• Asian Pacific Journal of Cancer Prevention
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• 제15권15호
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• pp.6145-6150
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• 2014

Toll-like receptors (TLRs) are expressed in immune and tumor cells and recognize pathogen-associated molecular patterns. Cervical cancer (CC) is directly linked to a persistent infection with high risk human papillomaviruses (HR-HPVs) and could be associated with alteration of TLRs expression. TLR9 plays a key role in the recognition of DNA viruses and better understanding of this signaling pathway in CC could lead to the development of novel immunotherapeutic approaches. The present study was undertaken to determine the level of TLR9 expression in cervical neoplasias from Tunisian women with 53 formalin-fixed and paraffin-embedded specimens, including 22 samples of invasive cervical carcinoma (ICC), 18 of cervical intraepithelial neoplasia (CIN), 7 of condyloma and 6 normal cervical tissues as control cases. Quantification of TLR9 expression was based on scoring four degrees of extent and intensity of immunostaining in squamous epithelial cells. TLR9 expression gradually increased from CIN1 (80% weak intensity) to CIN2 (83.3% moderate), CIN3 (57.1% strong) and ICC (100% very strong). It was absent in normal cervical tissue and weak in 71.4% of condyloma. The mean scores of TLR9 expression were compared using the Kruskall-Wallis test and there was a statistical significance between normal tissue and condyloma as well as between condyloma, CINs and ICC. These results suggest that TLR9 may play a role in progression of cervical neoplasia in Tunisian patients and could represent a useful biomarker for malignant transformation of cervical squamous cells.

• Biomolecules & Therapeutics
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• 제28권6호
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• pp.503-511
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• 2020

Autophagy is a major catabolic process that maintains cell metabolism by degrading damaged organelles and other dysfunctional proteins via the lysosome. Abnormal regulation of this process has been known to be involved in the progression of pathophysiological diseases, such as cancer and neurodegenerative disorders. Although the mechanisms for the regulation of autophagic pathways are relatively well known, the precise regulation of this pathway in the treatment of cancer remains largely unknown. It is still complicated whether the regulation of autophagy is beneficial in improving cancer. Many studies have demonstrated that autophagy plays a dual role in cancer by suppressing the growth of tumors or the progression of cancer development, which seems to be dependent on unknown characteristics of various cancer types. This review summarizes the key targets involved in autophagy and malignant transformation. In addition, the opposing tumor-suppressive and oncogenic roles of autophagy in cancer, as well as potential clinical therapeutics utilizing either regulators of autophagy or combinatorial therapeutics with anti-cancer drugs have been discussed.

• Asian Pacific Journal of Cancer Prevention
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• 제16권18호
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• pp.8047-8052
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• 2016

Proteases are important molecules that are involved in many key physiological processes. Protease signaling pathways are strictly controlled, and disorders in protease activity can result in pathological changes such as cardiovascular and inflammatory diseases, cancer and neurological disorders. Many proteases have been associated with increasing tumor metastasis in various human cancers, suggesting important functional roles in the metastatic process because of their ability to degrade the extracellular matrix barrier. Proteases are also capable of cleaving non-extracellular matrix molecules. Inhibitors of proteases to some extent can reduce invasion and metastasis of cancer cells, and slow down cancer progression. In this review, we focus on the role of a few proteases and their inhibitors in tumors as a basis for cancer prognostication and therapy.

• 대한한방내과학회지
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• 제19권1호
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• pp.291-300
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• 1998

Dementia is the neurodegenerative process that affects cognition, behavior and function and one of the most prominent diseases of dementia is Alzheimer's disease(AD). AD is a dementing illness characterized clinically by the progressive and irreversible deafferentation of the limbic system, association neocortex and basal forebrain. A number of conditions are known to be predisposing risk factors for AD. In several of these, initiation of glial-mediated inflammatory pathways as a mechanism of AD is getting a lot of attention. On the other hand, a biochemical marker for monitoring the onset and progression of the disease would be a valuable tool for disease management. Also such a marker might be used as an end point in clinical intervention protocols. This biochemical marker will have the potential for identifying subjects afflicted with the disease and possibly for monitoring the onset and longitudinal progression of the disease. Here we have reviewed the latest papers of different approaches to AD. Of course, there is a section of PET which is very useful clinically nowadays.

• Clinical and Experimental Pediatrics
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• 제64권10호
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• pp.511-518
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• 2021

The prevalence of childhood obesity is increasing worldwide at an alarming rate. While obesity is known to increase a variety of cardiovascular and metabolic diseases, it also acts as a risk factor for the development and progression of chronic kidney disease (CKD). During childhood and adolescence, severe obesity is associated with an increased prevalence and incidence of the early stages of kidney disease. Importantly, children born to obese mothers are also at increased risk of developing obesity and CKD later in life. The potential mechanisms underlying the association between obesity and CKD include hemodynamic factors, metabolic effects, and lipid nephrotoxicity. Weight reduction via increased physical activity, caloric restriction, treatment with angiotensin-converting enzyme inhibitors, and judicious bariatric surgery can be used to control obesity and obesity-related kidney disease. Preventive strategies to halt the obesity epidemic in the healthcare community are needed to reduce the widespread deleterious consequences of obesity including CKD development and progression.

