Special Issues
Table of Content

Cancer Mutations: From Mechanisms to Targeted Therapy

Submission Deadline: 31 July 2026 View: 1165 Submit to Special Issue

Guest Editors

Assist. Prof. Jonas Cicenas

Email: j.cicenas@mapkinases.eu

Affiliation: 1. Kaunas University of Applied Sciences , Kaunas, LT-50468, Lithuania 

2. UAB CDKjc, Kaunas, LT-51338, Lithuania

3. SMK College of Applied Sciences, Klaipeda, Lithuania

Homepage:

Research Interests: kinases, cancer, kinase inhibitors as targeted therapy

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Summary

Most cancers harbor a wide spectrum of gene alterations, including amplifications, deletions, translocations, inversions, frameshifts, and point substitutions. Disruptions in several key genes are nearly universal, occurring in approximately 75%–93% of patients, while mutations in other genes are less frequent but still contribute significantly to tumor initiation and progression. These genetic changes may arise from germline inheritance or occur spontaneously during a patient's lifetime. Gene mutations can either enhance protein function, sometimes rendering it constitutively active, or impair it, potentially abolishing normal activity. Such alterations disrupt critical cellular processes, including proliferation, motility, adhesion, apoptosis, autophagy, DNA repair, and genomic stability, thereby promoting tumor development, growth, and metastasis. This Special Issue aims to comprehensively explore the mechanisms, prevalence, and therapeutic implications of gene mutations across diverse solid tumors, as well as hematologic malignancies such as leukemias and lymphomas.


Keywords

cancer, mutations, therapy, genetic variant

Published Papers


  • Open Access

    ARTICLE

    CDK4 Mediates Cisplatin Resistance in Renal Cell Carcinoma (RCC) Cells by Regulating the ASH1L-CTR1 Axis

    Wenjian Zeng, Xianglong Li, Hao Cai, Qingyu Zhou, Shuangshuang Sun, Pingping Li, Sunlong Li, Zhi Chen
    Oncology Research, DOI:10.32604/or.2026.073934
    (This article belongs to the Special Issue: Cancer Mutations: From Mechanisms to Targeted Therapy)
    Abstract Objectives: Cisplatin resistance is a major obstacle in the treatment of renal cell carcinoma (RCC), severely compromising therapeutic efficacy and patient prognosis. This study aimed to clarify the role and molecular mechanism of cyclin-dependent kinase 4 (CDK4) in cisplatin resistance of RCC. Methods: Immunohistochemistry (IHC) was used to detect the expression of CDK4 in cisplatin-resistant RCC tissues. In RCC cells and their drug-resistant sublines, CDK4 overexpression/knockdown assays were performed to evaluate the effects on cisplatin resistance and malignant progression. An in vivo model was established, to verify the in vivo function of CDK4. Transcriptome sequencing (RNA-seq), Cleavage Under… More >

  • Open Access

    ARTICLE

    Real-World Outcomes of First-Line Palbociclib Plus Endocrine Therapy for HR+/HER2− Metastatic Breast Cancer in Japan: A Single-Center Retrospective Study

    Keiko Yanagihara, Masato Yoshida, Kensaku Awaji, Tamami Yamakawa, Sena Kato, Miki Tamura, Koji Nagata
    Oncology Research, Vol.34, No.1, 2026, DOI:10.32604/or.2025.073891
    (This article belongs to the Special Issue: Cancer Mutations: From Mechanisms to Targeted Therapy)
    Abstract Background: Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors have transformed the management of hormone receptor–positive/HER2–negative (HR+/HER2–) advanced breast cancer, yet evidence for elderly or poor-performance patients remains limited. This study examined real-world outcomes of palbociclib plus endocrine therapy in Asian patients, with additional subgroup analyses by age and performance status. Methods: We retrospectively analyzed 46 consecutive Asian patients with recurrent or de novo HR+/HER2− breast cancer treated with first-line palbociclib plus ET between April 2021 and March 2025. The primary endpoint was progression-free survival (PFS). Secondary endpoints included overall response rate (ORR), disease control rate (DCR), and safety.… More >

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