Extracellular Vesicle-Dependent Cross-Talk in Cancer—Focus on Pancreatic Cancer

Nannan, Lise; Oudart, Jean‐Baptiste; Monboisse, Jean-Claude; Ramont, Laurent; Brassart‐Pasco, Sylvie; Brassart, Bertrand

doi:10.3389/fonc.2020.01456

Cited by 19 publications

(23 citation statements)

References 109 publications

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“…ECM remodeling involves alterations in the expression of proteoglycans, a reorganization of the collagen interactome, proteolysis of macromolecules and activation of integrins. These alterations in ECM structure and function drive EMT (Catalano et al 2013 ; Nieberler et al 2017 ; Paolillo and Schinelli 2019 ; Brassart-Pasco et al 2020 ; Gerarduzzi et al 2020 ).…”

Section: Regulation Of the Epithelial-to-mesenchymal Transition By Tumour Microenvironmentmentioning

confidence: 99%

Cancer drug resistance induced by EMT: novel therapeutic strategies

et al. 2021

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Over the last decade, important clinical benefits have been achieved in cancer patients by using drug-targeting strategies. Nevertheless, drug resistance is still a major problem in most cancer therapies. Epithelial-mesenchymal plasticity (EMP) and tumour microenvironment have been described as limiting factors for effective treatment in many cancer types. Moreover, epithelial-to-mesenchymal transition (EMT) has also been associated with therapy resistance in many different preclinical models, although limited evidence has been obtained from clinical studies and clinical samples. In this review, we particularly deepen into the mechanisms of which intermediate epithelial/mesenchymal (E/M) states and its interconnection to microenvironment influence therapy resistance. We also describe how the use of bioinformatics and pharmacogenomics will help to figure out the biological impact of the EMT on drug resistance and to develop novel pharmacological approaches in the future.

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Section: Regulation Of the Epithelial-to-mesenchymal Transition By Tumour Microenvironmentmentioning

confidence: 99%

Cancer drug resistance induced by EMT: novel therapeutic strategies

et al. 2021

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“…Although a Dmean < 1 Gy was achieved using IMPT, it is still a less common and more expensive technique that cannot currently be taken as the standard of care for SBBC patients. In addition, skin toxicities seemed to be greater with proton therapy comparing with photon therapies [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Synchronous bilateral breast cancer treated with a 3-week hypofractionated radiotherapy schedule: clinical and dosimetric outcomes

et al. 2021

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Background and purpose Synchronous bilateral breast cancer (SBBC) accounts for 1–3.5% of breast cancer patients. The aim of this study was to evaluate dosimetric issues, clinical outcomes, and acute toxicities for SBBC patients receiving synchronous bilateral hypofractionated radiotherapy (SBHRT) and to compare them with patients treated with synchronous bilateral normofractionated RT schedule (SBNRT). Materials and methods From April 2016 to March 2020, 39 SBBC patients were referred to our institution. Patients were divided according to their prescription dose: Group A: 50 Gy/25fx (fractions), B: 60–64 Gy/25fx, C: 40.05 Gy/15fx; D: 48 Gy/15fx. Toxicity was evaluated using Common Terminology Criteria for Adverse Events (CTCAE)v.5.0. Results 34 patients were finally evaluated. Median follow-up was 24 months for NF schedule and 9 months for HF schedule. In the HF schedule, no acute side-effects > G2 were observed and no dermatitis was reported in 6 th month´s assessments. 95% of patients have no evidence of disease and only 1 patient presented local relapse in the first mammography after RT. No distant failures or deaths were observed. Regarding dosimetric issues, the inter-patient average D mean for the heart was: Group A: 5.0 Gy (4.6–5.5), Group B: 4.4 Gy (4.1–5.4), Group C: 4.8 Gy (4.5–5.1) and Group D: 5.3 Gy (4.4–5.6). For the lungs, the inter-patient average D mean was: Group A: 10.8 Gy (9.8–12.2), Group B: 11.5 Gy (11.3–12), Group C: 9.8 Gy (9.3–10.5) and Group D: 10.5 Gy (10–11.3). Conclusions This is the first study reporting the safety, feasibility, and tolerability of 40.05 Gy/15fx over 3 weeks for the treatment of SBBC patients. Further study with larger accrual is mandatory.

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“…TMVs can be separated from a patient’s biological fluids, such as peripheral blood, urine, saliva, and ascitic fluid. 51 TMVs contain many surface determinants, including CD44H, major histocompatibility complex I (MHC I), EMMPRIN, chemokine receptors (CCR6, CX3CR1), and epithelial cell adhesion molecules. TMVs also contain growth factors including vascular endothelial growth factor (VEGF) and hepatocyte growth factor.…”

Section: Tumor-derived Microvesiclesmentioning

confidence: 99%

Roles of Microvesicles in Tumor Progression and Clinical Applications

Zhu¹,

Li²,

Yi³

et al. 2021

IJN

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Microvesicles are extracellular vesicles with diameter ranging from 100 to 1000 nm that are secreted by tumor cells or other cells in the tumor microenvironment. A growing number of studies demonstrate that tumor-derived microvesicles are involved in tumor initiation and progression, as well as drug resistance. In addition, tumor-derived microvesicles carry a variety of immunogenic molecules and inhibit tumor response to immunotherapy; therefore, they can be exploited for use in tumor vaccines. Moreover, because of their high stability, tumor-derived microvesicles extracted from body fluids can be used as biomarkers for cancer diagnosis or assessment of prognosis. Tumor-derived microvesicles can also be deployed to reverse drug resistance of tumor regenerative cells, or to deliver chemotherapeutic drugs and oncolytic adenovirus for the treatment of cancer patients. This review summarizes the general characteristics of tumor-derived microvesicles, focusing on their biological characteristics, their involvement in tumor progression, and their clinical applications.

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Extracellular Vesicle-Dependent Cross-Talk in Cancer—Focus on Pancreatic Cancer

Cited by 19 publications

References 109 publications

Cancer drug resistance induced by EMT: novel therapeutic strategies

Cancer drug resistance induced by EMT: novel therapeutic strategies

Synchronous bilateral breast cancer treated with a 3-week hypofractionated radiotherapy schedule: clinical and dosimetric outcomes

Roles of Microvesicles in Tumor Progression and Clinical Applications

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