Cancer Communications最新文献

Volinia S, Terrazzan A, Kaminski TS, Jazdzewski K, Reali E, Bianchi N, Palatini J. Circulating tumor cells share RNA modules with early embryo trophectoderm and with metastatic cancer. Cancer Commun (Lond). 2025;45(5):500-504. doi:10.1002/cac2.12664

We spelled an author name incorrectly. We kindly request a change to the spelling:

Author: Jadzewski (wrong) to Jazdzewski (correct), adding the “z”, in the author list.

We apologize for this error.

Cancer immune checkpoint inhibitors (ICIs) have brought breakthroughs, but only about one-third of cancer patients benefit from ICIs. In recent years, targeting non-apoptotic regulated cell death (RCD) subtypes, such as ferroptosis, necroptosis, autophagy, cuproptosis, and pyroptosis, has emerged as a novel strategy in cancer therapy due to their ability to release damage-associated molecular patterns (DAMPs), enhance antigen presentation, and remodel the tumor immune microenvironment, thereby activating anti-tumor immune responses. A number of studies have shown that precise induction of these pathways by small molecules or nanoparticles can reverse the resistance to chemoradiotherapy and ICIs, promote the transformation of “cold tumors” to “hot tumors,” and ultimately establish durable immune memory. This article systematically reviewed the key mechanisms and immunomodulatory functions of five types of non-apoptotic RCD (ferroptosis, necroptosis, autophagy, cuproptosis, and pyroptosis), discussed the related treatment strategies, and prospects for the future application in combination with existing immunotherapy.

Radiopharmaceuticals are reshaping the landscape of cancer therapy, offering a unique theranostic advantage that is becoming increasingly central to precision medicine. By labeling the same molecular scaffold with different radionuclides, these agents enable seamless integration of diagnostic imaging and targeted therapy. Clinical breakthroughs with somatostatin receptor subtype 2 (SSTR2)- and prostate-specific membrane antigen (PSMA)-targeted radiopharmaceuticals have significantly enhanced both tumor visualization and therapeutic efficacy, establishing new benchmarks in oncology. Ongoing research is exploring novel molecular targets such as cholecystokinin-2 receptor (CCK2R), fibroblast activation protein (FAP), and C-X-C chemokine receptor type 4 (CXCR4). In parallel, there is growing interest in utilizing alternative radionuclides, including alpha-particle emitters and Auger electron emitters, beyond the commonly used beta-emitters, to improve therapeutic outcomes. Simultaneously, advances in ligand and linker design are being leveraged to optimize in vivo pharmacokinetics and tissue distribution. Among the emerging targets, CCK2R has attracted notable attention due to its overexpression in multiple malignancies. Research efforts have focused on improving ligand stability, receptor-binding affinity, and tumor retention, while also exploring strategies to enhance CCK2R expression on cancer cells. This review offers a comprehensive overview of the current landscape in cancer radiotheranostics, exploring the role of CCK2R in cancer biology and summarizing the latest advancements in the development of CCK2R-targeted radiopharmaceuticals. Using these advancements as a case study, we systematically examine key aspects of next-generation radiopharmaceutical design, from target selection and ligand engineering to pharmacokinetic optimization and clinical translation, providing a multidimensional framework for future innovation in cancer radiotheranostics.

Shu-Jin Li¹, Jia-Xian Chen¹, Zhijun Sun^1,2

¹The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine, Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, Hubei, People's Republic of China

²Department of Oral Maxillofacial-Head Neck Oncology, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, Hubei, People's Republic of China

Shu-Jin Li and Jia-Xian Chen contributed equally to this work.

Correspondence: Zhijun Sun ([email protected])

Following the publication of this article [1], it has come to our attention that proper citations were inadvertently omitted when introducing the concept of “immunostimulatory vascular-modulating cycle” and its illustration in Figure 4. The concept was originally proposed by Khan and Kerbel (2018) [2].

The revised text now reads:

“An immunostimulatory vascular-modulating cycle has been proposed to explain the synergistic effects observed between antiangiogenic agents and cancer immunotherapy, based on the mutual regulation between vascular normalization and immune responses [2] (Figure 4).”

The revised Figure 4 is provided below:

We sincerely apologize for our mistake.

[1] Li SJ, Chen JX, Sun ZJ. Improving antitumor immunity using antiangiogenic agents: Mechanistic insights, current progress, and clinical challenges. Cancer Commun. 2021;41(9):830–50.

[2] Khan KA, Kerbel RS. Improving immunotherapy outcomes with anti-angiogenic treatments and vice versa. Nat Rev Clin Oncol. 2018;15(5):310–24.

Wu M, Li W, Hu N, Liu C, Li J, Li Y, et al. Discovery of a Novel Viroid-Like Circular RNA in Colorectal Cancer. Cancer Commun. 2025;45(1):46-50. doi: 10.1002/cac2.12626.

This Expression of Concern is for the above article, published online on 09 November 2024 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Rui-Hua Xu; Sun Yat-sen University Cancer Center; and John Wiley & Sons Australia. The Expression of Concern has been agreed upon following information provided by a third party regarding the identification of the CRC-associated viroid. The authors reported this viroid-like circRNA as absent from the human genome based on the hg38 reference. However, the sequence is present at chromosome13:96543662-96543775 in the more complete T2T human genome reference, indicating it is not an exogenous RNA element. The authors have acknowledged the need for further investigation, particularly in light of the discrepancies from the difference between the hg38 and T2T human genomes. The editors have decided to issue this Expression of Concern to alert readers as further investigations proceed.

Lactylation, a newly identified post-translational modification, plays a multifaceted role in cancer biology by integrating epigenetic and non-epigenetic mechanisms. This review summarizes the latest research progress on lactylation, including its functions in epigenetic regulation and its broader impact on cellular processes. Lactate, as a metabolic byproduct, not only serves as an energy source for tumor cells but also acts as a signaling molecule driving various oncogenic processes. Lactylation facilitates cancer metabolic reprogramming, enabling tumor cells to adapt to hypoxic and nutrient-deprived microenvironments. Moreover, lactylation mediates immune suppression in the tumor microenvironment, promoting immune evasion and therapy resistance. This review further explores the clinical potential of targeting lactylation, offering new avenues for innovation in cancer research and treatment. These findings highlight the pivotal role of lactylation in cancer progression and its significant value as a potential therapeutic target.

Macrophages are prevalent in multiple tumors and exhibit diverse and potent functional activities. Therapeutic reprogramming of macrophage phenotypes represents a promising strategy for cancer immunotherapy. Engineering chimeric antigen receptors (CARs) to endow macrophages with anti-tumor capacities demonstrated encouraging efficacy, particularly in enhancing tumor-targeted phagocytosis. Furthermore, CAR macrophages (CAR-Ms) orchestrate adaptive immunity through secreting pro-inflammatory cytokines and presenting tumor antigens, thereby activating cytotoxic T lymphocyte responses. These multifaceted properties establish CAR-Ms as potent immunotherapeutic agents against therapy-refractory solid malignancies. Herein, we delineate the design principles, recent research advances, and rational combination strategies of CAR-Ms, with particular emphasis on emerging clinical evidence from ongoing CAR-M trials. We also explore potential applications of CAR-Ms in non-tumorous diseases and forecast future trends based on CAR-T therapy evolution. CAR-M development, combined with emerging technologies, will generate new perspectives for advancing cancer immunotherapy.