Role of iodide metabolism in physiology and cancer

2018 ◽  
Vol 25 (4) ◽  
pp. R225-R245 ◽  
Author(s):  
Antonio De la Vieja ◽  
Pilar Santisteban
Keyword(s):  
Human Cancer ◽  
Tumor Development ◽  
Cancer Type ◽  
Dependent Manner ◽  
Transmembrane Conductance Regulator ◽  
Sodium Iodide Symporter ◽  
Anoctamin 1 ◽  
Theranostic Agent ◽  
New Research

Iodide (I−) metabolism is crucial for the synthesis of thyroid hormones (THs) in the thyroid and the subsequent action of these hormones in the organism. I−is principally transported by the sodium iodide symporter (NIS) and by the anion exchanger PENDRIN, and recent studies have demonstrated the direct participation of new transporters including anoctamin 1 (ANO1), cystic fibrosis transmembrane conductance regulator (CFTR) and sodium multivitamin transporter (SMVT). Several of these transporters have been found expressed in various tissues, implicating them in I−recycling. New research supports the exciting idea that I−participates as a protective antioxidant and can be oxidized to hypoiodite, a potent oxidant involved in the host defense against microorganisms. This was possibly the original role of I−in biological systems, before the appearance of TH in evolution. I−per se participates in its own regulation, and new evidence indicates that it may be antineoplastic, anti-proliferative and cytotoxic in human cancer. Alterations in the expression of I−transporters are associated with tumor development in a cancer-type-dependent manner and, accordingly, NIS, CFTR and ANO1 have been proposed as tumor markers. Radioactive iodide has been the mainstay adjuvant treatment for thyroid cancer for the last seven decades by virtue of its active transport by NIS. The rapid advancement of techniques that detect radioisotopes, in particular I−, has made NIS a preferred target-specific theranostic agent.

scholarly journals Increasing Evidence for Involvement of SV40 in Human Cancer

2001 ◽  
Vol 17 (3) ◽  
pp. 167-172 ◽  
Author(s):  
Janet S. Butel
Keyword(s):  
Brain Tumors ◽  
Functional Role ◽  
Human Cancer ◽  
Tumor Development ◽  
Human Tumor ◽  
Dna Virus ◽  
Oncogenic Potential ◽  
Tumor Virus ◽  
Human Infections

SV40, a small DNA virus, is known to possess strong oncogenic potential. Millions of people were exposed to SV40 as an unknown contaminant of some early poliovaccines. This article briefly summarizes the increasing evidence of the association of SV40 with certain types of human cancer, including mesotheliomas and brain tumors. Unanswered questions pertaining to the pathogenesis of human infections by SV40 and the functional role of the virus in tumor development are noted. It is concluded that SV40 should be considered a candidate human tumor virus and that vigorous efforts to clarify the role of the virus in human disease should be supported.

scholarly journals Genetics of Colorectal Cancer: Role of p53

2020 ◽  
Vol 10 (6-s) ◽  
pp. 183-185
Author(s):  
Rajashri Champanery ◽  
Drashti Joshi
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tp53 Mutation ◽  
Human Cancer ◽  
Tumor Development ◽  
Tp53 Gene ◽  
Pathological Process ◽  
Functional Roles ◽  
Different Types

The tumor suppressor TP53 gene is one of the most frequently mutated in different types of human cancer. Particularly in colorectal cancer (CRC), it is believed that TP53 mutations play a role in the adenoma-carcinoma transition of tumors during pathological process. The TP53 mutation is the key step driving the transition from adenoma to adenocarcinoma. The functional roles of TP53 mutation in tumor development have been comprehensively investigated. In this mini review, we comprehensively summarize the p53 mutants in CRC progression and discuss the current strategies for p53 mutants in malignancies. Keywords: p53 mutants, colorectal cancer, Tp53 mutation

scholarly journals The Role of Gut Microbiota in Tumor Immunotherapy

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Miao Wu ◽  
Jiawei Bai ◽  
Chengtai Ma ◽  
Jie Wei ◽  
Xianjin Du
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Adverse Reactions ◽  
Tumor Development ◽  
Tumor Immunotherapy ◽  
Host Immune System ◽  
Hematological Tumors ◽  
New Research

