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Cancers
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Molecular Targets and Therapeutic Pathways in Cancer
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Molecular Targets and Therapeutic Pathways in Cancer

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

Deadline for manuscript submissions: 31 October 2026 | Viewed by 1780

Special Issue Editors

Dr. Ashish H. Shah

E-Mail Website
Guest Editor
Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA
Interests: mechanisms of viral oncogenesis; development of viral-based therapeutics for cancer; understanding the cancer virome and glioma immunology; identification of novel drug targets for brain tumors
Dr. Deepa Seetharam

E-Mail Website
Guest Editor
Department of Neurosurgery, Section of Virology and Immunotherapy, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA
Interests: abacavir; antiretroviral; drug repurposing; glioblastoma; lamivudine; reverse transcriptase inhibitors

Special Issue Information

Dear Colleagues,

Cancer remains one of the leading causes of mortality worldwide, making continued innovation in the development of therapeutic options a necessity. This Special Issue, “Molecular Targets and Therapeutic Pathways in Cancer”, aims to highlight recent advances in the identification of novel molecular targets and the elucidation of signaling pathways that drive the initiation, progression, and resistance of tumors. With the rapid expansion of genomics, proteomics, and high-throughput screening technologies, researchers are now better equipped to unravel the complex biology underlying cancer and translate these insights into more precise and effective therapies. We welcome original research articles, reviews, and perspectives that explore oncogenic signaling networks, targeted therapy development, resistance mechanisms, and emerging strategies such as synthetic lethality, immunomodulation, and drug repurposing. By showcasing cutting-edge work in this area, this Special Issue aims to foster collaboration and innovation at the interface of basic science and clinical translation.

Dr. Ashish H. Shah
Dr. Deepa Seetharam
Guest 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 special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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

  • cancer therapeutics
  • molecular targets
  • signal transduction pathways
  • targeted therapy
  • drug resistance
  • precision oncology
  • tumor microenvironment
  • immunotherapy
  • kinase inhibitors
  • translational cancer research

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

17 pages, 1358 KB  
Article
Therapeutic Targeting of miR-21 Restores SASH1 and Sensitizes HBV-HCC to Sorafenib
by Kyuyoung Han, Eun-Kyoung Jwa, Suhyeon Ha, Jiye Kim, Ryunjin Lee, Eunkyeong Lee, Seoon Kang, Hye Ok Kim, Hyunhee Kwon, Dong-Hwan Jung, Young-In Yoon, Gi-Won Song, Gil-Chun Park, Tae Won Kim, Jung-Man Namgoon, Shin Hwang, Eunyoung Tak and Sung-Gyu Lee
Cancers 2026, 18(6), 1038; https://doi.org/10.3390/cancers18061038 - 23 Mar 2026
Viewed by 557
Abstract
Background: Sorafenib resistance remains a major barrier to effective therapy in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). Introduction: Here, we identified a previously undefined mechanism by which miR-21 promotes sorafenib resistance by suppressing the tumor suppressor SASH1 and enhancing HBx-driven PI3K/AKT/mTOR signaling. [...] Read more.
Background: Sorafenib resistance remains a major barrier to effective therapy in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). Introduction: Here, we identified a previously undefined mechanism by which miR-21 promotes sorafenib resistance by suppressing the tumor suppressor SASH1 and enhancing HBx-driven PI3K/AKT/mTOR signaling. Methods: miR-21 expression was markedly elevated in HBV-HCC tissues, HBV-integrated HCC cell lines, and hypoxic conditions. Bioinformatic analyses and luciferase reporter assays confirmed SASH1 as a direct miR-21 target. Results: Mechanistically, SASH1 was functionally associated with HBx-related oncogenic signaling and influenced apoptotic responses. miR-21 inhibition reduced HBV-HCC cell proliferation, increased apoptosis, and restored sorafenib sensitivity in vitro. In an orthotopic HBV-HCC mouse model, the combined administration of miR-21 inhibitor and sorafenib elicited markedly greater tumor suppression and restoration of the SASH1 expression than either monotherapy did. Discussion: Therefore, these findings suggested that the miR-21/SASH1 pathway contributed to therapeutic resistance in HBV-associated HCC and highlighted that miR-21 targeting could be an efficient strategy to improve sorafenib response. Conclusions: The miR-21/SASH1 axis play a critical role in sorafenib resistance in HBV-associated HCC, and targeting miR-21 may provide a promising therapeutic strategy to enhance treatment efficacy. Full article
(This article belongs to the Special Issue Molecular Targets and Therapeutic Pathways in Cancer)
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12 pages, 2378 KB  
Article
DNA Damage Sensing and TP53 Function as Modulators of Sensitivity to Calicheamicin-Based Antibody–Drug Conjugates for Acute Leukemia
by Camryn M. Pettenger-Willey, George S. Laszlo, Margery Gang, Frances M. Cole, Colin D. Godwin, Sarah Erraiss, Pritha Chanana, Allie R. Kehret, Junyang Li, Jacob W. Barton, Meghann M. Yochim, Eduardo Rodríguez-Arbolí and Roland B. Walter
Cancers 2026, 18(1), 67; https://doi.org/10.3390/cancers18010067 - 25 Dec 2025
Viewed by 871
Abstract
Background/Objectives: Approved for treatment of acute leukemia, gemtuzumab ozogamicin (GO) and inotuzumab ozogamicin (InO) are antibody–drug conjugates (ADCs) that deliver a toxic calicheamicin (CLM) derivative. The resistance mechanisms to GO/InO remain incompletely understood. Methods: We performed a genome-wide clustered regularly interspaced short palindromic [...] Read more.
Background/Objectives: Approved for treatment of acute leukemia, gemtuzumab ozogamicin (GO) and inotuzumab ozogamicin (InO) are antibody–drug conjugates (ADCs) that deliver a toxic calicheamicin (CLM) derivative. The resistance mechanisms to GO/InO remain incompletely understood. Methods: We performed a genome-wide clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 screen for CLM sensitivity genes, and then performed confirmatory cytotoxicity assays. Results: Several DNA damage pathway regulation genes were identified, most notably TP53. Across 13 acute leukemia cell lines, the six TP53-mutant cell lines (TP53MUT) were indeed 10- to 1000-fold less sensitive to CLM than the seven TP53WT cell lines. In five TP53WT/KO syngeneic cell line pairs we generated, TP53KO cells were significantly less sensitive to CLM than their TP53WT counterparts. In TP53WT but not TP53MUT cells, the MDM2 inhibitor and p53 activator, idasanutlin, enhanced CLM cytotoxicity, demonstrating that decoupling of cells from MDM2-p53 regulation sensitizes leukemia cells to CLM. The ATM inhibitors AZD1390 and lartesertib also significantly enhanced CLM efficacy but did so independent of the TP53 status. In contrast, neither an ATR inhibitor, Chk1/Chk2 inhibitor, Chk2 inhibitor, or a PARP inhibitor significantly impacted CLM-induced cytotoxicity across the thirteen cell lines. Together, our studies identify ATM, MDM2, and TP53—which are in the same cellular response to DNA damage pathway—as key modulators of CLM-induced cytotoxicity in acute leukemia cells. Conclusions: These results support further evaluation of combination therapies with corresponding small-molecule inhibitors (currently pursued for therapy of other cancers) toward clinical testing as novel strategies to increase the efficacy of CLM-based ADCs such as GO and InO. Full article
(This article belongs to the Special Issue Molecular Targets and Therapeutic Pathways in Cancer)
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