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Molecular Targeted Therapies and Precision Medicine for Malignant Diseases
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Molecular Targeted Therapies and Precision Medicine for Malignant Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 May 2025 | Viewed by 9253

Special Issue Editor

Prof. Dr. Anica Dricu

E-Mail Website
Guest Editor
Department of Biochemistry, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania
Interests: molecular targeted cancer therapy; cancer immunotherapy; biomarkers; stem cells; brain tumors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the era of personalized medicine, the development of curative cancer therapies is supported by customized treatments concerning a patient's unique biology and metabolism, to ensure the best individualized therapeutic approach is taken. Cancer cells steadily amend gene transcription, translation and post-translational protein modifications to produce and use specific molecules that are essential in the process of growth, proliferation and expansion. When evaluating patients’ response to targeted therapy, genetic, epigenetic, transcriptional, proteomic, metabolic and environmental aspects are considered.

For this Special Issue, we invite original papers, reviews and communications focused on personalized medicine for cancer, including approaches to diagnosis, treatment and prevention that consider genes, proteins, other metabolites, family history, environmental conditions and lifestyles.

Prof. Dr. Anica Dricu
Guest Editor

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Keywords

  • personalized medicine
  • molecular targeted therapy
  • malignant diseases

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Published Papers (6 papers)

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Research

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13 pages, 246 KiB  
Article
A Haplotype GWAS in Syndromic Familial Colorectal Cancer
by Litika Vermani, Johanna Samola Winnberg, Wen Liu, Veronika Soller, Tilde Sjödin, Mats Lindblad and Annika Lindblom
Int. J. Mol. Sci. 2025, 26(2), 817; https://doi.org/10.3390/ijms26020817 - 19 Jan 2025
Viewed by 752
Abstract
A previous genome-wide association study (GWAS) in colorectal cancer (CRC) patients with gastric and/or prostate cancer in their families suggested genetic loci with a shared risk for these three cancers. A second haplotype GWAS was undertaken in the same colorectal cancer patients and [...] Read more.
A previous genome-wide association study (GWAS) in colorectal cancer (CRC) patients with gastric and/or prostate cancer in their families suggested genetic loci with a shared risk for these three cancers. A second haplotype GWAS was undertaken in the same colorectal cancer patients and different controls with the aim of confirming the result and finding novel loci. The haplotype GWAS analysis involved 685 patients with colorectal cancer cases and 1642 healthy controls from Sweden. A logistic regression model was used with a sliding window haplotype approach. Whole-genome and exome sequencing datawere used to find candidate SNPs to be tested in a nested case-control study. In the analysis of 685 colorectal cancer cases and 1642 controls, all ten candidate loci from the previous study were confirmed. Fifty candidate loci were suggested with a p-value < 5 × 10−6 and odds ratios between 1.35–6.52. Two of the 50 loci, on 13q33.3 and 16q23.3, were the same as in the previous study. Whole-genome or exome data from 122 colorectal cancer patients was used to search for candidate variants in these 50 loci. A nested case-control study was performed to test genetic variants at 11 loci in a cohort of 827 familial colorectal cancer and a sub-cohort of 293 familial CRC cases with colorectal, gastric, and/or prostate cancer within their families and 1530 healthy controls. One SNP, rs115943733 on 10q11.21, reached statistical significance (OR = 3.26, p = 0.009). Seven SNPs in 4 loci had a higher OR in the smaller cohort compared to the larger study CRC cases. The results in this GWAS gave support for suggested loci with an increased shared risk of CRC, gastric, and/or prostate cancer. Further studies are needed to confirm the shared risk to be able to use this information in cancer prevention. Full article
(This article belongs to the Special Issue Molecular Targeted Therapies and Precision Medicine for Malignant Diseases)
15 pages, 4068 KiB  
Article
