scholarly journals Role and underlying mechanisms of the interstitial protein periostin in the diagnosis and treatment of malignant tumors (Review)

2017 ◽  
Author(s):  
Dong Ye ◽  
Zhi Shen ◽  
Shi Qiu ◽  
Qun Li ◽  
Guo Wang
2021 ◽  
Vol 478 (9) ◽  
pp. 1663-1688
Author(s):  
Yonghua Li ◽  
Huan Jin ◽  
Yibing Chen ◽  
Ting Huang ◽  
Yanjun Mi ◽  
...  

Cancer cachexia often occurs in malignant tumors and is a multifactorial and complex symptom characterized by wasting of skeletal muscle and adipose tissue, resulting in weight loss, poor life quality and shorter survival. The pathogenic mechanism of cancer cachexia is complex, involving a variety of molecular substrates and signal pathways. Advancements in understanding the molecular mechanisms of cancer cachexia have provided a platform for the development of new targeted therapies. Although recent outcomes of early-phase trials have showed that several drugs presented an ideal curative effect, monotherapy cannot be entirely satisfactory in the treatment of cachexia-associated symptoms due to its complex and multifactorial pathogenesis. Therefore, the lack of definitive therapeutic strategies for cancer cachexia emphasizes the need to develop a better understanding of the underlying mechanisms. Increasing evidences show that the progression of cachexia is associated with metabolic alternations, which mainly include excessive energy expenditure, increased proteolysis and mitochondrial dysfunction. In this review, we provided an overview of the key mechanisms of cancer cachexia, with a major focus on muscle atrophy, adipose tissue wasting, anorexia and fatigue and updated the latest progress of pharmacological management of cancer cachexia, thereby further advancing the interventions that can counteract cancer cachexia.


Dermatology ◽  
2021 ◽  
pp. 1-13
Author(s):  
Mary D. Sun ◽  
Allan C. Halpern

Seborrheic keratoses (SKs) are ubiquitous, generally benign skin tumors that exhibit high clinical variability. While age is a known risk factor, the precise roles of UV exposure and immune abnormalities are currently unclear. The underlying mechanisms of this benign disorder are paradoxically driven by oncogenic mutations and may have profound implications for our understanding of the malignant state. Advances in molecular pathogenesis suggest that inhibition of Akt and APP, as well as existing treatments for skin cancer, may have therapeutic potential in SK. Dermoscopic criteria have also become increasingly important to the accurate detection of SK, and other noninvasive diagnostic methods, such as reflectance confocal microscopy and optical coherence tomography, are rapidly developing. Given their ability to mimic malignant tumors, SK cases are often used to train artificial intelligence-based algorithms in the computerized detection of skin disease. These technologies are becoming increasingly accurate and have the potential to significantly augment clinical practice. Current treatment options for SK cause discomfort and can lead to adverse post-treatment effects, especially in skin of color. In light of the discontinuation of ESKATA in late 2019, promising alternatives, such as nitric-zinc and trichloroacetic acid topicals, should be further developed. There is also a need for larger, head-to-head trials of emerging laser therapies to ensure that future treatment standards address diverse patient needs.


2021 ◽  
Vol 11 ◽  
Author(s):  
Peng Ge ◽  
Yalan Luo ◽  
Haiyang Chen ◽  
Jiayue Liu ◽  
Haoya Guo ◽  
...  

Pancreatic cancer (PC) is one of the most common malignant tumors in the digestive tract worldwide, with increased morbidity and mortality. In recent years, with the development of surgery, chemotherapy, radiotherapy, targeted therapy, and immunotherapy, and the change of the medical thinking model, remarkable progress has been made in researching comprehensive diagnosis and treatment of PC. However, the present situation of diagnostic and treatment of PC is still unsatisfactory. There is an urgent need for academia to fully integrate the basic research and clinical data from PC to form a research model conducive to clinical translation and promote the proper treatment of PC. This paper summarized the translation progress of mass spectrometry (MS) in the pathogenesis, diagnosis, prognosis, and PC treatment to promote the basic research results of PC into clinical diagnosis and treatment.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Xiao-Long Li ◽  
Ya-Ming Ji ◽  
Rui Song ◽  
Xiao-Ning Li ◽  
Lan-Shuan Guo

Gastric cancer (GC) is one of the most aggressive malignant tumors with low early diagnosis and high metastasis. Despite progress in treatment, to combat this disease, a better understanding of the underlying mechanisms and novel therapeutic targets is needed. KIF23, which belongs to the KIF family, plays a vital role in various cell processes, such as cytoplasm separation and axon elongation. Nowadays, KIF23 has been found to be highly expressed in multiple tumor tissues and cells, suggesting a potential link between KIF23 and tumorigenesis. Herein, we reported that KIF23 expression was correlated with poor prognosis of gastric cancer and found an association between KIF23 and pTNM stage. An in vitro assay proved that the proliferation of gastric cancer cells was significantly inhibited, which is caused by KIF23 depletion. Additionally, knockdown of KIF23 resulted in a marked inhibition of cell proliferation of gastric cancer in mice, with significant downregulation of Ki67 and PCNA expression. In conclusion, these data indicate that KIF23 is a potential therapeutic target for gastric cancer treatment.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Junyan Tao ◽  
Dantong Sun ◽  
Lina Dong ◽  
Hua Zhu ◽  
Helei Hou

Abstract The NF1 gene encodes neurofibromin, which is one of the primary negative regulatory factors of the Ras protein. Neurofibromin stimulates the GTPase activity of Ras to convert it from an active GTP-bound form to its inactive GDP-bound form through its GTPase activating protein-related domain (GRD). Therefore, neurofibromin serves as a shutdown signal for all vertebrate RAS GTPases. NF1 mutations cause a resultant decrease in neurofibromin expression, which has been detected in many human malignancies, including NSCLC, breast cancer and so on. NF1 mutations are associated with the underlying mechanisms of treatment resistance discovered in multiple malignancies. This paper reviews the possible mechanisms of NF1 mutation-induced therapeutic resistance to chemotherapy, endocrine therapy and targeted therapy in malignancies. Then, we further discuss advancements in targeted therapy for NF1-mutated malignant tumors. In addition, therapies targeting the downstream molecules of NF1 might be potential novel strategies for the treatment of advanced malignancies.


