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7.4
5.2
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Cancers
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Molecular Pathways in Cancers
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Molecular Pathways in Cancers

A topical collection in Cancers (ISSN 2072-6694). This collection belongs to the section "Molecular Cancer Biology".

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Editors

Dr. Ion Cristóbal

E-Mail Website
Collection Editor
Translational Oncology Division, Oncohealth Institute, IIS-Fundación Jiménez Díaz-UAM, 28040 Madrid, Spain
Interests: oncology; hematology; patient outcome; prognostic markers; healthcare quality; innovation; molecular processes
Special Issues, Collections and Topics in MDPI journals
Dr. Marta Rodríguez Moreno

E-Mail Website
Collection Editor
1. Pathology Department, IIS-Fundación Jiménez Díaz-UAM, Madrid, Spain
2. Center for the Biomedical Research Network in Oncology (CIBERONC), E-28040 Madrid, Spain
Interests: lymphoproliferative neoplasias; lymphoma; NOTCH signaling pathway; liquid biopsy; cancer bioinformatics
Special Issues, Collections and Topics in MDPI journals

Topical Collection Information

Dear Colleagues,

Despite continuous advances in anticancer therapies, the survival rates in most tumor types remain very poor, especially in those patients with advanced stages of the disease. There is a direct relationship between our level of understanding of each cancer’s molecular pathogenesis and our capacity to develop novel and effective therapeutic strategies.

For this Topical Collection, we welcome contributions that improve our knowledge of the molecular alterations that deregulate key signaling pathways and govern tumor progression in highly prevalent human cancers. This Topical Collection will focus on studies that combine basic and translational research and provide significant findings with a clear, clinical, and therapeutic impact.

Dr. Ion Cristóbal
Dr. Marta Rodríguez
Collection Editors

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 collection website. Research articles, review articles as well as short 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

  • highly prevalent cancers
  • tumor microenvironment
  • oncogenesis
  • progression
  • novel targeted therapy
  • prognosis

Published Papers (4 papers)