Synergistic Effects of the Combination of Alpelisib (PI3K Inhibitor) and Ribociclib (CDK4/6 Inhibitor) in Preclinical Colorectal Cancer Models
by Razia Aslam, Cathy E. Richards, Joanna Fay, Lance Hudson, Julie Workman, Cha Len Lee, Adrian Murphy, Brian O’Neill, Sinead Toomey and Bryan T. Hennessy
Int. J. Mol. Sci. 2024, 25(24), 13264; https://doi.org/10.3390/ijms252413264 - 10 Dec 2024
Cited by 1 | Viewed by 1252
Abstract
The CDK4/6 inhibitor Ribociclib has shown limited efficacy as a monotherapy in colorectal cancer (CRC). However, combining Ribociclib with targeted therapies could present a viable strategy for treating CRC. This study evaluated the combination of Ribociclib and the PI3K inhibitor Alpelisib across four [...] Read more.
The CDK4/6 inhibitor Ribociclib has shown limited efficacy as a monotherapy in colorectal cancer (CRC). However, combining Ribociclib with targeted therapies could present a viable strategy for treating CRC. This study evaluated the combination of Ribociclib and the PI3K inhibitor Alpelisib across four distinct cell lines representing different mutational statuses (PIK3CA/KRAS wild-type, KRAS-mutated, PIK3CA-mutated, and PIK3CA/KRAS-mutated). We analyzed the drugs’ impact on key proteins involved in the PI3K pathway, cell cycle regulation, and apoptosis. The combination of Alpelisib and Ribociclib demonstrated a synergistic anti-proliferative effect across all cell lines, leading to a simultaneous decrease in pRB, pAKT, and p-S6 levels, and a more comprehensive suppression of the PI3K/AKT/mTOR pathway. Additionally, there was an upregulation of the apoptotic marker, p-BCL2, in cells treated with the combination compared to controls. In vivo studies using Caco-2, LS1034, and SNUC4 xenografts revealed a significant reduction in tumour growth with the combination therapy compared to single-agent treatments. These findings suggest that combining Alpelisib and Ribociclib could be a promising therapeutic approach for CRC, warranting further clinical exploration. Full article
(This article belongs to the Special Issue Molecular Targeted Therapies and Precision Medicine for Malignant Diseases)
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16 pages, 5159 KiB  
Article
Disruption of the Physical Interaction Between Carbonic Anhydrase IX and the Monocarboxylate Transporter 4 Impacts Lactate Transport in Breast Cancer Cells
by Jacob E. Combs, Akilah B. Murray, Carrie L. Lomelino, Mam Y. Mboge, Mario Mietzsch, Nicole A. Horenstein, Susan C. Frost, Robert McKenna and Holger M. Becker
Int. J. Mol. Sci. 2024, 25(22), 11994; https://doi.org/10.3390/ijms252211994 - 8 Nov 2024
Viewed by 1204
Abstract
It has been previously established that breast cancer cells exhibit high expression of the monocarboxylate (lactate) transporters (MCT1 and/or MCT4) and carbonic anhydrase IX (CAIX) and form a functional metabolon for proton-coupled lactate export, thereby stabilizing intracellular pH. CD147 is the MCT accessory [...] Read more.
It has been previously established that breast cancer cells exhibit high expression of the monocarboxylate (lactate) transporters (MCT1 and/or MCT4) and carbonic anhydrase IX (CAIX) and form a functional metabolon for proton-coupled lactate export, thereby stabilizing intracellular pH. CD147 is the MCT accessory protein that facilitates the creation of the MCT/CAIX complex. This study describes how the small molecule Beta-Galactose 2C (BGal2C) blocks the physical and functional interaction between CAIX and either MCT1 or MCT4 in Xenopus oocytes, which reduces the rate of proton and lactate flux with an IC50 of ~90 nM. This value is similar to the Ki for inhibition of CAIX activity. Furthermore, it is shown that BGal2C blocks hypoxia-induced lactate transport in MDA-MB-231 and MCF-7 breast cancer cells, both of which express CAIX. As in oocytes, BGal2C interferes with the physical interaction between CAIX and MCTs in both cell types. Finally, X-ray crystallographic studies highlight unique interactions between BGal2C and a CAIX-mimic that are not observed within the CAII active site and which may underlie the strong specificity of BGal2C for CAIX. These studies demonstrate the utility of a novel sulfonamide in interfering with elevated proton and lactate flux, a hallmark of many solid tumors. Full article
(This article belongs to the Special Issue Molecular Targeted Therapies and Precision Medicine for Malignant Diseases)
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Review

