Advances in Novel Biomarkers and Emerging Immune/Targeted Therapies in Solid Tumors

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 1707

Special Issue Editors

Dartmouth-Hitchcock Medical Center, Lebanon, NH 03756, USA
Interests: biomarker; onco-immunology; lung cancer; precision oncology
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Guest Editor
Dartmouth-Hitchcock Medical Center, Lebanon, NH 03756, USA
Interests: cancer; tissue engineering; electrophysiology

Special Issue Information

Dear Colleagues,

In recent years, cancer research has experienced transformative advancements, particularly in our molecular understanding of solid tumors. Cutting-edge techniques such as genomic profiling, liquid biopsies, and onco-immunotherapy are revolutionizing how we approach cancer treatment, moving from a one-size-fits-all paradigm to a more precise, patient-centered model.

Immunotherapy and targeted therapies now represent key pillars in cancer treatment. Initially, immune checkpoint inhibitors (ICIs) and targeted therapies were limited to advanced or metastatic settings, often as salvage treatments in conjunction with chemotherapy. However, over the past decade, breakthroughs in these therapies have expanded their use to earlier stages, including neoadjuvant and adjuvant settings for resectable solid tumors. Clinical trials demonstrating their promise have led to the FDA approving several novel therapies for early-stage non-small-cell lung, breast, and bladder cancer and melanoma, among others. This paradigm shift offers the possibility of curing many early-stage cancer patients through the integration of immunotherapy and targeted treatments.

Our Special Issue, “Advances in Novel Biomarkers and Emerging Immune/Targeted Therapies in Solid Tumors”, guest-edited by Dr. Weijie Ma and Dr. Liang Lu, aims to gather groundbreaking research and reviews that enhance our understanding of the molecular mechanisms driving solid tumors and explore the clinical applications of targeted and immunotherapies. We encourage submissions covering a broad spectrum—from well-established molecular targets and emerging biomarkers to innovative treatment strategies. Topics of particular interest include overcoming acquired resistance to therapies, managing the side effects of these new treatments, integrating molecular therapies into existing treatment regimens, the role of pathological evaluation in optimizing therapies, and using tissue- and blood-based biomarkers for therapy selection and response monitoring.

We invite submissions from various disciplines, including molecular biology, pathology, pharmacology, and clinical oncology, to comprehensively collect the latest insights, aiming to enhance patient outcomes and guide future research in this rapidly evolving field.

Dr. Weijie Ma
Dr. Liang Lu
Guest Editors

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Keywords

  • solid tumor
  • biomarker
  • molecular targets
  • tyrosine kinase inhibitors (TKIs)
  • immune checkpoint inhibitors (ICIs)
  • oncogenic driver mutation
  • acquired resistance
  • precision oncology
  • cancer
  • next-generation sequence

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Published Papers (2 papers)

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Research

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14 pages, 1530 KB  
Article
miR-129 as a Molecular Biomarker in Gastric Cancer and Its Association with Neurodegenerative and Vascular Pathology
by Sabrina Birsan, Adrian-Gheorghe Boicean, Paula Anderco, Cristian Ichim, Samuel Bogdan Todor, Roman Iulian, Blanca Grama, Anca-Rafila Stîngaciu, Olga Brusnic, Tiberia Ilias and Corina Roman-Filip
Life 2025, 15(10), 1603; https://doi.org/10.3390/life15101603 - 14 Oct 2025
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Abstract
Background: MicroRNA-129 (miR-129) is a tumor suppressor involved in regulating oncogenic pathways, but its role in gastric adenocarcinoma and its potential connections to vascular and neurological dysfunction remain insufficiently defined. Objectives: To assess gastric juice-derived miR-129 as a diagnostic and prognostic biomarker for [...] Read more.
Background: MicroRNA-129 (miR-129) is a tumor suppressor involved in regulating oncogenic pathways, but its role in gastric adenocarcinoma and its potential connections to vascular and neurological dysfunction remain insufficiently defined. Objectives: To assess gastric juice-derived miR-129 as a diagnostic and prognostic biomarker for gastric cancer and to explore its associations with systemic inflammation, vascular impairment, and neurodegenerative changes. Methods: A prospective study was conducted in 38 patients undergoing upper gastrointestinal endoscopy (22 with histologically confirmed gastric adenocarcinoma, 16 controls). Gastric juice was aspirated prior to biopsy, and miR-129-2-3p expression was quantified by means of RT-qPCR normalized to U6 RNA. Tumor stage, serum biomarkers (CEA, CA 19-9, LDH, and CRP), carotid index (Doppler ultrasound), and neuroimaging (MRI) were recorded. Statistical analyses included ANOVA, Mann–Whitney U, ROC curve analysis, and correlation testing. Results: miR-129 expression was significantly reduced in gastric cancer compared with controls (ANOVA: F(3,34) = 3.70, p = 0.021, η2 = 0.25). ΔCt values increased progressively from controls to T2–T4 tumors, indicating stage-dependent downregulation. ROC analysis demonstrated moderate diagnostic performance (AUC = 0.75, 95% CI 0.54–0.92). Lower miR-129 levels correlated inversely with serum tumor markers (CEA, CA 19-9), LDH, and CRP. Patients with elevated carotid index (>1.3) and abnormal brain imaging findings exhibited significantly lower miR-129 expression (both p < 0.05). Conclusion: Gastric juice-derived miR-129 is downregulated in gastric adenocarcinoma, with progressive decline across tumor stages. Its inverse association with systemic tumor and inflammatory markers, as well as vascular and neurological impairment, suggests that miR-129 may function as a minimally invasive, multi-system biomarker for integrated cancer and vascular–neurological risk assessment. Full article
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Review