2020 ◽  
Author(s):  
Wang Zhang ◽  
Binchao Liu ◽  
Miaomiao Jiang ◽  
Shi Yan ◽  
Xian Han ◽  
...  

Abstract Background: Although many biomarkers have been reported for detecting glioma, the prognosis for the disease remains poor, and therefore, new biomarkers need to be identified. GNG5, which is part of the G-protein family, has been associated with different malignant tumors, though the role of GNG5 in glioma has not been studied. Therefore, we aimed to identify the relationship between GNG5 expression and glioma prognosis and to identify a new biomarker for the diagnosis and treatment of gliomas.Methods: We used datasets from databases including TCGA and GEO, and results from GEPIA, RT-qPCR, and HPA to determine the expression of GNG5 in glioma. Based on datasets obtained from the CGGA database, we identified the correlation between GNG5 expression and multiple molecular and clinical features as well as clinical prognosis using a variety of analytical methods. Co-expression analysis and GSEA were performed to detect GNG5-related genes in gliomas and possible signaling pathways involved. ESTIMATE, ssGSEA, and TIMER were used to detect the relationship between GNG5 and the immune microenvironment.Results: A total of 1826 glioma related datasets were used in our study, including sequencing data, microarray data, and RT-qPCR data. We found that GNG5 is highly expressed in gliomas, and its expression level is positively correlated with pathological grade, histological type, age, and tumor recurrence and negatively correlated with isocitrate dehydrogenase mutation, 1p/19 co-deletion, and chemotherapy. Moreover, GNG5 as an independent risk factor was negatively correlated with the overall survival time. GSEA analysis revealed the potential signaling pathways involved in GNG5 function in gliomas, such as ECM-receptor interaction and the toll-like receptor signaling pathway. The ssGSEA, ESTIMATE, and TIMER based analysis indicated a correlation between GNG5 expression and various immune cells in glioma, such as B cell, macrophage, and dendritic cells.Conclusions: Based on the large data platform and the use of different databases to corroborate results obtained using various datasets, our study reveals for the first time that GNG5, as an oncogene, is overexpressed in gliomas and can lead to poor prognosis of patients. Thus, GNG5 is a potential novel biomarker for the clinical diagnosis and treatment of gliomas.


2020 ◽  
Author(s):  
Wang Zhang ◽  
Binchao Liu ◽  
Miaomiao Jiang ◽  
Shi Yan ◽  
Xian Han ◽  
...  

Abstract Background: Although many biomarkers have been reported for detecting glioma, the prognosis for the disease remains poor, and therefore, new biomarkers need to be identified. GNG5, which is part of the G-protein family, has been associated with different malignant tumors, though the role of GNG5 in glioma has not been studied. Therefore, we aimed to identify the relationship between GNG5 expression and glioma prognosis and to identify a new biomarker for the diagnosis and treatment of gliomas.Methods: We used datasets from databases including TCGA and GEO, and results from GEPIA, RT-qPCR, and HPA to determine the expression of GNG5 in glioma. Based on datasets obtained from the CGGA database, we identified the correlation between GNG5 expression and multiple molecular and clinical features as well as clinical prognosis using a variety of analytical methods. Co-expression analysis and GSEA were performed to detect GNG5-related genes in gliomas and possible signaling pathways involved. ESTIMATE, ssGSEA, and TIMER were used to detect the relationship between GNG5 and the immune microenvironment.Results: A total of 1826 glioma related datasets were used in our study, including sequencing data, microarray data, and RT-qPCR data. We found that GNG5 is highly expressed in gliomas, and its expression level is positively correlated with pathological grade, histological type, age, and tumor recurrence and negatively correlated with isocitrate dehydrogenase mutation, 1p/19 co-deletion, and chemotherapy. Moreover, GNG5 as an independent risk factor was negatively correlated with the overall survival time. GSEA analysis revealed the potential signaling pathways involved in GNG5 function in gliomas, such as ECM-receptor interaction and the toll-like receptor signaling pathway. The ssGSEA, ESTIMATE, and TIMER based analysis indicated a correlation between GNG5 expression and various immune cells in glioma, such as B cell, macrophage, and dendritic cells.Conclusions: Based on the large data platform and the use of different databases to corroborate results obtained using various datasets, our study reveals for the first time that GNG5, as an oncogene, is overexpressed in gliomas and can lead to poor prognosis of patients. Thus, GNG5 is a potential novel biomarker for the clinical diagnosis and treatment of gliomas.


2008 ◽  
Vol 61 (10) ◽  
pp. 998-1003 ◽  
Author(s):  
Yoshito Akagi ◽  
Kazuo Shirouzu ◽  
Nobuya Ishibashi ◽  
Tetsushi Kinugasa

Sign in / Sign up

Export Citation Format

Share Document