The autophagy is associated with many diseases such as tumors, neurodegenerative diseases, immune diseases, cardiovascular diseases, aging and diabetes. Defining its mechanism can further understand the regularity of disease occurrence and provide new ideas for exploring new therapeutic targets.
Autophagy is a steady-state process and a cellular defense mechanism that participates in many life activities of mammals and plays an important role. Further studies for the mechanisms of autophagy and epigenetic modification should be made to explore the potential therapeutic targets for clinical treatment.
Autophagy can maintain the homeostasis of cells by removing the accumulated proteins, damaged organelles and pathogens. Studies have shown that autophagy is closely related to a variety of life activities, and its dysfunction often leads to tumor, degenerative diseases and other diseases. Epigenetic modification is widely involved in autophagy and plays an important role in the occurrence and development of many diseases. In order to further understand the mechanism of autophagy, we review the related signaling pathways and epigenetic modifications of autophagy.
GSPP did not have inhibitory effects on the proliferation and migration of human fibrosarcoma HT1080 cells.
Thus further research should be carried out in order to study the mechanism of GSPP and bFGF acting on the tumor stroma.
Background: Fibrosarcoma is a malignant soft tissue tumor of mesenchymal origin. Gekko sulfated glycopeptide (GSPP), an anticancer drug in traditional Chinese medicine, could inhibited the tumor angiogenesis by targeting basic fibroblast growth factor (bFGF). bFGF promoted the proliferation of fibroblasts. Both fibrosarcoma and fibroblasts derived from fibrous connective tissue. This study investigated whether GSPP has the inhibitory effects on human fibrosarcoma HT1080 cells. Materials and methods: The trypan blue exclusion assay was used to determine cell viability and cell numbers. Cells migration was observed by wound-healing and transwell. Results: From the first day to seventh day, HT1080 cells number of GSPP, bFGF, GSPP combined bFGF groups had not change compared with control. HT1080 cells migration distance and the number of migrating cells of GSPP, bFGF, GSPP combined bFGF groups were not significantly reduced. Conclusions: GSPP did not have inhibitory effects on the proliferation and migration of human fibrosarcoma HT1080 cells. Thus further research should be carried out in order to study the mechanism of GSPP and bFGF acting on the tumor stroma.
Rhizome Curcumae, as one of the traditional Chinese medicines, plays an important role in many diseases.
In recent years, Rhizome Curcumae has more and more anti-tumor experiments in vitro, and various results indicate that its effect on tumors is multifaceted.
In the clinical treatment of malignant tumors, Rhizome Curcumae has been used as an injection. There is increasing evidence that it inhibits a variety of tumor cells. More and more pharmacological mechanisms have been discovered.
The anti-cancer mechanism of Rhizome Curcumae mainly includes inhibiting the proliferation of tumor cells, promoting the apoptosis of tumor cells, inhibiting tumor angiogenesis, increasing the effect of chemotherapy drugs and reducing its side effects, reversing tumor multidrug resistance and improving immunity. This paper summarizes and describes the extracts and anticancer actives of Rhizome Curcumae in recent years, as well as their anticancer mechanism. It provides theoretical basis and ideas for the research of Rhizome Curcumae in the field of anticancer.
This study retrospectively evaluated the clinical significance of the serum thymidine kinase 1 (TK1) and prognosis nutrition index (PNI) in the prognosis of elderly patients with advanced non-small cell lung cancer (NSCLC).And found that the higher serum TK1 and lower PNI were in worse long-term outcomes in geriatric patients with advanced NSCLC.
This study proved that the elevated serum TK1 and descendant PNI were independent prognostic factors, which might be potential treatment target for geriatric patients with NSCLC.
