scholarly journals CHITINASE-LIKE PROTEINS AS PROMISING MARKERS IN CANCER PATIENTS

2018 ◽  
Vol 17 (4) ◽  
pp. 99-105 ◽  
Author(s):  
I. V. Larionova ◽  
T. N. Sevastyanova ◽  
A. A. Rakina ◽  
N. V. Cherdyntseva ◽  
Ju. G. Kzhyshkowska

In the present review we collected the main studies regarding the role of chitinase-like proteins (CLPs), belonging to the family of Glyco_18 domain-containing proteins, in different cancers. In  humans, 3 chitinaselike proteins have been identified: YKL-40 (CHI3L1), YKL-39 (CHI3L2) and  stabilin-1-interacting chitinase-like protein (SI-CLP). CLPs are produced by several types of cells  and combine the properties of cytokines and growth factors. The high levels of CLPs were  identified in the circulation of the patients with inflammatory diseases and various types of  tumors. We highlighted the main known functions of CLPs in normal and pathological conditions, their contribution to metastasis development, angiogenesis, invasion and other processes in  cancer, the correlation of the levels of CLPs with tumour progression. Our data also contribute to the understanding of question how CLP could be useful for cancer patient benefit.

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
C. Lehmann ◽  
S. Islam ◽  
S. Jarosch ◽  
J. Zhou ◽  
D. Hoskin ◽  
...  

Since iron can contribute to detrimental radical generating processes through the Fenton and Haber-Weiss reactions, it seems to be a reasonable approach to modulate iron-related pathways in inflammation. In the human organism a counterregulatory reduction in iron availability is observed during inflammatory diseases. Under pathological conditions with reduced or increased baseline iron levels different consequences regarding protection or susceptibility to inflammation have to be considered. Given the role of iron in development of inflammatory diseases, pharmaceutical agents targeting this pathway promise to improve the clinical outcome. The objective of this review is to highlight the mechanisms of iron regulation and iron chelation, and to demonstrate the potential impact of this strategy in the management of several acute and chronic inflammatory diseases, including cancer.


Author(s):  
А.А. Газданова ◽  
В.Г. Кукес ◽  
О.К. Парфенова ◽  
Н.Г. Сидоров ◽  
А.В. Перков ◽  
...  

Миостатин - белок, принадлежащий к классу миокинов, семейству трансформирующих факторов роста β (TGF-β). В обзорной статье, анализирующей данные литературы, показана ключевая роль миостатина в развитии старческой саркопении и кахексии при различных патологических состояниях, таких как рак, ХСН, ХБП, ХОБЛ и др. В статье рассматривается структура миостатина, подробная схема синтеза и его активации, механизм действия как негативного регулятора роста и дифференцировки мышц при этих патологических состояниях. Выделены основные физиологические свойства и клиническое значение. Рассмотрены экзогенные и эндогенные факторы, регулирующие экспрессию миостатина, и возможные механизмы их действия. Myostatin is a protein belonging to the myokine class, the family of transforming growth factors β (TGF-β). The review article, based on the analysis of literature data, shows the key role of myostatin in the development of senile sarcopenia and cachexia in various pathological conditions, such as cancer, chronic heart failure, chronic renal failure, COPD, etc. The article discusses the structure of myostatin, provides a detailed diagram of the synthesis and activation of myostatin, the ways of implementing the mechanism of action as a negative regulator of muscle growth and differentiation in these pathological conditions. The main physiological properties and clinical significance are highlighted. Exogenous and endogenous factors regulating myostatin expression and possible mechanisms of their action are considered.


2016 ◽  
pp. 109-118
Author(s):  
Campbell S.D. Roxburgh ◽  
Donald C. McMillan

The chapter focuses on the role of immunity and inflammation in established cancer. From the evidence reviewed it is clear that immune and inflammatory responses, innate, humoral and adaptive, local and systemic, are intimately linked to the tumour and themselves and impact on cancer survival. It is also possible to identify key mediators that may be targeted in the cancer patient. However, further work is required to elucidate the mechanisms by which these immune and inflammatory responses are activated, maintained, and interact. Therapeutic intervention using non-selective anti-inflammatory agents is widely advocated and likely to become part of routine clinical practice in the near future. Selective therapeutic intervention directed at the immune and inflammatory responses in cancer is in its infancy. Therefore, it would appear that, at least in non-hereditary disease, immune and inflammatory responses are of key, if not of prime, importance in tumour progression and dissemination.