Tumor immunotherapy is the fourth therapy after surgery, chemotherapy, and radiotherapy. It has made great breakthroughs in the treatment of some epithelial tumors and hematological tumors. However, its adverse reactions are common or even more serious, and the response rate in some solid tumors is not satisfactory. With the maturity of genomics and metabolomics technologies, the effect of intestinal microbiota in tumor development and treatment has gradually been recognized. The microbiota may affect tumor immunity by regulating the host immune system and tumor microenvironment. Some bacteria help fight tumors by activating immunity, while some bacteria mediate immunosuppression to help cancer cells escape from the immune system. More and more studies have revealed that the effects and complications of tumor immunotherapy are related to the composition of the gut microbiota. The composition of the intestinal microbiota that is sensitive to treatment or prone to adverse reactions has certain characteristics. These characteristics may be used as biomarkers to predict the prognosis of immunotherapy and may also be developed as “immune potentiators” to assist immunotherapy. Some clinical and preclinical studies have proved that microbial intervention, including microbial transplantation, can improve the sensitivity of immunotherapy or reduce adverse reactions to a certain extent. With the development of gene editing technology and nanotechnology, the design and development of engineered bacteria that contribute to immunotherapy has become a new research hotspot. Based on the relationship between the intestinal microbiota and immunotherapy, the correct mining of microbial information and the development of reasonable and feasible microbial intervention methods are expected to optimize tumor immunotherapy to a large extent and bring new breakthroughs in tumor treatment.

scholarly journals The emerging role of SPOP protein in tumorigenesis and cancer therapy

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Yizuo Song ◽  
Yichi Xu ◽  
Chunyu Pan ◽  
Linzhi Yan ◽  
Zhi-wei Wang ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Human Cancer ◽  
Critical Role ◽  
Cancer Type ◽  
Nuclear Speckle ◽  
Ring E3 Ligase ◽  
Promising Therapeutic Target ◽  
Liver Cancers ◽  
Ring E3

AbstractThe nuclear speckle-type pox virus and zinc finger (POZ) protein (SPOP), a representative substrate-recognition subunit of the cullin-RING E3 ligase, has been characterized to play a dual role in tumorigenesis and cancer progression. Numerous studies have determined that SPOP suppresses tumorigenesis in a variety of human malignancies such as prostate, lung, colon, gastric, and liver cancers. However, several studies revealed that SPOP exhibited oncogenic function in kidney cancer, suggesting that SPOP could exert its biological function in a cancer type-specific manner. The role of SPOP in thyroid, cervical, ovarian, bone and neurologic cancers has yet to be determined. In this review article, we describe the structure and regulation of SPOP in human cancer. Moreover, we highlight the critical role of SPOP in tumorigenesis based on three major categories: physiological evidence (animal models), pathological evidence (human cancer specimens) and biochemical evidence (downstream ubiquitin substrates). Furthermore, we note that SPOP could be a promising therapeutic target for cancer treatment.

scholarly journals The Paradoxical Role of Cellular Senescence in Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Jing Yang ◽  
Mengmeng Liu ◽  
Dongchun Hong ◽  
Musheng Zeng ◽  
Xing Zhang
Keyword(s):  
Cellular Senescence ◽  
Tumor Development ◽  
Dependent Manner ◽  
Proliferating Cells ◽  
Cancer Aggressiveness ◽  
Suppressor Mechanism ◽  
Secretory Phenotype ◽  
The One ◽  
Inappropriate Expression

Cellular senescence occurs in proliferating cells as a consequence of various triggers including telomere shortening, DNA damage, and inappropriate expression of oncogenes. The senescent state is accompanied by failure to reenter the cell cycle under mitotic stimulation, resistance to cell death and enhanced secretory phenotype. A growing number of studies have convincingly demonstrated a paradoxical role for spontaneous senescence and therapy-induced senescence (TIS), that senescence may involve both cancer prevention and cancer aggressiveness. Cellular senescence was initially described as a physiological suppressor mechanism of tumor cells, because cancer development requires cell proliferation. However, there is growing evidence that senescent cells may contribute to oncogenesis, partly in a senescence-associated secretory phenotype (SASP)-dependent manner. On the one hand, SASP prevents cell division and promotes immune clearance of damaged cells, thereby avoiding tumor development. On the other hand, SASP contributes to tumor progression and relapse through creating an immunosuppressive environment. In this review, we performed a review to summarize both bright and dark sides of senescence in cancer, and the strategies to handle senescence in cancer therapy were also discussed.