Objective: This study was designed to evaluate the clinical significance of the serum thymidine kinase 1 (TK1) and prognosis nutrition index (PNI) in the prognosis of elderly patients with advanced non-small cell lung cancer (NSCLC). Methods: A total of 126 elderly patients with advanced non-small cell lung cancer from Jan. 2015 to Apr. 2016 were enrolled. The clinical, pathological and survival information were collected. The serum TK1 level was measured as well as PNI was calculated when the patient was admitted to our hospital for the first time. The relationship between serum TK1, PNI, and clinical prognostic characteristics was analyzed. The clinical significance of serum TK1 and PNI in the prognosis of elderly patients with advanced non-small cell lung cancer was investigated. Results: The results showed that the survival time of the patients was related to TK1 and PNI.The further Kaplan-Meier method and log-rank tests showed that the long-term outcome of the high-TK1 group was significantly worse than low-TK1 group (mOS, 27 m vs. 15 m, P = 0.047). Besides, the Kaplan-Meier method and log-rank tests also showed that the long-term outcome of high-PNI group was significantly better than low-PNI group (mOS, 31.5 m vs. 16 m, P = 0.015). However, the Spearman’s correlation analysis showed there was no correlation between PNI and TK1. The univariate and multivariate analysis showed that TK1, PNI and the number of metastatic sites were independent prognostic factors. Conclusions: The study confirmed the TK1 and PNI were independent prognostic factors of advanced NSCLC in the elderly. More attention worth is paid in routine clinical practice for patients cell proliferation and nutritional status.
The problem of immune checkpoint blockers drug resistance is one of the hotspots in current research. This study describes the drug resistance patterns of immune checkpoint blockers and strategies to reverse drug resistance.
The combination of multiple treatment methods including radiotherapy, chemotherapy, and traditional Chinese medicine combined with immune checkpoint blockers are expected to become new strategies to reverse the drug resistance of immune checkpoint blockers.
Recent years, the immune checkpoint blockers (ICBs) become more and more important in tumor therapy with the development of tumor immunology and achieved significant clinical effects in various solid tumors. ICBs is a type of tumor immunotherapy method which controls and clears tumor by activating the autoimmune system and restoring the body's normal anti-tumor immune response. However, the resistance of ICBs cannot be ignored and still faces many challenges. The mechanism and the solution of ICBs resistance need to be further research.
In recent years, prostate cancer has been known to have an increasing incidence worldwide. In 2012, prostate cancer was recognized as the second most frequent cancer to occur in men and fifth leading cause of cancer mortality in men. It is known to affect one of every eight men in the world, and even more common in men above the age of 65. However, the long-term survival rate for an average cancer patient continues to decline, creating a need for therapies that could enhance survival rate with favorable advantages. With the minimal side effects and toxicity of the new treatments, it is obvious that these new treatments are the way forward in fighting cancer. This review elaborates the new therapy for prostate cancer treatment that has been developed in very recent times. The goal is not only to create awareness of these new treatments but also gives patients as well as doctors more treatment options. This review builds a foundation on the knowledge of cancer, importantly cancer immunology, and also forms groundwork majorly on prostate cancer, focusing on the mechanism of how immunotherapy could be a better choice over the previously common prostate cancer treatments, proposing a perspective on future directions in the treatment of prostate cancer.
order to find a genetic marker to predict the prognosis of patients with
ovarian cancer based on multi-omics data. Methods: We download RNA-Seq
SNP, CNV data and clinical follow-up information from TCGA database and
randomly divide them into training set and test set. GSE17260 dataset in GEO is
taken as an external validation set. Prognosis-related genes, copy number
difference genes and mutant genes are screened in the training set. After the
integration of genes, the random forest algorithm is further used for feature
selection, ultimately obtaining a robust biomarker. On this basis, a
gene-related prognostic model is established and verified in the test set and
verification set. Results: We have obtained 2097 prognostic related
genes, 447 copy amplification genes, 1069 copy deletion genes and 654
significant mutations genes. Through the feature selection of random forest
algorithm, five feature genes (PSMB1, COL6A6, SLC22A2, KLHL23 and CD3G) are
obtained by integrating these genes, some of which have been reported to be
related to tumor progress. Furthermore, the prognostic risk assessment model of
5-gene signature is established by Cox regression analysis. The model can
evaluate the risk of patient samples in training set, test set and external
verification set. 5-gene signature shows strong robustness and clinical
independence. The results of GSEA analysis also show that the pathway of 5-gene
signature enrichment is significantly related to the pathway and biological
process of the occurrence and development of ovarian cancer. Conclusion: In
this study, 5-gene signature is constructed as a new prognostic marker to
predict the survival of patients with ovarian cancer.
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