2019 ◽  
Vol 11 ◽  
pp. 175883591988008 ◽  
Author(s):  
Maurizio Muscaritoli ◽  
Jann Arends ◽  
Matti Aapro

Tackling malnutrition in cancer patients remains one of the most challenging tasks in clinical practice. Even though robust evidence exists stressing the role of nutritional status in relation to treatment outcome, its appropriate consideration in clinical practice is often lacking. In this review, we discuss the significance of nutritional status and of malnutrition for the cancer patient. Drawn from experience and from current recommendations of the European Society for Clinical Nutrition and Metabolism (ESPEN), we propose concrete and manageable steps to routinely incorporate nutritional aspects in today’s oncological clinical practice.


2016 ◽  
Vol 64 (3) ◽  
pp. 529
Author(s):  
Kathleen Salazar-Ramírez ◽  
Jhonny Molinares-Rodríguez ◽  
Samir Bolívar-González

Autophagy is an evolutionary process preserved in eukaryotes, which removes harmful components and maintains cell homeostasis in response to a variety of extracellular stimuli. It is involved in both physiological and pathological conditions, including cancer.The role of autophagy in the treatment of cancer is described as a “double-edged sword”, which reflects its involvement in tumor suppression, survival and subsequent proliferation of tumor cells. Recent advances are useful for planning appropriate adjustments to inhibit or promote autophagy in order to obtain therapeutic efficacy in cancer patients. The objectives of this review are to clarify the role of autophagy in cancer and to highlight the need for more research in the field.


Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2408
Author(s):  
Valeria Manganelli ◽  
Agostina Longo ◽  
Vincenzo Mattei ◽  
Serena Recalchi ◽  
Gloria Riitano ◽  
...  

ER lipid raft-associated protein 1 (ERLIN1) and 2 (ERLIN2) are 40 kDa transmembrane glycoproteins belonging to the family of prohibitins, containing a PHB domain. They are generally localized in the endoplasmic reticulum (ER), where ERLIN1 forms a heteroligomeric complex with its closely related ERLIN2. Well-defined functions of ERLINS are promotion of ER-associated protein degradation, mediation of inositol 1,4,5-trisphosphate (IP3) receptors, processing and regulation of lipid metabolism. Until now, ERLINs have been exclusively considered protein markers of ER lipid raft-like microdomains. However, under pathophysiological conditions, they have been described within mitochondria-associated endoplasmic reticulum membranes (MAMs), tethering sites between ER and mitochondria, characterized by the presence of specialized raft-like subdomains enriched in cholesterol and gangliosides, which play a key role in the membrane scrambling and function. In this context, it is emerging that ER lipid raft-like microdomains proteins, i.e., ERLINs, may drive mitochondria-ER crosstalk under both physiological and pathological conditions by association with MAMs, regulating the two main processes underlined, survival and death. In this review, we describe the role of ERLINs in determining cell fate by controlling the “interchange” between apoptosis and autophagy pathways, considering that their alteration has a significant impact on the pathogenesis of several human diseases.


2021 ◽  
Vol 11 ◽  
Author(s):  
Priyanka Hirani ◽  
Valentine Gauthier ◽  
Carys E. Allen ◽  
Thomas N. Wight ◽  
Oliver M. T. Pearce

A growing body of literature links events associated with the progression and severity of immunity and inflammatory disease with the composition of the tissue extracellular matrix as defined by the matrisome. One protein in the matrisome that is common to many inflammatory diseases is the large proteoglycan versican, whose varied function is achieved through multiple isoforms and post-translational modifications of glycosaminoglycan structures. In cancer, increased levels of versican are associated with immune cell phenotype, disease prognosis and failure to respond to treatment. Whether these associations between versican expression and tumour immunity are the result of a direct role in the pathogenesis of tumours is not clear. In this review, we have focused on the role of versican in the immune response as it relates to tumour progression, with the aim of determining whether our current understanding of the immunobiology of versican warrants further study as a cancer immunotherapy target.


2014 ◽  
Vol 19 (9) ◽  
pp. 981-998 ◽  
Author(s):  
Woohyun Yoo ◽  
Dhavan V. Shah ◽  
Bret R. Shaw ◽  
Eunkyung Kim ◽  
Paul Smaglik ◽  
...  

Lupus ◽  
2009 ◽  
Vol 18 (13) ◽  
pp. 1233-1238 ◽  
Author(s):  
DS Domiciano ◽  
JF Carvalho ◽  
Y. Shoenfeld

Anti-endothelial cells antibodies have been detected in numerous autoimmune and inflammatory diseases, including systemic lupus erythematous, rheumatoid arthritis, vasculitis and sarcoidosis. Anti-endothelial cells antibodies bind to endothelial cell antigens and induce endothelial damage. Their effects on the endothelial cell have been considered responsible, at least in part, by the vascular injury which occurs in these pathological conditions.


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