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New Approaches in Molecular and Cellular Cancer Biology: Translating Basic Research to the Clinic

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Oncology".

Deadline for manuscript submissions: 29 April 2027 | Viewed by 113

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Guest Editor Assistant
Signal Transduction & Proteomics Lab, Institute for Neurosciences of Castilla y León (INCyL), Department of Biochemistry and Molecular Biology, University of Salamanca, Salamanca, Spain
Interests: brain tumors; brain metastasis; proteomic; phosphoproteomics

Special Issue Information

Dear Colleagues,

Cancer remains one of the leading causes of mortality worldwide, presenting a continuous challenge to global healthcare systems. While conventional treatments like surgery, chemotherapy, radiotherapy and immunotherapy have prolonged survival, their efficacy is frequently limited by systemic toxicity and the inevitable emergence of drug resistance. Recent discoveries in molecular and cellular biology have fundamentally transformed our understanding of tumor heterogeneity and the complexity of signaling networks driving malignancy. However, translating these basic scientific discoveries into successful, long-term clinical interventions remains a critical difficulty. To overcome these limitations, it is essential to explore innovative approaches that decipher and target the precise molecular and cellular mechanisms underlying tumor progression, survival, and evasion.

Accordingly, the main aim of this Special Issue, “New Approaches in Molecular and Cellular Cancer Biology: Translating Basic Research to the Clinic”, is to bring together cutting-edge research that addresses these challenges through novel biological perspectives. We welcome original research articles and comprehensive reviews focusing on innovative molecular targets, intracellular signaling pathways, and cellular interactions within the tumor microenvironment. Key topics of interest include, but are not limited to, cellular plasticity, epigenetic regulation, non-coding RNAs, mechanisms of therapeutic resistance, advanced multi-omics approaches, angiogenesis, anticancer compounds, apoptotic inducers, cytotoxic peptide conjugate-based cancer therapies, kinases, and transcription factors. Studies utilizing novel in vitro or in vivo models to elucidate structure–function relationships of oncogenic drivers are also highly encouraged. Ultimately, we hope this collection provides a comprehensive platform to advance translational oncology, facilitating the development of safer, more accurate, and effective cancer therapies.

Dr. Rafael Coveñas Rodríguez
Guest Editor

Dr. Maruan Hijazi Vega
Guest Editor Assistant

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Keywords

  • cell signaling
  • proteomics
  • phosphoproteomics
  • mass spectrometry
  • kinase inhibitors
  • kinase activity
  • signaling networks
  • computational biology
  • peptide receptor antagonists
  • anticancer and cancer peptides

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Published Papers (1 paper)

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Research

30 pages, 10381 KB  
Article
Colitis-Associated Colorectal Cancer—STAT3 Inhibition as a Preventive Strategy
by Prema Robinson, Tan Hoang, Zara Italia, Zal Italia, Chia-Chi Chang, Ashish V. Damania, Nadim J. Ajami, Emma Rodriguez, Moses Kasembeli, Leticia Hamana Zorrilla, Luisa Maren Solis Soto, Caelyn Pham, Jacob Nguyen, Yousef Zamil, César Andrés Chávez Durán, Uddalak Bharadwaj, Rajasekaran Mahalingam and David J. Tweardy
Int. J. Mol. Sci. 2026, 27(18), 8381; https://doi.org/10.3390/ijms27188381 (registering DOI) - 20 Sep 2026
Abstract
Colorectal cancer (CRC) occurs with higher frequency in patients with inflammatory bowel disease (IBD) and has increased morbidity and mortality compared with CRC in patients in the general population. STAT3 has been implicated in CRC development, but strategies to target it have yet [...] Read more.
Colorectal cancer (CRC) occurs with higher frequency in patients with inflammatory bowel disease (IBD) and has increased morbidity and mortality compared with CRC in patients in the general population. STAT3 has been implicated in CRC development, but strategies to target it have yet to be employed to prevent its occurrence in groups at high risk for CRC. Our group developed TTI-101, a small-molecule STAT3 inhibitor, which was effective in treating colitis in the dextran sodium sulfate (DSS) mouse model. In the current study, we examined the ability of TTI-101 to prevent CRC in the azoxymethane (AOM)-DSS mouse model of CRC. Mice received AOM followed by DSS and were treated with either TTI-101 or vehicle control for 10 weeks. While vehicle-treated AOM-DSS mice developed polyps and adenocarcinomas, TTI-101-treated AOM-DSS mice did not. Levels of activated STAT3 (pY-STAT3) were increased in both the epithelial and stromal compartments of adenocarcinomas vs. normal colon mucosa and correlated with adenocarcinoma burden. Pharmacologically relevant concentrations of TTI-101 were detected in plasma and colon; plasma levels correlated with colon levels and correlated inversely with adenocarcinoma number. Transcriptomic analyses revealed that TTI-101 normalized expression of AOM-DSS-induced CRC-associated genes in the colon, many of which are regulated by STAT3. The addition of DSS to AOM resulted in a distinct cecal microbiome diversity and composition that was muted by the addition of TTI-101. Thus, TTI-101 prevented colitis-associated CRC in the AOM-DSS model through targeting STAT3’s pro-oncogenic effects on the colon transcriptome and modulating colitis-associated dysbiosis; targeting STAT3 in patients with IBD merits consideration for CRC prevention, as well as IBD treatment. Full article
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