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1.
Cancer Commun (Lond) ; 41(11): 1195-1227, 2021 11.
Article in English | MEDLINE | ID: mdl-34699681

ABSTRACT

Nasopharyngeal carcinoma (NPC) is a malignant epithelial tumor originating in the nasopharynx and has a high incidence in Southeast Asia and North Africa. To develop these comprehensive guidelines for the diagnosis and management of NPC, the Chinese Society of Clinical Oncology (CSCO) arranged a multi-disciplinary team comprising of experts from all sub-specialties of NPC to write, discuss, and revise the guidelines. Based on the findings of evidence-based medicine in China and abroad, domestic experts have iteratively developed these guidelines to provide proper management of NPC. Overall, the guidelines describe the screening, clinical and pathological diagnosis, staging and risk assessment, therapies, and follow-up of NPC, which aim to improve the management of NPC.


Subject(s)
Nasopharyngeal Neoplasms , China , Humans , Medical Oncology , Nasopharyngeal Carcinoma/diagnosis , Nasopharyngeal Carcinoma/therapy , Nasopharyngeal Neoplasms/diagnosis , Nasopharyngeal Neoplasms/therapy
2.
Genes Dis ; 7(3): 351-358, 2020 Sep.
Article in English | MEDLINE | ID: mdl-32884989

ABSTRACT

The phenomenon of enhanced invasion and metastasis of residual tumor cells has been observed in an increasing number of patients receiving chemoradiotherapy recently, and tumor metastasis will undoubtedly limit patient prognosis. However, the key mechanism by which chemoradiotherapy affects the invasion and metastasis of tumor cells remains unclear. Studies have shown that chemoradiotherapy may directly act on tumor cells and alter the tumor microenvironment, or induce cell apoptosis and autophagy to promote tumor cell survival and metastasis. In this review, we summarize the potential mechanisms by which chemoradiotherapy may affect the biological behavior of tumor cells and open up new avenues for reducing tumor recurrence and metastasis after treatment. These insights will improve the efficacy of chemoradiotherapy.

3.
Biomed Res Int ; 2017: 8421614, 2017.
Article in English | MEDLINE | ID: mdl-28656150

ABSTRACT

Preoperative 5-fluorouracil- (5-FU-) based chemoradiotherapy is a standard treatment for locally advanced colorectal cancer (CRC). However, the effect of 5-FU-based chemoradiotherapy on CRC is limited due to the development of chemoradiation resistance (CRR), and the molecular mechanisms underlying this resistance are yet to be investigated. Recently, circular RNAs (circRNAs), which can function as microRNA sponges, were found to be involved in the development of several cancers. In this study, we focused on clarifying the modulation of the expression profiles of circRNAs in CRR. Microarray analysis identified 71 circRNAs differentially expressed in chemoradiation-resistant CRC cells. Among them, 47 were upregulated and 24 were downregulated by more than twofold. Furthermore, expression modulation of five representative circRNAs was validated by quantitative reverse transcription PCR (qRT-PCR). Moreover, these modulated circRNAs were predicted to interact with 355 miRNAs. Furthermore, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that the most modulated circRNAs regulate several cancers and cancer-related pathways, and the possible mechanism underlying CRR was discussed. This is the first report revealing the circRNA modulations in 5-FU chemoradiation-resistant CRC cells by microarray. The study provided a useful database for further understanding CRR and presents potential targets to overcome CRR in CRC.


Subject(s)
Colorectal Neoplasms/genetics , Fluorouracil/adverse effects , Gene Expression Regulation, Neoplastic/genetics , RNA/blood , Chemoradiotherapy/adverse effects , Colorectal Neoplasms/drug therapy , Colorectal Neoplasms/pathology , Colorectal Neoplasms/radiotherapy , Drug Resistance, Neoplasm/genetics , HCT116 Cells , Humans , Neoplasm Proteins/genetics , Oligonucleotide Array Sequence Analysis , RNA, Circular
4.
Asian Pac J Cancer Prev ; 16(8): 3395-402, 2015.
Article in English | MEDLINE | ID: mdl-25921151

ABSTRACT

BACKGROUND: Preoperative 5-fluorouracil (5-FU)-based chemoradiotherapy is a standard treatment for locally advanced colorectal cancer (CRC). However, CRC cells often develop chemoradiation resistance (CRR). Recent studies have shown that long non-coding RNA (lncRNA) plays critical roles in a myriad of biological processes and human diseases, as well as chemotherapy resistance. Since the roles of lncRNAs in 5-FU-based CRR in human CRC cells remain unknown, they were investigated in this study. MATERIALS AND METHODS: A 5-FU-based concurrent CRR cell model was established using human CRC cell line HCT116. Microarray expression profiling of lncRNAs and mRNAs was undertaken in parental HCT116 and 5-FU-based CRR cell lines. RESULTS: In total, 2,662 differentially expressed lncRNAs and 2,398 mRNAs were identified in 5-FU-based CRR HCT116 cells when compared with those in parental HCT116. Moreover, 6 lncRNAs and 6 mRNAs found to be differentially expressed were validated by quantitative real time PCR (qRT-PCR). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis for the differentially expressed mRNAs indicated involvement of many, such as Jak- STAT, PI3K-Akt and NF-kappa B signaling pathways. To better understand the molecular basis of 5-FU-based CRR in CRC cells, correlated expression networks were constructed based on 8 intergenic lncRNAs and their nearby coding genes. CONCLUSIONS: Changes in lncRNA expression are involved in 5-FU-based CRR in CRC cells. These findings may provide novel insight for the prognosis and prediction of response to therapy in CRC patients.


Subject(s)
Antineoplastic Agents , Colorectal Neoplasms/genetics , Drug Resistance, Neoplasm/genetics , Fluorouracil , Gene Expression Regulation, Neoplastic , RNA, Long Noncoding/metabolism , RNA, Messenger/metabolism , Radiation Tolerance/genetics , Chemoradiotherapy , Colorectal Neoplasms/therapy , Gene Expression Profiling , HCT116 Cells , Humans , Janus Kinases/genetics , Microarray Analysis , NF-kappa B/genetics , Phosphatidylinositol 3-Kinases/genetics , Proto-Oncogene Proteins c-akt/genetics , RNA, Long Noncoding/genetics , Real-Time Polymerase Chain Reaction , STAT Transcription Factors/genetics , Signal Transduction/genetics
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