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Current Research on Cancer Biology and Therapeutics: Fourth Edition
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Current Research on Cancer Biology and Therapeutics: Fourth Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 29 June 2026 | Viewed by 1482

Special Issue Editor

Dr. Rafael Coveñas Rodríguez

E-Mail Website
Guest Editor
Laboratory of Neuroanatomy of the Peptidergic Systems, Institute of Neuroscience of Castilla and León (INCYL), University of Salamanca, c/Pintor Fernando Gallego 1, 37007 Salamanca, Spain
Interests: cancer and anticancer peptides; substance P/neurokinin-1 receptor system; neurokinin-1 receptor antagonists
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer caused 10 million deaths in 2020 and remains a major health problem worldwide. Surgery, chemotherapy, and radiotherapy are the current cancer treatments, but unfortunately, their results are, in many cases, unsatisfactory. The development of promising cancer research fields (new cytostatics, stem cells, and the human genome) has not been translated into better perspectives for many cancer patients. To improve the diagnosis and treatment of tumors, novel specific anticancer strategies showing enhanced antitumor effects and decreased toxicity must be explored.

Cancer cells evade the immune system and show resistance to anticancer therapies, leading to cancer cell proliferation, survival, invasion, and metastasis. These mechanisms, as well as angiogenesis, are regulated by different ligands, receptors, and intracellular cascades that regulate the genetic/protein machinery of cancer cells; thus, anticancer drugs must specifically block these cellular events. This has opened up new research lines for exploring new therapeutic strategies focused on targetable molecules. Accordingly, the main aim of this Special Issue is to increase knowledge about potential targetable molecules involved in previous mechanisms, such as peptides, signal transduction molecules, transcription factors, kinases, DNA damage repair enzymes, and epigenetic regulatory proteins. Thus, new antiproliferative, antimetastatic, and antiangiogenic strategies are welcome, as well as apoptotic inducers, signal transduction inhibitors, cytotoxic peptide conjugate-based cancer therapy, gene expression modulators, hormone therapies, and peptide receptor radionuclide therapy. Studies focused on the function–structure relationships between ligands and receptors for the design and synthesis of new and more effective anticancer compounds are also welcome.

I hope that this Special Issue opens the door to developing promising molecular targets, blocking tumor development, and developing new compounds capable of specifically destroying tumor cells. New anticancer strategies targeting tumor-specific molecular derangements must serve to improve the diagnosis and treatment of tumors and increase the cure rate and quality of life of cancer patients

Dr. Rafael Coveñas Rodríguez
Guest Editor

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • cancer and anticancer peptides
  • substance P/neurokinin-1 receptor system
  • neurokinin-1 receptor antagonists

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Published Papers (4 papers)

