Cancer Drug Resistance Achieves an Impact Factor of 7.6, Marking Four Consecutive Years of Growth

Cancer Drug Resistance (CDR) is pleased to announce that it has received a 2025 Journal Impact Factor (JIF) of 7.6, representing a 46% increase from the previous year's JIF of 5.2.

According to the latest Journal Citation Reports (JCR), CDR is now ranked within the top 15% of journals in the Oncology category, reflecting the journal's growing influence and recognition within the international cancer research community.

Since being indexed in the Web of Science Core Collection in 2022 and receiving its first Impact Factor in 2023, CDR has achieved four consecutive years of citation growth. This progress reflects the continued efforts of our authors, reviewers, Editorial Board members, Guest Editors, and readers worldwide, who have contributed to building CDR as a platform dedicated to understanding and overcoming one of the most pressing challenges in cancer treatment: drug resistance.

Advancing the Understanding of Cancer Drug Resistance

Over the past year, CDR has continued to focus on areas where resistance mechanisms are rapidly reshaping clinical decision-making.

One major area of emphasis has been acquired resistance to targeted therapies and strategies to overcome treatment failure. As KRAS G12C inhibitors transition from clinical trials into routine practice, their resistance landscape has become increasingly complex. Among the notable contributions published in CDR was a comprehensive review that systematically categorized clinical resistance mechanisms into three major classes: on-target alterations, bypass pathway activation, and phenotypic transformation. Beyond cataloguing resistance events, this framework provides a practical foundation for designing rational combination strategies following treatment failure.

During the same period, the journal also highlighted emerging resistance mechanisms associated with third-generation EGFR tyrosine kinase inhibitors and PARP inhibitors. Topics such as BRCA reversion mutations, replication fork protection, and adaptive signaling networks were discussed not only from a mechanistic perspective but also in the context of potential therapeutic interventions.

A second major focus has been heterogeneity of resistance to immune checkpoint blockade and the optimization of subsequent treatment strategies. Rather than asking whether immunotherapy works, many contributions published in CDR addressed a more clinically relevant question: where does resistance arise, and how should therapy be adapted once it occurs?

Published studies and reviews explored multiple layers of immune resistance, including defects in antigen presentation, T-cell dysfunction and exhaustion, and physical barriers created by the tumor microenvironment. Particularly noteworthy was a review examining CAR-T cell dysfunction in solid tumors, which clearly distinguished intrinsic T-cell exhaustion from tumor microenvironment-mediated immune exclusion. By clarifying these conceptual boundaries, the work provided valuable guidance for the next generation of engineered cellular therapies and was recognized by independent experts as an important contribution to the field.

Collectively, these efforts reflect CDR's commitment to publishing research that not only describes resistance mechanisms but also informs the development of clinically actionable solutions.

Looking Ahead: Priority Topics for 2026–2027

As cancer treatment continues to evolve, understanding and overcoming therapeutic resistance remains a central challenge across oncology. To support emerging areas of investigation, CDR welcomes submissions addressing the following priority topics:

• Resistance mechanisms and management strategies for antibody–drug conjugates (ADCs), including payload resistance, linker instability, and target antigen downregulation;
• Acquired resistance to immune checkpoint inhibitors and optimization of sequential treatment strategies;
• Liquid biopsy approaches for predicting, monitoring, and tracking therapeutic resistance, including ctDNA, circulating tumor cells, extracellular vesicles, and multi-omics integration;
• Failure mechanisms of CAR-T cells and bispecific antibodies in solid tumors, with particular attention to microenvironmental barriers and T-cell persistence;
• Combination strategies following resistance to RAS/RAF pathway inhibitors, including KRAS G12C and KRAS G12D-targeted therapies;
• Resistance mechanisms to targeted protein degraders, including PROTACs and molecular glues;
• Extrachromosomal DNA (ecDNA)-driven drug resistance and tumor evolution;
• Tumor evolution, lineage plasticity, epithelial-mesenchymal transition (EMT), and stem-cell state switching in disease recurrence;
• Tumor microenvironment reprogramming and systemic resistance involving cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), and extracellular matrix remodeling;
• Artificial intelligence and machine learning approaches for predicting drug resistance using multi-omics data, with an emphasis on both computational innovation and experimental validation.

Continuing Our Mission

While citation-based metrics provide one measure of journal performance, the mission of CDR remains unchanged: to serve as a trusted forum for high-quality research that advances the understanding, prevention, and reversal of cancer drug resistance.

As we celebrate this milestone, we remain committed to rigorous peer review, publication ethics, scientific integrity, and the dissemination of research that can ultimately improve outcomes for patients with cancer worldwide.

Contact the Editorial Office

Researchers interested in submitting manuscripts, proposing Special Topics, or exploring editorial collaborations are welcome to contact the Editorial Office.

• Editorial Office Email: [email protected]
• Submission System: https://www.oaecenter.com/login?JournalId=cdr

Editor: Louise Pan
Language Editor: Amir Khan
Production Editor: Ting Xu
Respectfully Submitted by the Editorial Office of Cancer Drug Resistance