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1.
Biochim Biophys Acta Rev Cancer ; 1877(3): 188707, 2022 05.
Artículo en Inglés | MEDLINE | ID: mdl-35247506

RESUMEN

It is widely established that chromosomal rearrangements induce oncogenesis in solid tumors. However, discovering chromosomal rearrangements that are targetable and actionable remains a difficulty. Targeting gene fusion or chromosomal rearrangement seems to be a powerful strategy to address malignancies characterized by gene rearrangement. Oncogenic NRG1 fusions are relatively rare drivers that infrequently occur across most tumor types. NRG1 fusions exhibit unique biological properties and are difficult to identify owing to their large intronic regions. NRG1 fusions can be detected using a variety of techniques, including fluorescence in situ hybridization, immunohistochemistry, or next-generation sequencing (NGS), with NGS-based RNA sequencing being the most sensitive. Previous studies have shown that NRG1 fusion protein induces tumorigenesis, and numerous therapies targeting the ErbB signaling pathway, such as ErbB kinase inhibitors and monoclonal antibodies, have initially demonstrated encouraging anticancer efficacy in malignant tumors carrying NRG1 fusions. In this review, we present the characteristics and prevalence of NRG1 fusions in solid tumors. Additionally, we discuss the laboratory approaches for diagnosing NRG1 gene fusions. More importantly, we outline promising strategies for treating malignancies with NRG1 fusion.


Asunto(s)
Neoplasias Pulmonares , Reordenamiento Génico , Humanos , Hibridación Fluorescente in Situ , Neoplasias Pulmonares/tratamiento farmacológico , Neurregulina-1/genética , Neurregulina-1/metabolismo , Neurregulina-1/uso terapéutico , Proteínas de Fusión Oncogénica/genética
2.
Front Oncol ; 11: 686556, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34113573

RESUMEN

Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) is a rare autosomal dominant hereditary cancer syndrome characterized by a predisposition to cutaneous leiomyomas, uterine leiomyomas, and renal cell carcinoma (RCC). It is known to be caused by germline mutations of the fumarate hydratase (FH) gene, which encodes an enzyme component of the citric acid cycle and catalyzes the conversion of fumarate to L-malate. Currently, there is no standardized treatment for HLRCC, which may be due in part to a lack of understanding of the underlying mechanisms. Here, the underlying molecular mechanisms by which the inactivation of FH causes HLRCC are discussed. Additionally, potential therapeutic pharmacological strategies are also summarized to provide new perspectives for the prevention and treatment of HLRCC.

3.
Biomed Pharmacother ; 131: 110795, 2020 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-33152951

RESUMEN

With the widespread popularity of hyperuricemia, it has become a severe threat to human public health. Accumulating evidence suggests that dietary fructose has a close relationship with hyperuricemia, but the role of fructose intake in hyperuricemia remains unclear. Hyperuricemia is characterized by excessive production and deposition of urate crystals. Metabolism of fructose leads to the increased serum concentration of urate. In this review, we depict an update of fructose consumption worldwide and the epidemiology of hyperuricemia and summarize the progress in studying the relationship between fructose intake and the risk of hyperuricemia. This review highlights the metabolic process of fructose in the liver, small intestine, and kidney. Furthermore, we discuss molecular insights on fructose metabolism to reveal the underlying mechanism of fructose metabolism. Additionally, we elaborate on the effect of fructose metabolism on hyperuricemia to deeply understand the pathogenesis of hyperuricemia caused by fructose intake. Fructose consumption has a close correlation with an enhanced risk of developing hyperuricemia. More prospective studies are inevitable to understand the role of fructose intake in the development of hyperuricemia.


Asunto(s)
Dieta , Fructosa/efectos adversos , Hiperuricemia/epidemiología , Animales , Fructosa/administración & dosificación , Fructosa/metabolismo , Humanos , Riesgo , Ácido Úrico/sangre
4.
Artículo en Inglés | MEDLINE | ID: mdl-22007256

RESUMEN

The pyrolytic kinetics of Phragmites australis was investigated using thermogravimetric analysis (TGA) method with linear temperature programming process under an inert atmosphere. Kinetic expressions for the degradation rate in devolatilization and combustion steps have been obtained for P. australis with Dollimore method. The values of apparent activation energy, the most probable mechanism functions, and the corresponding preexponential factor were determined. The results show that the model agrees well with the experimental data and provide useful information for the design of pyrolytic processing system using P. australis as feedstock to produce biofuel.

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