scholarly journals Chemical Oral Cancerogenesis Is Impaired in PI3Kγ Knockout and Kinase-Dead Mice

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 4211
Author(s):  
Giovanni Nicolao Berta ◽  
Federica Di Scipio ◽  
Zhiqian Yang ◽  
Alessandra Oberto ◽  
Giuliana Abbadessa ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cancer Cell ◽  
Human Cancer ◽  
Cancer Cell Line ◽  
Squamous Carcinoma ◽  
Dependent Manner ◽  
Cell Vitality ◽  
Oral Squamous Carcinoma ◽  
Dose Dependent

We investigated the role of PI3Kγ in oral carcinogenesis by using a murine model of oral squamous carcinoma generated by exposure to 4-nitroquinoline 1-oxide (4NQO) and the continuous human cancer cell line HSC-2 and Cal-27. PI3Kγ knockout (not expressing PI3Kγ), PI3Kγ kinase-dead (carrying a mutation in the PI3Kγ gene causing loss of kinase activity) and wild-type (WT) C57Bl/6 mice were administered 4NQO via drinking water to induce oral carcinomas. At sacrifice, lesions were histologically examined and stained for prognostic tumoral markers (EGFR, Neu, cKit, Ki67) and inflammatory infiltrate (CD3, CD4, CD8, CD19 and CD68). Prevalence and incidence of preneoplastic and exophytic lesions were significantly and similarly delayed in both transgenic mice versus the control. The expression of prognostic markers, as well as CD19+ and CD68+ cells, was higher in WT, while T lymphocytes were more abundant in tongues isolated from transgenic mice. HSC-2 and Cal-27 cells were cultured in the presence of the specific PI3Kγ-inhibitor (IPI-549) which significantly impaired cell vitality in a dose-dependent manner, as shown by the MTT test. Here, we highlighted two different mechanisms, namely the modulation of the tumor-infiltrating cells and the direct inhibition of cancer-cell proliferation, which might impair oral cancerogenesis in the absence/inhibition of PI3Kγ.

scholarly journals Aurora Borealis (Bora), Which Promotes Plk1 Activation by Aurora A, Has an Oncogenic Role in Ovarian Cancer

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 886 ◽  
Author(s):  
Alfonso Parrilla ◽  
Marta Barber ◽  
Blanca Majem ◽  
Josep Castellví ◽  
Juan Morote ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ex Vivo ◽  
Human Cancer ◽  
Critical Role ◽  
Tumor Development ◽  
Loss Of Function ◽  
Aurora Borealis ◽  
Mitotic Kinase ◽  
Cancer Management

Identifying novel actionable factors that critically contribute to tumorigenesis is essential in ovarian cancer, an aggressive and disseminative tumor, with limited therapeutic options available. Here we show that Aurora Borealis (BORA), a mitotic protein that plays a key role in activating the master mitotic kinase polo-like kinase 1 (PLK1), has an oncogenic role in ovarian cancer. Gain and loss of function assays on mouse models and ex vivo patient-derived ascites cultures revealed an oncogenic role of BORA in tumor development and a transcriptome-analysis in clinically representative models depicted BORA’s role in survival, dissemination and inflammatory cancer related-pathways. Importantly, combinatory treatments of FDA-approved inhibitors against oncogenic downstream effectors of BORA displayed synergistic effect in ovarian cancer models, offering promising therapeutic value. Altogether, our findings uncovered for the first time a critical role of BORA in the viability of human cancer cells providing potential novel therapeutic opportunities for ovarian cancer management.