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17 pages, 299 KB  
Review
Indications and Mechanisms of Action of the Main Treatment Modalities for Non-Melanoma Skin Cancer
by Marcio F. Chedid, Aline C. Tregnago, Floriano Riva, Lucas Prediger, Anisha Agarwal and Jane Mattei
Life 2025, 15(9), 1447; https://doi.org/10.3390/life15091447 - 16 Sep 2025
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Abstract
Skin cancer is the most common cancer worldwide. The incidence of skin cancer has been increasing worldwide. Nearly 75% of all skin cancers are basal cell carcinomas (BCC), cutaneous squamous cell carcinoma (cSCC) represents approximately 20%, and those remaining are melanomas (4%) or [...] Read more.
Skin cancer is the most common cancer worldwide. The incidence of skin cancer has been increasing worldwide. Nearly 75% of all skin cancers are basal cell carcinomas (BCC), cutaneous squamous cell carcinoma (cSCC) represents approximately 20%, and those remaining are melanomas (4%) or other rare tumors (1%). Given the high cure rates and the ability to histologically confirm tumor clearance, surgical therapy is the gold standard for the treatment of skin cancer. Conventional surgery is the most employed technique for the removal of non-melanoma skin cancer (NMSCs). Mohs Micrographic Surgery (MMS) is the most precise surgical method for the treatment of non-melanoma skin cancer, allowing for 100% margin evaluation, being the gold-standard method for surgical treatment of non-melanoma skin cancer. Whenever it is possible to obtain wide margins (4 to 6 mm), cure rates vary from 70% to 99%. Imiquimod, a synthetic imidazoquinolinone amine, is a topical immune response modifier approved by the U.S. Food and Drug Administration (FDA) for the treatment of external anogenital warts, actinic keratosis (AK), and superficial basal cell carcinoma (sBCC). The efficacy of imiquimod is primarily attributed to its ability to modulate both innate and adaptive immune responses, as well as its direct effects on cancer cells. Imiquimod exerts its immunomodulatory effects by activating Toll-like receptors 7 and 8 (TLR7/8) on various immune cells, including dendritic cells, macrophages, and natural killer (NK) cells. Upon binding to these receptors, imiquimod triggers the MyD88-dependent signaling pathway, leading to the activation of nuclear factor kappa B (NF-κB) and interferon regulatory factors (IRFs). This cascade leads to the production of pro-inflammatory cytokines, including interferon-alpha (IFN-α), tumor necrosis factor-alpha (TNF-α), interleukin-12 (IL-12), and interleukin-6 (IL-6). These cytokines enhance local inflammation, recruit additional immune cells to the tumor site, and stimulate antigen presentation, thereby promoting an anti-tumor immune response. Radiation therapy (RTh) may be employed as a primary treatment to BCC. It may also be employed as an adjuvant treatment to surgery for SCC and aggressive subtypes of BCC. RTh triggers both direct and indirect DNA damage on cancer cells and generates reactive oxygen species (ROS) within cells. ROS trigger oxidative damage to DNA, proteins, and lipids, exacerbating the cellular stress and contributing to tumor cell death. Recently, immunotherapy emerged as a revolutionary treatment for all stages of SCC. Cemiplimab is a human programmed cell death 1 (PD-1)-blocking antibody that triggers a response to over 50% of patients with locally advanced and metastatic SCC. A randomized clinical trial (RCT) published in 2022 revealed that cemiplimab was highly effective in the neoadjuvant treatment of large SCCs. The drug promoted a significant tumor size decrease, enabling organ-sparing operations and a much better cosmetic effect. A few months ago, a RCT of cemiplimab on adjuvant therapy for locally aggressive SCC was published. Interestingly, cemiplimab was administered to patients with local or regional cutaneous squamous cell carcinoma after surgical resection and postoperative radiotherapy, at high risk for recurrence owing to nodal features, revealed that cemiplimab led to much lower risks both of locoregional recurrence and distant recurrence. Full article
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