scholarly journals Liver-Directed Therapy for Neuroendocrine Metastases: From Interventional Radiology to Nuclear Medicine Procedures

Cancers ◽  
2021 ◽  
Vol 13 (24) ◽  
pp. 6368
Author(s):  
Roberto Luigi Cazzato ◽  
Fabrice Hubelé ◽  
Pierre De Marini ◽  
Eric Ouvrard ◽  
Julien Salvadori ◽  
...  
Keyword(s):  
Nuclear Medicine ◽  
Interventional Radiology ◽  
Therapeutic Strategy ◽  
Tumor Volume ◽  
Current Knowledge ◽  
Tumor Development ◽  
Hepatic Metastases ◽  
Percutaneous Ablation ◽  
Neuroendocrine Neoplasms ◽  
Interventional Radiology Procedures

Neuroendocrine neoplasms (NENs) are rare and heterogeneous epithelial tumors most commonly arising from the gastroenteropancreatic (GEP) system. GEP-NENs account for approximately 60% of all NENs, and the small intestine and pancreas represent two most common sites of primary tumor development. Approximately 80% of metastatic patients have secondary liver lesions, and in approximately 50% of patients, the liver is the only metastatic site. The therapeutic strategy depends on the degree of hepatic metastatic invasion, ranging from liver surgery or percutaneous ablation to palliative treatments to reduce both tumor volume and secretion. In patients with grade 1 and 2 NENs, locoregional nonsurgical treatments of liver metastases mainly include percutaneous ablation and endovascular treatments, targeting few or multiple hepatic metastases, respectively. In the present work, we provide a narrative review of the current knowledge on liver-directed therapy for metastasis treatment, including both interventional radiology procedures and nuclear medicine options in NEN patients, taking into account the patient clinical context and both the strengths and limitations of each modality.

Interrupting the FGF19-FGFR4 Axis to Therapeutically Disrupt Cancer Progression

2018 ◽  
Vol 19 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Liwei Lang ◽  
Austin Y. Shull ◽  
Yong Teng
Keyword(s):  
Cancer Progression ◽  
Therapeutic Strategy ◽  
Tumor Development ◽  
Vital Role ◽  
Signaling Cascades ◽  
Cancer Cell Proliferation ◽  
Clinical Use ◽  
Fibroblast Growth ◽  
Apoptosis Resistance ◽  
Downstream Signaling

Coordination between the amplification of the fibroblast growth factor FGF19, overexpression of its corresponding receptor FGFR4, and hyperactivation of the downstream transmembrane enzyme β-klotho has been found to play pivotal roles in mediating tumor development and progression. Aberrant FGF19-FGFR4 signaling has been implicated in driving specific tumorigenic events including cancer cell proliferation, apoptosis resistance, and metastasis by activating a myriad of downstream signaling cascades. As an attractive target, several strategies implemented to disrupt the FGF19-FGFR4 axis have been developed in recent years, and FGF19-FGFR4 binding inhibitors are being intensely evaluated for their clinical use in treating FGF19-FGFR4 implicated cancers. Based on the established work, this review aims to detail how the FGF19-FGFR4 signaling pathway plays a vital role in cancer progression and why disrupting communication between FGF19 and FGFR4 serves as a promising therapeutic strategy for disrupting cancer progression.

Awareness of radiation doses and risks among radiology residents, fellows, specialists, consultants and technologists in Jeddah, Saudi Arabia: Cross-Sectional Study. (Preprint)

2019 ◽  
Author(s):  
Bashayer Hassan Shuaib ◽  
Rahaf Hisham Niazi ◽  
Ahmed Haitham Abduljabbar ◽  
Mohammed Abdulraheem Wazzan
Keyword(s):  
Interventional Radiology ◽  
Ionizing Radiation ◽  
Statistical Significance ◽  
Knowledge Score ◽  
P Value ◽  
Radiation Doses ◽  
Cross Sectional ◽  
The Right ◽  
Interventional Radiology Procedures ◽  
Radiology Staff

