenty year, we have come to know that the portion of the genome responsible for protein coding constitutes just approximately 1.5%. The remaining 98.5% of the genome not responsible for protein coding have been regarded as 'junk DNA'. More recently, however, 'Encyclopedia of DNA elements project' revealed that most of the junk DNA were transcribed to RNA regardless of being translated into proteins. In addition, many reports support that a lot of these non-coding RNAs play a role in gene regulation. In fact, there are various functioning short non-coding RNAs including rRNA, tRNA, small interfering RNA, and micro RNA. Mechanisms of these RNAs are relatively well-known. Until recently, however, little is known about long non-coding RNAs which consist of 200 nucleotides or more. In this article, we will review the representative long non-coding RNAs which have been reported to be related to gastrointestinal cancers and to play a certain role in its pathogenesis.
Gastrointestinal Neoplasms/*genetics/*metabolism/pathology ; Humans ; Liver Neoplasms/genetics/metabolism/pathology ; RNA, Long Noncoding/genetics/*metabolism

With the improvement of high-throughput genomic technology such as microarray and next-generation sequencing over the last ten to twenty year, we have come to know that the portion of the genome responsible for protein coding constitutes just approximately 1.5%. The remaining 98.5% of the genome not responsible for protein coding have been regarded as 'junk DNA'. More recently, however, 'Encyclopedia of DNA elements project' revealed that most of the junk DNA were transcribed to RNA regardless of being translated into proteins. In addition, many reports support that a lot of these non-coding RNAs play a role in gene regulation. In fact, there are various functioning short non-coding RNAs including rRNA, tRNA, small interfering RNA, and micro RNA. Mechanisms of these RNAs are relatively well-known. Until recently, however, little is known about long non-coding RNAs which consist of 200 nucleotides or more. In this article, we will review the representative long non-coding RNAs which have been reported to be related to gastrointestinal cancers and to play a certain role in its pathogenesis.
Gastrointestinal Neoplasms/*genetics/*metabolism/pathology ; Humans ; Liver Neoplasms/genetics/metabolism/pathology ; RNA, Long Noncoding/genetics/*metabolism

Long non-coding RNAs (lncRNAs) are strongly related to the occurrence and development of digestive tract cancer in human. Firstly, lncRNAs target and regulate the expression of downstream cancer genes to affect the growth, metastasis, apoptosis, metabolism and immune escape of cancer cells. Secondly, lncRNAs are considered to be important regulating factors for lipid metabolism in cancer, which is related to signaling pathways of adipogenesis and involved in the occurrence and development of digestive tract cancer. Finally, lncRNAs have application value in the diagnosis and treatment of digestive tract cancer. For example, lncRNAMALAT1 has been reported as a target for diagnosis and treatment of hepatocellular carcinoma. This article reviews current progress on the regulatory role of lncRNAs in digestive tract cancer, to provide references for the research and clinical application in the prevention and treatment of digestive tract cancer.
Humans ; RNA, Long Noncoding/genetics* ; Gastrointestinal Neoplasms/genetics* ; Apoptosis ; Liver Neoplasms

Colorectal cancers (CRC)-and probably all cancers-are caused by alterations in genes. This includes activation of oncogenes and inactivation of tumor suppressor genes (TSGs). There are many ways to achieve these alterations. Oncogenes are frequently activated by point mutation, gene amplification, or changes in the promoter (typically caused by chromosomal rearrangements). TSGs are typically inactivated by mutation, deletion, or promoter methylation, which silences gene expression. About 15% of CRC is associated with loss of the DNA mismatch repair system, and the resulting CRCs have a unique phenotype that is called microsatellite instability, or MSI. This paper reviews the types of genetic alterations that can be found in CRCs and hepatocellular carcinoma (HCC), and focuses upon the epigenetic alterations that result in promoter methylation and the CpG island methylator phenotype (CIMP). The challenge facing CRC research and clinical care at this time is to deal with the heterogeneity and complexity of these genetic and epigenetic alterations, and to use this information to direct rational prevention and treatment strategies.
Colorectal Neoplasms/genetics ; DNA Methylation/*genetics ; Gastrointestinal Neoplasms/*etiology/*genetics ; Humans ; Microsatellite Instability ; Promoter Regions, Genetic/*genetics

Gastrointestinal stromal tumors(GIST) are known for their molecular alterations in KIT or PDGFR genes, and have become the paradigm of molecularly targeted therapies for solid tumors. Recent researches of genotype and phenotype demonstrate that molecular subtypes can predict the response to treatment with tyrosine kinase inhibitors and are related with prognosis. Different strategies will be recommended according to different molecular subtypes of GIST in the future for treatment optimization and individualization.
Gastrointestinal Neoplasms ; genetics ; therapy ; Gastrointestinal Stromal Tumors ; genetics ; therapy ; Genotype ; Humans ; Prognosis ; Proto-Oncogene Proteins c-kit

Mutation of c-kit and platelet-derived growth factor receptor alpha (PDGFRA) is the most important molecular feature of gastrointestinal stromal tumor (GIST). Mutation detection of these two genes is of great significance when establishing the diagnosis of a kit-negative GIST, or when predicting response to tyrosine kinase inhibitor. Furthermore, more and more researches focus on the feasibility of the mutation status using as a prognostic factor in recent years.
Gastrointestinal Neoplasms ; diagnosis ; drug therapy ; genetics ; Gastrointestinal Stromal Tumors ; diagnosis ; drug therapy ; genetics ; Humans ; Mutation ; Proto-Oncogene Proteins c-kit ; genetics ; Receptor, Platelet-Derived Growth Factor alpha ; genetics

Long non-coding RNAs (lncRNAs) are a class of non-coding transcripts which are greater than 200 nucleotides in length and have a variety of biological functions. Studies have found that lncRNAs play an important role in the development of gastrointestinal cancers and can affect tumor cell growth, angiogenesis, metastasis and drug resistance. This paper has reviewed lncRNAs associated with gastrointestinal cancers and explored their roles in the occurrence, diagnosis and treatment of gastrointestinal cancers.
Animals ; Gastrointestinal Neoplasms ; genetics ; metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; RNA, Long Noncoding ; genetics ; metabolism

OBJECTIVE: To study genetic alterations in 13 CODIS STR loci in various tumor tissue samples from human digestive system. METHODS: Malignant tumor tissues and blood samples taken from 55 different unrelated individuals were collected. DNA samples were extracted using Chelex100 extraction kit, amplified using Profiler and Cofiler PCR amplification kit and analyzed using API 310 analyzer. RESULTS: Aberrant cell divisions were detected in all of the 55 tumor tissue samples, with STR alternations detected in two samples including allelic alteration, partial and complete loss or unbalance of heterozygosity. Moreover, the alternations might occur simultaneously at more than one loci. CONCLUSION Caution must be taken in STR analysis of tumor tissue samples since the exclusion loci in forensic identification or paternity testing may be resulted from mutations in the tumor tissue.
Alleles ; DNA, Neoplasm/analysis* ; Digestive System Neoplasms/genetics* ; Gastrointestinal Neoplasms/genetics* ; Genetic Variation ; Genotype ; Humans ; Loss of Heterozygosity ; Pancreatic Neoplasms/genetics* ; Polymerase Chain Reaction ; Tandem Repeat Sequences/genetics*

Adolescent ; Adult ; Aged ; Exons ; Female ; Gastrointestinal Neoplasms ; genetics ; Gastrointestinal Stromal Tumors ; genetics ; Humans ; Male ; Middle Aged ; Mutation ; Proto-Oncogene Proteins c-kit ; genetics ; metabolism ; Young Adult