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Cancers
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The Role of Platelets in Tumor Microenvironment
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The Role of Platelets in Tumor Microenvironment

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 14108

Special Issue Editor

Dr. Yacine Boulaftali

E-Mail Website
Guest Editor
Institut National de la Santé et de la Recherche Médicale, UMR_S 1148, Université de Paris, 75018 Paris, France
Interests: Inflammation; Platelets; Thrombosis; Fibrinolysis; Hemostasis; Mouse Models; Flow Cytometry; Platelet; Thromboinflammatory Diseases Aggregation; Platelet Activation

Special Issue Information

Dear Colleagues,

Over the last few decades, an increasing number of studies have reported on the role of platelets in the tumor microenvironment, independent of their well-established contributions to hemostasis and thrombosis. The relationship between platelets and tumor cells is bidirectional. Tumor cells can activate platelets and, conversely, platelets can influence tumor growth and metastasis. Platelets also promote tumor cells’ intravasation and extravasation.

The mechanism by which platelets contribute to the tumor microenvironment is still under debate. Some studies have reported a role for platelet-derived factors in tumor cell proliferation, while others suggest an antiproliferative effect of platelet-derived microparticles.

Preclinical and clinical research show that solid tumor growth is dependent on angiogenesis. It is now well established that platelets are involved in tumor-induced angiogenesis, and recent studies have also shown that they also participate in tumor vessel homeostasis. These observations raise the intriguing possibility that targeting platelets can destabilize the tumor vasculature and may improve the delivery of chemotherapeutic agents.

In this Special Issue, the role of platelets in tumor angiogenesis and in the maintenance of vascular integrity, as well as the role of platelets in chemotherapy resistance will be discussed.

Dr. Yacine Boulaftali
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • platelets
  • solid tumor
  • angiogenesis
  • vascular integrity
  • chemotherapy resistance

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Published Papers (4 papers)

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Research

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14 pages, 27354 KiB  
Article
Platelet-Derived PDGFB Promotes Recruitment of Cancer-Associated Fibroblasts, Deposition of Extracellular Matrix and Tgfβ Signaling in the Tumor Microenvironment
by Yanyu Zhang, Ehsan Manouchehri Doulabi, Melanie Herre, Jessica Cedervall, Qi Qiao, Zuoxiu Miao, Anahita Hamidi, Lars Hellman, Masood Kamali-Moghaddam and Anna-Karin Olsson
Cancers 2022, 14(8), 1947; https://doi.org/10.3390/cancers14081947 - 12 Apr 2022
Cited by 13 | Viewed by 3607
Abstract
Platelets constitute a major reservoir of platelet-derived growth factor B (PDGFB) and are continuously activated in the tumor microenvironment, exposing tumors to the plethora of growth factors contained in platelet granules. To address the specific role of platelet-derived PDGFB in the tumor microenvironment, [...] Read more.
Platelets constitute a major reservoir of platelet-derived growth factor B (PDGFB) and are continuously activated in the tumor microenvironment, exposing tumors to the plethora of growth factors contained in platelet granules. To address the specific role of platelet-derived PDGFB in the tumor microenvironment, we have created a mouse model with conditional knockout of PDGFB in platelets (pl-PDGFB KO). Lack of PDGFB in platelets resulted in 10-fold lower PDGFB concentration in the tumor microenvironment, fewer cancer-associated fibroblasts and reduced deposition of the extracellular matrix (ECM) molecules fibronectin and collagen I in the orthotopic RIP1-Tag2 model for pancreatic neuroendocrine cancer. Myosin light chain phosphorylation, promoting cell contraction and, consequently, the mechano-induced release of active transforming growth factor (TGF) β from extracellular compartments, was reduced in tumors from pl-PDGFB KO mice. In agreement, TGFβ signaling, measured as phosphorylated Smad2, was significantly hampered in tumors from mice lacking PDGFB in their platelets, providing a plausible explanation for the reduced deposition of extracellular matrix. These findings indicate a major contribution of platelet-derived PDGFB to a malignant transformation of the tumor microenvironment and address for the first time the role of PDGFB released specifically from platelets in the remodeling of the ECM in tumors. Full article
(This article belongs to the Special Issue The Role of Platelets in Tumor Microenvironment)
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14 pages, 17416 KiB  
Article
Platelet-Expressed Synaptophysin (pSyn) as Novel Biomarker in Neuroendocrine Malignancies
by Martina Hinterleitner, Bence Sipos, Verena Wagner, Julia M. Grottenthaler, Ulrich M. Lauer, Lars Zender and Clemens Hinterleitner
Cancers 2021, 13(10), 2286; https://doi.org/10.3390/cancers13102286 - 11 May 2021
Cited by 5 | Viewed by 2520
Abstract
Neuroendocrine neoplasms (NENs) encompass a heterogeneous group of tumors. Whereas low-grade neuroendocrine tumors (NETs) are histologically well-differentiated, highly aggressive neuroendocrine carcinomas (NECs) are characterized by a high proliferation rate and a worse clinical outcome. Since most NEN patients need monitoring of tumor progress [...] Read more.
Neuroendocrine neoplasms (NENs) encompass a heterogeneous group of tumors. Whereas low-grade neuroendocrine tumors (NETs) are histologically well-differentiated, highly aggressive neuroendocrine carcinomas (NECs) are characterized by a high proliferation rate and a worse clinical outcome. Since most NEN patients need monitoring of tumor progress and response to treatment for a long period of time, especially in metastatic disease, reliable, dynamic, and easy-to-assess biomarkers are needed. In this prospective study, we identified platelet-expressed synaptophysin (pSyn) as a novel biomarker in NENs. The level of pSyn in NENs was significantly upregulated compared to healthy donors. pSyn was positively correlated with higher tumor stages, the occurrence of metastasis, histological grading, and higher tumor proliferation (Ki67). Most importantly, high pSyn expression in our NEN cohort was shown to predict shorter progression-free survival (PFS). In conclusion, our data highlight the potential of pSyn as a novel biomarker in NENs reflecting tumor stages, grading, and prognosis. Full article
(This article belongs to the Special Issue The Role of Platelets in Tumor Microenvironment)
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Review