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Research

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18 pages, 2181 KB  
Article
GLI2 and FLNB Define Periocular Morphoeic Basal Cell Carcinoma
by John C. Bladen, Jun Wang, Mariya Moosajee, Muhammad Rahman, Ajanthah Sangaralingam, Vijay K. Gogna, Claude Chelala, Edel A. O’Toole and Michael P. Philpott
Int. J. Mol. Sci. 2025, 26(23), 11377; https://doi.org/10.3390/ijms262311377 - 25 Nov 2025
Viewed by 303
Abstract
Morphoeic basal cell carcinoma (mBCC) has a higher risk of local recurrence than the more indolent nodular (nodBCC) subtype. Little is known about the genetic and molecular makeup of mBCC that determines its invasive behaviour: a comparison of mBCC with nodBCC was carried [...] Read more.
Morphoeic basal cell carcinoma (mBCC) has a higher risk of local recurrence than the more indolent nodular (nodBCC) subtype. Little is known about the genetic and molecular makeup of mBCC that determines its invasive behaviour: a comparison of mBCC with nodBCC was carried out. Whole-exome sequencing (WES) of 20 BCC tumours (10 eyelid morphoeic and 10 nodular) underwent driver gene detection using OncodriveFM and MutSigCV, followed by a randomisation analysis procedure. Samples underwent RNA sequencing, gene-set enrichment analysis and candidates verified by RT-PCR. PTCH1, FLNB, and double-knockdown human keratinocyte models were used to validate phenotype and gene expression. Hedgehog pathway analysis of 20 additional BCCs underwent immunostaining verification. Our analysis revealed FLNB as a potential driver with a mutational cluster in FLNB Filamin domain 24 and a 4-fold reduction in expression compared to normal eyelids in mBCC only. FLNB knockdown demonstrated an mBCC phenotype. Aberrant Gli2 dominant hedgehog (Hh) signalling was seen in mBCC on three molecular levels: mutational significance, transcriptome profile, and protein expression. Gli2-dominant Hh overexpression was seen in the tumour plus stroma of eyelid morphoeic but not nodular BCC. FLNB is a potential tumour suppressor, with its loss producing a morphoeic phenotype in vitro. Full article
(This article belongs to the Special Issue Current Research on Cancer Biology and Therapeutics: Fourth Edition)
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16 pages, 681 KB  
Article
SOX9, GATA3, and GATA4 Overexpression in Liposarcomas: Insights into the Molecular Biology of Adipocytic Sarcomas
by Andrei-Ionuț Patrichi, Zsolt Kovács, Ioan Jung and Simona Gurzu
Int. J. Mol. Sci. 2025, 26(22), 10981; https://doi.org/10.3390/ijms262210981 - 13 Nov 2025
Viewed by 277
Abstract
Liposarcomas represent a heterogeneous group of malignant mesenchymal neoplasms, with diverse histological subtypes and molecular alterations. This study aimed to investigate the gene expression profiles of SOX9, GATA3, and GATA4 in liposarcoma subtypes and to assess their associations with clinicopathological parameters. Forty-two formalin-fixed, [...] Read more.
Liposarcomas represent a heterogeneous group of malignant mesenchymal neoplasms, with diverse histological subtypes and molecular alterations. This study aimed to investigate the gene expression profiles of SOX9, GATA3, and GATA4 in liposarcoma subtypes and to assess their associations with clinicopathological parameters. Forty-two formalin-fixed, paraffin-embedded liposarcoma samples were analyzed. Total RNA was extracted, reverse-transcribed, and quantified by qRT-PCR using GAPDH as an endogenous control. Relative quantification (RQ) values were categorized, and statistical analyses included Fisher’s exact test, Kaplan–Meier survival analysis, and Cox proportional hazards modeling. SOX9 expression significantly varied among histological subtypes (p = 0.017), with ALT/WDLS cases showing a predominance of high-level expression (RQ > 50 in 12/15 cases), in contrast to myxoid subtypes clustering mainly in the 10–50 RQ range. GATA4 overexpression correlated with smaller tumor size (<100 mm) (p = 0.049), being more frequent in 15/20 small tumors compared to 10/22 larger ones. GATA3 and GATA4 demonstrated the strongest inter-gene correlation (r = 0.68, p < 0.05), suggesting possible functional interplay. Kaplan–Meier analysis revealed no statistically significant survival differences for individual gene expression, but a high combined GATA3–GATA4 signature was associated with a favorable trend. These findings indicate that SOX9, GATA3, and GATA4 are broadly upregulated in liposarcomas, with subtype- and size-dependent expression patterns. The strong association between GATA3 and GATA4 expression supports their potential synergistic role in tumor biology. Integration of these molecular markers into diagnostic and prognostic workflows may enhance subtype characterization and inform targeted therapeutic strategies. Further studies in larger cohorts are warranted to validate these biomarkers and explore their mechanistic interplay in liposarcoma pathogenesis. Full article
(This article belongs to the Special Issue Current Research on Cancer Biology and Therapeutics: Fourth Edition)
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18 pages, 2130 KB  
Article
STAT3 Inhibition to Treat Ulcerative Colitis-Associated Colorectal Cancer
by Prema Robinson, Zal Italia, Zara Italia, Tan Hoang, Emma Rodriguez, T. Kris Eckols, Moses Kasembeli, Leticia Hamana Zorrilla, Luisa Maren Solis Soto, Rajasekaran Mahalingam and David J. Tweardy
Int. J. Mol. Sci. 2025, 26(21), 10808; https://doi.org/10.3390/ijms262110808 - 6 Nov 2025
Viewed by 736
Abstract
In patients with inflammatory bowel disease (IBD), colorectal cancer (CRC) occurs with 20-to-30-fold higher frequency, is more advanced at diagnosis, and has a worse prognosis than in the general population. To improve their treatment options, we determined if targeting STAT3 with TTI-101, a [...] Read more.
In patients with inflammatory bowel disease (IBD), colorectal cancer (CRC) occurs with 20-to-30-fold higher frequency, is more advanced at diagnosis, and has a worse prognosis than in the general population. To improve their treatment options, we determined if targeting STAT3 with TTI-101, a small-molecule STAT3 inhibitor, was beneficial in the azoxymethane (AOM)-disodium sulfate (DSS) mouse model of colitis-associated CRC. C57BL/6 mice received a single intraperitoneal injection of AOM followed by three cycles of 5% DSS in drinking water before receiving TTI-101 (50 mg/kg by oral gavage, OG, and daily) or vehicle for 28 days. TTI-101 treatment reduced adenoma numbers by 89% from 1.14 ± 1.07 in vehicle-treated mice to 0.13 ± 0.35 in TTI-101-treated mice (p ≤ 0.05, Kruskal–Wallis test). Levels of activated STAT3 (pY-STAT3) were increased 3.3-fold in the epithelium and stroma of dysplastic mucosa (147 ± 46; mean ± SD; and n = 4) vs. normal mucosa (45 ± 26; n = 7; and p ≤ 0.05, Kruskal–Wallis test) and were correlated with the adenoma number. TTI-101 was detected at pharmacologically relevant levels in the plasma and colons of TTI-101-treated AOM-DSS mice and was concentrated within colon tissue; plasma TTI-101 levels inversely correlated to pY-STAT3 levels. Importantly, TTI-101 normalized the colon transcriptome of AOM-DSS mice and reduced the expression of STAT3- and STAT1-upregulated genes associated with CRC oncogenesis. Thus, TTI-101 treatment may benefit IBD patients with CRC. Full article
(This article belongs to the Special Issue Current Research on Cancer Biology and Therapeutics: Fourth Edition)
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Review