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22 pages, 1265 KiB  
Review
Current Research Trends in Glioblastoma: Focus on Receptor Tyrosine Kinases
by Edmond Nicolae Barcan, Carmen Duta, Georgiana Adeline Staicu, Stefan Alexandru Artene, Oana Alexandru, Alexandra Costachi, Andreea Silvia Pirvu, Daniela Elise Tache, Irina Stoian, Stefana Oana Popescu, Ligia Gabriela Tataranu and Anica Dricu
Int. J. Mol. Sci. 2025, 26(8), 3503; https://doi.org/10.3390/ijms26083503 - 9 Apr 2025
Viewed by 484
Abstract
Glioblastoma (GBM) is an aggressive brain tumor characterized by molecular complexity and resistance to conventional treatments, including surgery, radiation, and chemotherapy. Despite these challenges, advancements in receptor tyrosine kinase (RTK) research, combined with multi-omics approaches, hold promise for improving patient outcomes and survivability. [...] Read more.
Glioblastoma (GBM) is an aggressive brain tumor characterized by molecular complexity and resistance to conventional treatments, including surgery, radiation, and chemotherapy. Despite these challenges, advancements in receptor tyrosine kinase (RTK) research, combined with multi-omics approaches, hold promise for improving patient outcomes and survivability. RTKs are central to GBM progression, influencing cell proliferation, survival, and angiogenesis. However, the complexity of RTK signaling necessitates a broader, integrative perspective, which has been enabled by the emergence of -omics sciences. Multi-omics technologies—including genomics, transcriptomics, proteomics, and metabolomics—offer unprecedented insights into the molecular landscape of GBM and its RTK-driven pathways. Genomic studies have revealed mutations and amplifications in RTK-related genes, while transcriptomics has uncovered alterations in gene expression patterns, providing a clearer picture of how these aberrations drive tumor behavior. Proteomics has further delineated changes in protein expression and post-translational modifications linked to RTK signaling, highlighting novel therapeutic targets. Metabolomics complements these findings by identifying RTK-associated metabolic reprogramming, such as shifts in glycolysis and lipid metabolism, which sustain tumor growth and therapy resistance. The integration of these multi-omics layers enables a comprehensive understanding of RTK biology in GBM. For example, studies have linked metabolic alterations with RTK activity, offering new biomarkers for tumor classification and therapeutic targeting. Additionally, single-cell transcriptomics has unveiled intratumoral heterogeneity, a critical factor in therapy resistance. This article highlights the transformative potential of multi-omics in unraveling the complexity of RTK signaling in GBM. By combining these approaches, researchers are paving the way for precision medicine strategies that may significantly enhance diagnostic accuracy and treatment efficacy, providing new hope for patients facing this devastating disease. Full article
(This article belongs to the Special Issue Molecular Targeted Therapies and Precision Medicine for Malignant Diseases)
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21 pages, 2126 KiB  
Review
Glioblastoma and Immune Checkpoint Inhibitors: A Glance at Available Treatment Options and Future Directions
by Silvia Mara Baez Rodriguez, Ligia Gabriela Tataranu, Amira Kamel, Serban Turliuc, Radu Eugen Rizea and Anica Dricu
Int. J. Mol. Sci. 2024, 25(19), 10765; https://doi.org/10.3390/ijms251910765 - 7 Oct 2024
Cited by 2 | Viewed by 2545
Abstract
Glioblastoma is known to be one of the most aggressive and fatal human cancers, with a poor prognosis and resistance to standard treatments. In the last few years, many solid tumor treatments have been revolutionized with the help of immunotherapy. However, this type [...] Read more.
Glioblastoma is known to be one of the most aggressive and fatal human cancers, with a poor prognosis and resistance to standard treatments. In the last few years, many solid tumor treatments have been revolutionized with the help of immunotherapy. However, this type of treatment has failed to improve the results in glioblastoma patients. Effective immunotherapeutic strategies may be developed after understanding how glioblastoma achieves tumor-mediated immune suppression in both local and systemic landscapes. Biomarkers may help identify patients most likely to benefit from this type of treatment. In this review, we discuss the use of immunotherapy in glioblastoma, with an emphasis on immune checkpoint inhibitors and the factors that influence clinical response. A Pubmed data search was performed for all existing information regarding immune checkpoint inhibitors used for the treatment of glioblastoma. All data evaluating the ongoing clinical trials involving the use of ICIs either as monotherapy or in combination with other drugs was compiled and analyzed. Full article
(This article belongs to the Special Issue Molecular Targeted Therapies and Precision Medicine for Malignant Diseases)
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13 pages, 1181 KiB  
Review
Modifications of Nanobubble Therapy for Cancer Treatment
by Katarzyna M. Terlikowska, Bozena Dobrzycka and Slawomir J. Terlikowski
Int. J. Mol. Sci. 2024, 25(13), 7292; https://doi.org/10.3390/ijms25137292 - 2 Jul 2024
Cited by 4 | Viewed by 2315
Abstract
Cancer development is related to genetic mutations in primary cells, where 5–10% of all cancers are derived from acquired genetic defects, most of which are a consequence of the environment and lifestyle. As it turns out, over half of cancer deaths are due [...] Read more.
Cancer development is related to genetic mutations in primary cells, where 5–10% of all cancers are derived from acquired genetic defects, most of which are a consequence of the environment and lifestyle. As it turns out, over half of cancer deaths are due to the generation of drug resistance. The local delivery of chemotherapeutic drugs may reduce their toxicity by increasing their therapeutic dose at targeted sites and by decreasing the plasma levels of circulating drugs. Nanobubbles have attracted much attention as an effective drug distribution system due to their non-invasiveness and targetability. This review aims to present the characteristics of nanobubble systems and their efficacy within the biomedical field with special emphasis on cancer treatment. In vivo and in vitro studies on cancer confirm nanobubbles’ ability and good blood capillary perfusion; however, there is a need to define their safety and side effects in clinical trials. Full article
(This article belongs to the Special Issue Molecular Targeted Therapies and Precision Medicine for Malignant Diseases)
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