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16 pages, 917 KiB  
Review
Intratumoral Platelets: Harmful or Incidental Bystanders of the Tumor Microenvironment?
by Ophélie Le Chapelain and Benoît Ho-Tin-Noé
Cancers 2022, 14(9), 2192; https://doi.org/10.3390/cancers14092192 - 27 Apr 2022
Cited by 3 | Viewed by 2882
Abstract
The tumor microenvironment (TME) has gained considerable interest because of its decisive impact on cancer progression, response to treatment, and disease recurrence. The TME can favor the proliferation, dissemination, and immune evasion of cancer cells. Likewise, there is accumulating evidence that intratumoral platelets [...] Read more.
The tumor microenvironment (TME) has gained considerable interest because of its decisive impact on cancer progression, response to treatment, and disease recurrence. The TME can favor the proliferation, dissemination, and immune evasion of cancer cells. Likewise, there is accumulating evidence that intratumoral platelets could favor the development and aggressiveness of solid tumors, notably by influencing tumor cell phenotype and shaping the vascular and immune TME components. Yet, in contrast to other tumor-associated cell types like macrophages and fibroblasts, platelets are still often overlooked as components of the TME. This might be due, in part, to a deficit in investigating and reporting the presence of platelets in the TME and its relationships with cancer characteristics. This review summarizes available evidence from clinical and animal studies supporting the notion that tumor-associated platelets are not incidental bystanders but instead integral and active components of the TME. A particular emphasis is given to the description of intratumoral platelets, as well as to the functional consequences and possible mechanisms of intratumoral platelet accumulation. Full article
(This article belongs to the Special Issue The Role of Platelets in Tumor Microenvironment)
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14 pages, 1441 KiB  
Review
Platelet and Cancer-Cell Interactions Modulate Cancer-Associated Thrombosis Risk in Different Cancer Types
by Ana-Luisa Palacios-Acedo, Mélanie Langiu, Lydie Crescence, Diane Mège, Christophe Dubois and Laurence Panicot-Dubois
Cancers 2022, 14(3), 730; https://doi.org/10.3390/cancers14030730 - 30 Jan 2022
Cited by 17 | Viewed by 4369
Abstract
The first cause of death in cancer patients, after tumoral progression itself, is thrombo-embolic disease. This cancer-associated hypercoagulability state is known as Trousseau’s syndrome, and the risk for developing thrombotic events differs according to cancer type and stage, as well as within patients. [...] Read more.
The first cause of death in cancer patients, after tumoral progression itself, is thrombo-embolic disease. This cancer-associated hypercoagulability state is known as Trousseau’s syndrome, and the risk for developing thrombotic events differs according to cancer type and stage, as well as within patients. Massive platelet activation by tumor cells is the key mediator of thrombus formation in Trousseau’s syndrome. In this literature review, we aimed to compare the interactions between cancer cells and platelets in three different cancer types, with low, medium and high thrombotic risk. We chose oral squamous cell carcinoma for the low-thrombotic-risk, colorectal adenocarcinoma for the medium-thrombotic-risk, and pancreatic carcinoma for the high-thrombotic-risk cancer type. We showcase that understanding these interactions is of the highest importance to find new biomarkers and therapeutic targets for cancer-associated thrombosis. Full article
(This article belongs to the Special Issue The Role of Platelets in Tumor Microenvironment)
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