BACKGROUND Radiology now plays a major role to diagnose, monitoring, and management of several diseases; numerous diagnostic and interventional radiology procedures involve exposure to ionizing radiation. Radiology now plays a major role to diagnose, monitoring, and management of several diseases; numerous diagnostic and interventional radiology procedures involve exposure to ionizing radiation. OBJECTIVE This study aimed to discover and compare the awareness level of radiation doses, protection issues, and risks among radiology staff in Jeddah hospitals. METHODS A cross-sectional survey containing 25 questions on personal information and various aspects of radiation exposure doses and risks was designed using an online survey tool and the link was emailed to all radiology staff in eight tertiary hospitals in Jeddah. The authors were excluded from the study. A P-value of < .05 was used to identify statistical significance. All analyses were performed using SPSS, version 21. RESULTS Out of 156 participants the majority 151 (96.8%) had poor knowledge score, where the mean scores were 2.4±1.3 for doses knowledge, 2.1±1.1for cancer risks knowledge, 2.3±0.6 for general information, and 6.7±1.9 for the total score. Only 34.6% of the participants were aware of the dosage of a single-view chest x-ray, and 9.0% chose the right answer for the approximate effective dose received by a patient in a two-view. 42.9% were able to know the correct dose of CT abdomen single phase. There is a significant underestimation of cancer risk of CT studies especially for CT abdomen where only 23.7% knew the right risk. A p-value of <0.05 was used to identify statistical significance. No significant difference of knowledge score was detected regarding gender (P =.2) or work position (P=.66). CONCLUSIONS Our survey results show considerable inadequate knowledge in all groups without exception. We recommended a conscientious effort to deliver more solid education and obtain more knowledge in these matters and providing periodic training courses to teach how to minimize the dose of radiation and to avoid risk related. CLINICALTRIAL not applicable

scholarly journals Aurora Kinase B Inhibition: A Potential Therapeutic Strategy for Cancer

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1981
Author(s):  
Naheed Arfin Borah ◽  
Mamatha M. Reddy
Keyword(s):  
Drug Resistance ◽  
Cell Cycle Progression ◽  
Therapeutic Strategy ◽  
Tumor Development ◽  
Aurora Kinase ◽  
Aurora Kinase B ◽  
Development Therapy ◽  
Chromosomal Passenger ◽  
Combination Studies ◽  
Related Drug

Aurora kinase B (AURKB) is a mitotic serine/threonine protein kinase that belongs to the aurora kinase family along with aurora kinase A (AURKA) and aurora kinase C (AURKC). AURKB is a member of the chromosomal passenger protein complex and plays a role in cell cycle progression. Deregulation of AURKB is observed in several tumors and its overexpression is frequently linked to tumor cell invasion, metastasis and drug resistance. AURKB has emerged as an attractive drug target leading to the development of small molecule inhibitors. This review summarizes recent findings pertaining to the role of AURKB in tumor development, therapy related drug resistance, and its inhibition as a potential therapeutic strategy for cancer. We discuss AURKB inhibitors that are in preclinical and clinical development and combination studies of AURKB inhibition with other therapeutic strategies.

scholarly journals Autophagy Modulation in Cancer: Current Knowledge on Action and Therapy

2018 ◽  
Vol 2018 ◽  
pp. 1-18 ◽  
Author(s):  
Mija Marinković ◽  
Matilda Šprung ◽  
Maja Buljubašić ◽  
Ivana Novak
Keyword(s):  
Therapeutic Strategy ◽  
Current Knowledge ◽  
Therapeutic Agents ◽  
Therapeutic Strategies ◽  
Human Diseases ◽  
The Core ◽  
Future Drug ◽  
Autophagic Activity ◽  
Tumor Types ◽  
Catabolic Process