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32 pages, 1788 KB  
Review
Luteinizing Hormone-Releasing Hormone (LHRH)-Targeted Treatment in Ovarian Cancer
by Pallavi Nayak, Michela Varani, Anna Giorgio, Giuseppe Campagna, Donatella Caserta and Alberto Signore
Int. J. Mol. Sci. 2025, 26(24), 11884; https://doi.org/10.3390/ijms262411884 - 9 Dec 2025
Abstract
Ovarian cancer remains one of the most lethal gynecologic malignancies and requires more effective and targeted treatment strategies. Luteinizing hormone-releasing hormone (LHRH), or gonadotropin-releasing hormone (GnRH), receptors are expressed in approximately 80% of ovarian tumors, representing a promising target for targeted drug delivery. [...] Read more.
Ovarian cancer remains one of the most lethal gynecologic malignancies and requires more effective and targeted treatment strategies. Luteinizing hormone-releasing hormone (LHRH), or gonadotropin-releasing hormone (GnRH), receptors are expressed in approximately 80% of ovarian tumors, representing a promising target for targeted drug delivery. This narrative review aimed to explore the development and advancements of LHRH-receptor targeted therapies in ovarian cancer. A bibliographic search was performed using PubMed, Scopus, Google Scholar, and Web of Science. The search strategy included studies on LHRH-peptide drug delivery systems and LHRH-conjugate nanosystems. Literature search covered in vitro studies, preclinical models, and ongoing clinical trials from 2000 to 2025. A total of 19 studies were included for peptide-drug delivery, and 30 studies were included for LHRH-conjugated nanosystems. Overall findings demonstrated enhanced preclinical efficacy, achieving ~50–80% tumor-growth inhibition and 2–4-fold higher cellular uptake, alongside reduced systemic toxicity. Early clinical studies, although limited, reported an overall response/disease-control rate of approximately 50%, supporting improved tumor accumulation of drugs, small interfering RNA (siRNA), and diagnostic agents. Ovarian cancer-specific therapy, targeting LHRH receptors, represents a promising strategy to enhance therapeutic outcomes. Further efforts in preclinical and clinical research are essential to refine personalized treatments and integrate them with a combination of therapies. Full article
(This article belongs to the Special Issue Current Research on Cancer Biology and Therapeutics: Fourth Edition)
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