Role of EP1 and EP4 PGE2subtype receptors in serum-induced 3T6 fibroblast cycle progression and proliferation

2002 ◽  
Vol 282 (2) ◽  
pp. C280-C288 ◽  
Author(s):  
Teresa Sanchez ◽  
Juan Jose Moreno
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cellular Proliferation ◽  
Tumor Development ◽  
Inhibitory Effect ◽  
S Phase ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Cycle Progression

Recent studies have suggested that prostaglandin E2 (PGE2) subtype receptors (EP) are involved in cellular proliferation and tumor development. We studied the role of EP1 and EP4PGE2 subtype receptor antagonists AH-6809 and AH-23848B, respectively, in serum-induced 3T6 fibroblast proliferation. This was significantly reduced in a dose-dependent manner (IC50∼100 and ∼30 μM, respectively) to an almost complete inhibition, without any cytotoxic effect. However, the effect of each antagonist on 3T6 cell cycle progression clearly differed. Whereas the EP1 antagonist increased the G0/G1population, the EP4 antagonist brought about an accumulation of cells in early S phase. These effects were associated with a decrease in cyclin D and E levels in AH-6809-treated 3T6 cells and lower cyclin A levels in AH-23848B-treated fibroblasts with respect to control cells. The G0/G1 accumulation caused by AH-6809 seems to be intracellular Ca2+ concentration ([Ca2+]i) dependent, because a 6-h 1 μM thapsigargin treatment allowed G0/G1-arrested cells to enter S phase. Similarly, treatment with 20 μM forskolin for 6 h allowed S-phase and G2/M progression of AH-23848B-treated cells. This study shows that the inhibitory effect of the EP1 and EP4 antagonists on serum-induced 3T6 fibroblast growth is due to their effect at various levels of the cell cycle machinery, suggesting that PGE2 interaction with its different subtype receptors regulates progression through the cell cycle by modulating cAMP and [Ca2+]i.

MATERIAL HANDLING MACHINES AND SYSTEMS – UMI-TWINN PROJECT CONTRIBUTION

2019 ◽  
Vol 12 (1) ◽  
pp. 7-20
Author(s):  
Péter Telek ◽  
Béla Illés ◽  
Christian Landschützer ◽  
Fabian Schenk ◽  
Flavien Massi
Keyword(s):  
Material Handling ◽  
Digital Data ◽  
Flow Process ◽  
Research Directions ◽  
Scientific Excellence ◽  
Research Activities ◽  
New Research ◽  
Eu Project ◽  
The University

Nowadays, the Industry 4.0 concept affects every area of the industrial, economic, social and personal sectors. The most significant changings are the automation and the digitalization. This is also true for the material handling processes, where the handling systems use more and more automated machines; planning, operation and optimization of different logistic processes are based on many digital data collected from the material flow process. However, new methods and devices require new solutions which define new research directions. In this paper we describe the state of the art of the material handling researches and draw the role of the UMi-TWINN partner institutes in these fields. As a result of this H2020 EU project, scientific excellence of the University of Miskolc can be increased and new research activities will be started.

Review of Computed Tomographic Colonography from a Surgeon’s Perspective

2015 ◽  
Vol 24 (2) ◽  
pp. 215-223 ◽  
Author(s):  
Charles Bellows ◽  
Giuseppe Gagliardi ◽  
Lorenzo Bacigalupo
Keyword(s):  
Cancer Screening ◽  
Computed Tomographic Colonography ◽  
Clinical Practices ◽  
Optical Colonoscopy ◽  
Computed Tomographic ◽  
Primary Colon Cancer ◽  
Primary Colon ◽  
New Research ◽  
Additional Value

Abstract New research has addressed many of the early concerns of Computed Tomographic colonography (CTC) and these studies are now beginning to shape clinical practices. A review of the literature demonstrates that the sensitivity of CTC in screening for large polyps (≥ 1cm) or cancers in the large intestine is as high as that of conventional optical colonoscopy, however, the sensitivity decreases with the diameter of the polyp. Despite this, CTC is well tolerated, more acceptable to patients than optical colonoscopy and therefore may improve colorectal cancer screening compliance. This review not only describes the diagnostic accuracy and sensitivity of CTC, and the evolving role of CTC as a primary colon cancer screening option, but also the recent studies that have demonstrated the additional value of CTC utilization for practicing clinicians.

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