• Genomics & Informatics
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• 제16권4호
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• pp.18.1-18.9
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• 2018

Long non-coding RNAs (lncRNAs) are classified as RNAs that are longer than 200 nucleotides and cannot be translated into protein. Several studies have demonstrated that lncRNAs are directly or indirectly involved in a variety of biological processes and in the regulation of gene expression. In addition, lncRNAs have important roles in many diseases including cancer. It has been shown that abnormal expression of lncRNAs is observed in several human solid tumors. Several studies have shown that many lncRNAs can function as oncogenes in cancer development through the induction of cell cycle progression, cell proliferation and invasion, anti-apoptosis, and metastasis. Oncogenic lncRNAs have the potential to become promising biomarkers and might be potent prognostic targets in cancer therapy. However, the biological and molecular mechanisms of lncRNA involvement in tumorigenesis have not yet been fully elucidated. This review summarizes studies on the regulatory and functional roles of oncogenic lncRNAs in the development and progression of various types of cancer.

• Biomolecules & Therapeutics
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• 제29권4호
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• pp.365-372
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• 2021

Type 2 diabetes mellitus (T2DM) leads to many health problems like diabetic nephropathy (DN). One of the key factors for chronic kidney disease and end-stage renal disease (ESRD) is T2DM. Extensive work is being done to delineate the pathogenesis of DN and to extend possible remedies. This review is intended to understand the nature of DN risk factors, progression, effects of glycemic levels, and stages of DN. We also explored the novel diagnostic and therapeutic approaches for DN such as gene therapy and stem cell treatments.

• Clinical and Experimental Pediatrics
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• 제65권3호
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• pp.115-126
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• 2022

Retinopathy of prematurity (ROP) is among the most common causes of childhood blindness. Three phases of ROP epidemics have been observed worldwide since ROP was first described in the 1940s. Despite advances in neonatal care, the occurrence of ROP and associated visual impairment has been increasing somewhere on Earth and remains difficult to control. Conventional treatment options for preventing ROP progression include retinal ablation using cryotherapy or laser therapy. With the emergence of anti-vascular endothelial growth factor (anti-VEGF) treatment for ocular diseases, the efficacy and safety of anti-VEGF therapy for ROP have recently been actively discussed. In the advanced stage of ROP with retinal detachment, surgical treatment including scleral buckling or vitrectomy is needed to maintain or induce retinal attachment. At this stage, the visual outcome is usually poor despite successful anatomical retinal attachment. Therefore, preventing ROP progression by timely screening examinations and treatment remains the most important part of ROP management.

• Clinical and Experimental Pediatrics
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• 제64권3호
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• pp.103-110
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• 2021

Inflammatory or immune-mediated demyelinating central nervous system (CNS) syndromes include a broad spectrum of clinical phenotype and different overlapping diseases. Antibodies against myelin oligodendrocyte glycoprotein (MOG-Ab) have been found in some cases of these demyelinating diseases, particularly in children. MOG-Ab is associated with a wider clinical phenotype not limited to neuromyelitis optica spectrum disorder, with most patients presenting with optic neuritis, acute disseminated encephalomyelitis (ADEM) or ADEM-like encephalitis with brain demyelinating lesions, and/or myelitis. Using specific cell-based assays, MOG-Ab is becoming a potential biomarker of inflammatory demyelinating disorders of the CNS. A humoral immune reaction against MOG was recently found in monophasic diseases and recurrent/multiphasic clinical progression, particularly in pediatric patients. This review summarizes the data regarding MOG-Ab as an impending biological marker for discriminating between these diverse demyelinating CNS diseases and discusses recent developments, clinical applications, and findings regarding the immunopathogenesis of MOG-Ab-associated disorders.

• Childhood Kidney Diseases
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• 제19권2호
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• pp.176-179
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• 2015

Rituximab (RTX), a monoclonal antibody against the B-cell marker CD20, is commonly used as a treatment for antibody-mediated diseases or B-lymphocyte-mediated diseases. Destruction of B cells may reverse the disease course in many conditions; however, patients who are treated with RTX cannot respond appropriately to de novo infection due to lack of B lymphocytes. Here, we report one such case. A 7-year-old renal allograft recipient presented with severe anemia due to parvovirus infection after RTX treatment. The patient had focal segmental glomerulosclerosis and had received cadaveric kidney transplantation 6 months previously. She was treated with high-dose steroid for acute rejection and RTX for Epstein Barr Virus infection 3 months previously. At presentation, her hemoglobin level was 5.4 g/dL and leukocyte and platelet counts were normal. She had microcytic normochromic anemia and high viral load of parvovirus B19(70,578 copies/mL). Intravenous immunoglobulin ($200mg/kg{\cdot}d$) treatment controlled the progression of anemia and parvovirus infection. De novo parvovirus infection during the B lymphocyte-depletion period may have precipitated the severe anemia in this case. Close monitoring of infection is required after RTX therapy.