In the last two decades, accumulating evidence pointed to the importance of autophagy in various human diseases. As an essential evolutionary catabolic process of cytoplasmatic component digestion, it is generally believed that modulating autophagic activity, through targeting specific regulatory actors in the core autophagy machinery, may impact disease processes. Both autophagy upregulation and downregulation have been found in cancers, suggesting its dual oncogenic and tumor suppressor properties during malignant transformation. Identification of the key autophagy targets is essential for the development of new therapeutic agents. Despite this great potential, no therapies are currently available that specifically focus on autophagy modulation. Although drugs like rapamycin, chloroquine, hydroxychloroquine, and others act as autophagy modulators, they were not originally developed for this purpose. Thus, autophagy may represent a new and promising pharmacologic target for future drug development and therapeutic applications in human diseases. Here, we summarize our current knowledge in regard to the interplay between autophagy and malignancy in the most significant tumor types: pancreatic, breast, hepatocellular, colorectal, and lung cancer, which have been studied in respect to autophagy manipulation as a promising therapeutic strategy. Finally, we present an overview of the most recent advances in therapeutic strategies involving autophagy modulators in cancer.

scholarly journals CXCL12 and Its Isoforms: Different Roles in Pancreatic Cancer?

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Alessandra Righetti ◽  
Matteo Giulietti ◽  
Berina Šabanović ◽  
Giulia Occhipinti ◽  
Giovanni Principato ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Microenvironment ◽  
Stromal Cells ◽  
Tumor Invasion ◽  
Epithelial To Mesenchymal Transition ◽  
Current Knowledge ◽  
Tumor Development ◽  
Physiological Role ◽  
Mesenchymal Transition ◽  
Splicing Isoforms

CXCL12 is a chemokine that acts through CXCR4 and ACKR3 receptors and plays a physiological role in embryogenesis and haematopoiesis. It has an important role also in tumor development, since it is released by stromal cells of tumor microenvironment and alters the behavior of cancer cells. Many studies investigated the roles of CXCL12 in order to understand if it has an anti- or protumor role. In particular, it seems to promote tumor invasion, proliferation, angiogenesis, epithelial to mesenchymal transition (EMT), and metastasis in pancreatic cancer. Nevertheless, some evidence shows opposite functions; therefore research on CXCL12 is still ongoing. These discrepancies could be due to the presence of at least six CXCL12 splicing isoforms, each with different roles. Interestingly, three out of six variants have the highest levels of expression in the pancreas. Here, we report the current knowledge about the functions of this chemokine and then focus on pancreatic cancer. Moreover, we discuss the methods applied in recent studies in order to understand if they took into account the existence of the CXCL12 isoforms.

scholarly journals Dual oxidase 1 limits the IFNγ-associated antitumor effect of macrophages

2020 ◽  
Vol 8 (1) ◽  
pp. e000622
Author(s):  
Lydia Meziani ◽  
Marine Gerbé de Thoré ◽  
Pauline Hamon ◽  
Sophie Bockel ◽  
Ruy Andrade Louzada ◽  
...  
Keyword(s):  
Antitumor Effect ◽  
Therapeutic Strategy ◽  
Critical Role ◽  
Tumor Development ◽  
Intratumoral Injection ◽  
Histocompatibility Complex ◽  
Dual Oxidase

BackgroundMacrophages play pivotal roles in tumor progression and the response to anticancer therapies, including radiotherapy (RT). Dual oxidase (DUOX) 1 is a transmembrane enzyme that plays a critical role in oxidant generation.MethodsSince we found DUOX1 expression in macrophages from human lung samples exposed to ionizing radiation, we aimed to assess the involvement of DUOX1 in macrophage activation and the role of these macrophages in tumor development.ResultsUsing Duox1−/− mice, we demonstrated that the lack of DUOX1 in proinflammatory macrophages improved the antitumor effect of these cells. Furthermore, intratumoral injection of Duox1−/− proinflammatory macrophages significantly enhanced the antitumor effect of RT. Mechanistically, DUOX1 deficiency increased the production of proinflammatory cytokines (IFNγ, CXCL9, CCL3 and TNFα) by activated macrophages in vitro and the expression of major histocompatibility complex class II in the membranes of macrophages. We also demonstrated that DUOX1 was involved in the phagocytotic function of macrophages in vitro and in vivo. The antitumor effect of Duox1−/− macrophages was associated with a significant increase in IFNγ production by both lymphoid and myeloid immune cells.ConclusionsOur data indicate that DUOX1 is a new target for macrophage reprogramming and suggest that DUOX1 inhibition in macrophages combined with RT is a new therapeutic strategy for the management of cancers.

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