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Cancers
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Targeted and Combination Therapy: Multi-Omic Approaches and Patient-Derived Models for...
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Targeted and Combination Therapy: Multi-Omic Approaches and Patient-Derived Models for Ultra-Precise Cancer Therapy

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

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 6204

Special Issue Editor

Dr. Hatem E. Sabaawy

E-Mail Website
Guest Editor
Rutgers Cancer Institute of New Jersey
Interests: precision medicine; patient-derived organoids (PDOs); orthotopic xenografts; glioblastoma; prostate cancer; combination therapy

Special Issue Information

This Special Issue will focus on presenting targeted therapy and combination therapy approaches to cancers such as glioblastoma, advanced prostate cancer, and other advanced cancers. This would include genomic, epigenetic, and proteomic profiling of patient tissues, identification of targetable pathways, preclinical studies using patient-derived cells (PDCs), spheres or spheroids (PDSs), organoids (PDOs), and xenografts (PDXs), and early phase or translational studies. The emphasis will be on approaches to identifying intratumor heterogeneity, predicting therapeutic resistance, evolving treatment against tumor-driving clones for personalized therapy, and, at each stage of the disease, achieving ultimate therapeutic responses with ultra-precise therapy.

Dr. Hatem E. Sabaawy
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 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

  • precision medicine
  • organoids
  • PDO
  • PDX
  • glioblastoma
  • prostate cancer
  • combination therapy

 

Published Papers (2 papers)

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Research

20 pages, 6315 KiB  
Article
A RAS-Independent Biomarker Panel to Reliably Predict Response to MEK Inhibition in Colorectal Cancer
by Ulrike Pfohl, Jürgen Loskutov, Sanum Bashir, Ralf Kühn, Patrick Herter, Markus Templin, Soulafa Mamlouk, Sergei Belanov, Michael Linnebacher, Florian Bürtin, Marcus Vetter, Christoph Reinhard, Lena Wedeken and Christian R. A. Regenbrecht
Cancers 2022, 14(13), 3252; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14133252 - 01 Jul 2022
Cited by 2 | Viewed by 2835
Abstract
Background: In colorectal cancer (CRC), mutations of genes associated with the TGF-β/BMP signaling pathway, particularly affecting SMAD4, are known to correlate with decreased overall survival and it is assumed that this signaling axis plays a key role in chemoresistance. Methods: Using CRISPR [...] Read more.
Background: In colorectal cancer (CRC), mutations of genes associated with the TGF-β/BMP signaling pathway, particularly affecting SMAD4, are known to correlate with decreased overall survival and it is assumed that this signaling axis plays a key role in chemoresistance. Methods: Using CRISPR technology on syngeneic patient-derived organoids (PDOs), we investigated the role of a loss-of-function of SMAD4 in sensitivity to MEK-inhibitors. CRISPR-engineered SMAD4R361H PDOs were subjected to drug screening, RNA-Sequencing, and multiplex protein profiling (DigiWest®). Initial observations were validated on an additional set of 62 PDOs with known mutational status. Results: We show that loss-of-function of SMAD4 renders PDOs sensitive to MEK-inhibitors. Multiomics analyses indicate that disruption of the BMP branch within the TGF-β/BMP pathway is the pivotal mechanism of increased drug sensitivity. Further investigation led to the identification of the SFAB-signature (SMAD4, FBXW7, ARID1A, or BMPR2), coherently predicting sensitivity towards MEK-inhibitors, independent of both RAS and BRAF status. Conclusion: We identified a novel mutational signature that reliably predicts sensitivity towards MEK-inhibitors, regardless of the RAS and BRAF status. This finding poses a significant step towards better-tailored cancer therapies guided by the use of molecular biomarkers. Full article
(This article belongs to the Special Issue Targeted and Combination Therapy: Multi-Omic Approaches and Patient-Derived Models for Ultra-Precise Cancer Therapy)
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19 pages, 2340 KiB  
Article
Multi-Omics Analysis of Glioblastoma Cells’ Sensitivity to Oncolytic Viruses
by Anastasiya V. Lipatova, Alesya V. Soboleva, Vladimir A. Gorshkov, Julia A. Bubis, Elizaveta M. Solovyeva, George S. Krasnov, Dmitry V. Kochetkov, Pavel O. Vorobyev, Irina Y. Ilina, Sergei A. Moshkovskii, Frank Kjeldsen, Mikhail V. Gorshkov, Peter M. Chumakov and Irina A. Tarasova
Cancers 2021, 13(21), 5268; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13215268 - 20 Oct 2021
Cited by 15 | Viewed by 2743
Abstract
Oncolytic viruses have gained momentum in the last decades as a promising tool for cancer treatment. Despite the progress, only a fraction of patients show a positive response to viral therapy. One of the key variable factors contributing to therapy outcomes is interferon-dependent [...] Read more.
Oncolytic viruses have gained momentum in the last decades as a promising tool for cancer treatment. Despite the progress, only a fraction of patients show a positive response to viral therapy. One of the key variable factors contributing to therapy outcomes is interferon-dependent antiviral mechanisms in tumor cells. Here, we evaluated this factor using patient-derived glioblastoma multiforme (GBM) cultures. Cell response to the type I interferons’ (IFNs) stimulation was characterized at mRNA and protein levels. Omics analysis revealed that GBM cells overexpress interferon-stimulated genes (ISGs) and upregulate their proteins, similar to the normal cells. A conserved molecular pattern unambiguously differentiates between the preserved and defective responses. Comparing ISGs’ portraits with titration-based measurements of cell sensitivity to a panel of viruses, the “strength” of IFN-induced resistance acquired by GBM cells was ranked. The study demonstrates that suppressing a single ISG and encoding an essential antiviral protein, does not necessarily increase sensitivity to viruses. Conversely, silencing IFIT3 and PLSCR1 genes in tumor cells can negatively affect the internalization of vesicular stomatitis and Newcastle disease viruses. We present evidence of a complex relationship between the interferon response genes and other factors affecting the sensitivity of tumor cells to viruses. Full article
(This article belongs to the Special Issue Targeted and Combination Therapy: Multi-Omic Approaches and Patient-Derived Models for Ultra-Precise Cancer Therapy)
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