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2023

Jump to: 2022

15 pages, 2319 KiB  
Article
Inhibition of Dipeptidyl Peptidase-4 Activates Autophagy to Promote Survival of Breast Cancer Cells via the mTOR/HIF-1α Pathway
by Emi Kawakita, Fan Yang, Sen Shi, Yuta Takagaki, Daisuke Koya and Keizo Kanasaki
Cancers 2023, 15(18), 4529; https://doi.org/10.3390/cancers15184529 - 12 Sep 2023
Cited by 1 | Viewed by 1792
Abstract
Autophagy plays a complex role in breast cancer cell survival, metastasis, and chemotherapeutic resistance. Dipeptidyl peptidase (DPP)-4, a therapeutic target for type 2 diabetes mellitus, is also involved in autophagic flux. The potential influence of DPP-4 suppression on cancer biology remains unknown. Here, [...] Read more.
Autophagy plays a complex role in breast cancer cell survival, metastasis, and chemotherapeutic resistance. Dipeptidyl peptidase (DPP)-4, a therapeutic target for type 2 diabetes mellitus, is also involved in autophagic flux. The potential influence of DPP-4 suppression on cancer biology remains unknown. Here, we report that DPP-4 deficiency promotes breast cancer cell survival via the induction of autophagy by the C-X-C motif chemokine 12 (CXCL12)/C-X-C receptor 4 (CXCR4)/mammalian target of rapamycin (mTOR)/hypoxia inducible factor (HIF)-1α axis. DPP-4 knockdown and DPP-4 inhibitor KR62436 (KR) treatment both increased the levels of LC3II and HIF-1α in cultured human breast and mouse mammary cancer cells. The KR-induced autophagic phenotype in cancer cells was inhibited by treatment with the CXCR4 inhibitor AMD3100 and rapamycin. HIF-1α knockdown also suppressed breast cancer autophagy induced by KR. The autophagy inhibitor 3-methyladenine significantly blocked the KR-mediated suppression of cleaved caspase-3 levels and apoptosis in breast cancer cell lines. Finally, we found that the metformin-induced apoptosis of DPP-4-deficient 4T1 mammary cancer cells was associated with the suppression of autophagy. Our findings identify a novel role for DPP-4 inhibition in the promotion of breast cancer survival by inducing CXCL12/CXCR4/mTOR/HIF-1α axis-dependent autophagy. Metformin is a potential drug that counteracts the breast cancer cell survival system. Full article
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20 pages, 7203 KiB  
Article
A Matched Molecular and Clinical Analysis of the Epithelioid Haemangioendothelioma Cohort in the Stafford Fox Rare Cancer Program and Contextual Literature Review
by Arwa Abdelmogod, Lia Papadopoulos, Stephen Riordan, Melvin Wong, Martin Weltman, Ratana Lim, Christopher McEvoy, Andrew Fellowes, Stephen Fox, Justin Bedő, Jocelyn Penington, Kym Pham, Oliver Hofmann, Joseph H. A. Vissers, Sean Grimmond, Gayanie Ratnayake, Michael Christie, Catherine Mitchell, William K. Murray, Kelly McClymont, Peter Luk, Anthony T. Papenfuss, Damien Kee, Clare L. Scott, David Goldstein and Holly E. Barkeradd Show full author list remove Hide full author list
Cancers 2023, 15(17), 4378; https://doi.org/10.3390/cancers15174378 - 01 Sep 2023
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Abstract
Background: Epithelioid haemangioendothelioma (EHE) is an ultra-rare malignant vascular tumour with a prevalence of 1 per 1,000,000. It is typically molecularly characterised by a WWTR1::CAMTA1 gene fusion in approximately 90% of cases, or a YAP1::TFE3 gene fusion in approximately 10% of cases. EHE [...] Read more.
Background: Epithelioid haemangioendothelioma (EHE) is an ultra-rare malignant vascular tumour with a prevalence of 1 per 1,000,000. It is typically molecularly characterised by a WWTR1::CAMTA1 gene fusion in approximately 90% of cases, or a YAP1::TFE3 gene fusion in approximately 10% of cases. EHE cases are typically refractory to therapies, and no anticancer agents are reimbursed for EHE in Australia. Methods: We report a cohort of nine EHE cases with comprehensive histologic and molecular profiling from the Walter and Eliza Hall Institute of Medical Research Stafford Fox Rare Cancer Program (WEHI-SFRCP) collated via nation-wide referral to the Australian Rare Cancer (ARC) Portal. The diagnoses of EHE were confirmed by histopathological and immunohistochemical (IHC) examination. Molecular profiling was performed using the TruSight Oncology 500 assay, the TruSight RNA fusion panel, whole genome sequencing (WGS), or whole exome sequencing (WES). Results: Molecular analysis of RNA, DNA or both was possible in seven of nine cases. The WWTR1::CAMTA1 fusion was identified in five cases. The YAP1::TFE3 fusion was identified in one case, demonstrating unique morphology compared to cases with the more common WWTR1::CAMTA1 fusion. All tumours expressed typical endothelial markers CD31, ERG, and CD34 and were negative for pan-cytokeratin. Cases with a WWTR1::CAMTA1 fusion displayed high expression of CAMTA1 and the single case with a YAP1::TFE3 fusion displayed high expression of TFE3. Survival was highly variable and unrelated to molecular profile. Conclusions: This cohort of EHE cases provides molecular and histopathological characterisation and matching clinical information that emphasises the molecular patterns and variable clinical outcomes and adds to our knowledge of this ultra-rare cancer. Such information from multiple studies will advance our understanding, potentially improving treatment options. Full article
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15 pages, 5951 KiB  
Article
Set Protein Is Involved in FLT3 Membrane Trafficking
by Nerea Marcotegui, Silvia Romero-Murillo, Javier Marco-Sanz, Irene Peris, Blanca S. Berrozpe, Carmen Vicente, María D. Odero and Elena Arriazu
Cancers 2023, 15(8), 2233; https://doi.org/10.3390/cancers15082233 - 10 Apr 2023
Viewed by 1356
Abstract
The in-frame internal tandem duplication (ITD) of the FLT3 gene is an important negative prognostic factor in acute myeloid leukemia (AML). FLT3-ITD is constitutive active and partially retained in the endoplasmic reticulum (ER). Recent reports show that 3′UTRs function as scaffolds that can [...] Read more.
The in-frame internal tandem duplication (ITD) of the FLT3 gene is an important negative prognostic factor in acute myeloid leukemia (AML). FLT3-ITD is constitutive active and partially retained in the endoplasmic reticulum (ER). Recent reports show that 3′UTRs function as scaffolds that can regulate the localization of plasma membrane proteins by recruiting the HuR-interacting protein SET to the site of translation. Therefore, we hypothesized that SET could mediate the FLT3 membrane location and that the FLT3-ITD mutation could somehow disrupt the model, impairing its membrane translocation. Immunofluorescence and immunoprecipitation assays demonstrated that SET and FLT3 co-localize and interact in FLT3-WT cells but hardly in FLT3-ITD. SET/FLT3 interaction occurs before FLT3 glycosylation. Furthermore, RNA immunoprecipitation in FLT3-WT cells confirmed that this interaction occurs through the binding of HuR to the 3′UTR of FLT3. HuR inhibition and SET nuclear retention reduced FLT3 in the membrane of FLT3-WT cells, indicating that both proteins are involved in FLT3 membrane trafficking. Interestingly, the FLT3 inhibitor midostaurin increases FLT3 in the membrane and SET/FLT3 binding. Therefore, our results show that SET is involved in the transport of FLT3-WT to the membrane; however, SET barely binds FLT3 in FLT3-ITD cells, contributing to its retention in the ER. Full article
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2022

Jump to: 2023

4 pages, 231 KiB  
Editorial
Role of the PP2A Pathway in Cholangiocarcinoma: State of the Art and Future Perspectives
by Ion Cristóbal and Angela Lamarca
Cancers 2022, 14(21), 5422; https://doi.org/10.3390/cancers14215422 - 03 Nov 2022
Cited by 3 | Viewed by 938
Abstract
Cholangiocarcinoma represents a heterogeneous disease at both a clinical and molecular level [...] Full article
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