Molecular Targeted Therapy in Cancer

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

Deadline for manuscript submissions: closed (15 December 2024) | Viewed by 4024

Special Issue Editor


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Guest Editor
College of Science and Engineering, University of Derby, Derby, UK
Interests: targeted cancer therapy; tumour-targeted superantigens (TTS); protein engineering; superantigens; antibody-directed enzyme prodrug therapy; long-acting drugs

Special Issue Information

Dear Colleagues,

Paul Ehrlich proposed the "magic bullet" concept in the 1890s, aiming that treatment could be specific to the target without toxicity to the healthy cells. With the advance in cancer biology, especially the DNA changes and proteins that drive cancer, this concept has recently been implemented efficiently in cancer treatment.

Molecular targeted cancer therapy consists mainly of small molecule inhibitors or monoclonal antibodies that inhibit the signal transduction pathways involved in growth, proliferation, and survival. Immune checkpoint inhibitors, cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), antibody‒drug conjugates (ADC), and antibody-directed enzyme prodrug therapy (ADEPT) are some of the recent molecular targeted cancer therapies.

Although molecular targeted therapy has achieved remarkable survival benefits in many types of cancer, they are not for every cancer patient and cause side effects and toxicity in some cases, in addition to drug resistance.   

This Special Issue aims to receive relevant contributions and recent insight into identifying druggable targets and discovering new drugs with different chemical entities or modes of action. We also seek contributions to finding or developing cancer small molecule inhibitors with higher specificity to cancer cells to increase efficacy and minimize toxicity. We are also keen to collect contributions to the patient microbiome's role in molecular targeted cancer therapy, such as cancer development, cancer progression and metastasis, and drug resistance and toxicity.

Prof. Dr. Sayed K. Goda
Guest Editor

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Keywords

  • molecular targeted therapy
  • signal transduction inhibitors
  • small molecules of cancer drugs
  • targeted cancer therapy
  • host microbiome in cancer-targeted therapy
  • anticancer drugs
  • cancer drug resistance
  • solid tumors
  • monoclonal antibodies in cancer therapy

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Published Papers (2 papers)

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Research

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16 pages, 3685 KiB  
Article
ASPH Is a Metastatic Factor and Therapeutic Target in Chondrosarcoma
by Xiaojuan Sun, Jesse Hart, Ross Taliano, Janine Molino, Joseph H. Schwab, Sjoerd Nota, Katsuya Nagaoka, Songhua Zhang, Mark Olsen, Rolf Carlson, Jack Wands and Richard M. Terek
Cancers 2025, 17(6), 951; https://doi.org/10.3390/cancers17060951 - 12 Mar 2025
Cited by 1 | Viewed by 621
Abstract
Background: Chondrosarcoma (CS) is a highly aggressive primary malignant bone tumor for which there are no effective systemic treatments. We assessed aspartate β-hydroxylase (ASPH) as a potential treatment target. ASPH is a transforming cell surface receptor, but its role in chondrosarcoma has not [...] Read more.
Background: Chondrosarcoma (CS) is a highly aggressive primary malignant bone tumor for which there are no effective systemic treatments. We assessed aspartate β-hydroxylase (ASPH) as a potential treatment target. ASPH is a transforming cell surface receptor, but its role in chondrosarcoma has not been evaluated. Our goals were to analyze the expression of ASPH in conventional chondrosarcoma, evaluate its utility as a biomarker, and determine if ASPH inhibition diminishes tumor progression in a preclinical model. Methods: An annotated tissue microarray was constructed with conventional chondrosarcoma tissues. ASPH expression was quantified with immunohistochemistry. A small molecule inhibitor (SMI) designed to inhibit ASPH activity was evaluated in two CS cell lines with intact ASPH expression and after knockout. Cell viability, invasion, and matrix metalloproteinase (MMP) expression were measured. A mouse xenograft chondrosarcoma model was used to evaluate the effect of the SMI on tumor growth, MMP activity in tumors, and lung metastatic burden. Results: Higher ASPH scores were associated with a greater risk of death and metastasis. The SMI decreased CS cell proliferation, invasion, and secretion of MMPs in vitro, and the effects were lost after ASPH knockout. In vivo, systemic administration of the SMI decreased tumor growth, MMP activity and content in xenograft tumors, and lung metastatic burden. Conclusions: These data validate ASPH as a biomarker in CS and as a factor in the metastatic phenotype. Systemic treatment with an SMI directed against ASPH inhibits tumor progression in a preclinical model, suggesting that ASPH-targeted therapy may be a new treatment strategy for chondrosarcoma expressing ASPH. Full article
(This article belongs to the Special Issue Molecular Targeted Therapy in Cancer)
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Review

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42 pages, 2557 KiB  
Review
Deciphering the Role of Cancer Stem Cells: Drivers of Tumor Evolution, Therapeutic Resistance, and Precision Medicine Strategies
by Mohamed El-Tanani, Syed Arman Rabbani, Shakta Mani Satyam, Imran Rashid Rangraze, Adil Farooq Wali, Yahia El-Tanani and Alaa A. A. Aljabali
Cancers 2025, 17(3), 382; https://doi.org/10.3390/cancers17030382 - 24 Jan 2025
Cited by 1 | Viewed by 2322
Abstract
Cancer stem cells (CSCs) play a central role in tumor progression, recurrence, and resistance to conventional therapies, making them a critical focus in oncology research. This review provides a comprehensive analysis of CSC biology, emphasizing their self-renewal, differentiation, and dynamic interactions with the [...] Read more.
Cancer stem cells (CSCs) play a central role in tumor progression, recurrence, and resistance to conventional therapies, making them a critical focus in oncology research. This review provides a comprehensive analysis of CSC biology, emphasizing their self-renewal, differentiation, and dynamic interactions with the tumor microenvironment (TME). Key signaling pathways, including Wnt, Notch, and Hedgehog, are discussed in detail to highlight their potential as therapeutic targets. Current methodologies for isolating CSCs are critically examined, addressing their advantages and limitations in advancing precision medicine. Emerging technologies, such as CRISPR/Cas9 and single-cell sequencing, are explored for their transformative potential in unraveling CSC heterogeneity and informing therapeutic strategies. The review also underscores the pivotal role of the TME in supporting CSC survival, promoting metastasis, and contributing to therapeutic resistance. Challenges arising from CSC-driven tumor heterogeneity and dormancy are analyzed, along with strategies to mitigate these barriers, including novel therapeutics and targeted approaches. Ethical considerations and the integration of artificial intelligence in designing CSC-specific therapies are discussed as essential elements of future research. The manuscript advocates for a multi-disciplinary approach that combines innovative technologies, advanced therapeutics, and collaborative research to address the complexities of CSCs. By bridging existing gaps in knowledge and fostering advancements in personalized medicine, this review aims to guide the development of more effective cancer treatment strategies, ultimately improving patient outcomes. Full article
(This article belongs to the Special Issue Molecular Targeted Therapy in Cancer)
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