Cancer is characterized by abnormal cell proliferation. Cyclins and cyclin-dependent kinases (CDKs) have been recognized as essential regulators of the intricate cell cycle, orchestrating DNA replication and transcription, RNA splicing, and protein synthesis. Dysregulation of the CDK pathway is prevalent in the development and progression of human cancers, rendering cyclins and CDKs attractive therapeutic targets. Several CDK4/6 inhibitors have demonstrated promising anti-cancer efficacy and have been successfully translated into clinical use, fueling the development of CDK-targeted therapies. With this enthusiasm for finding novel CDK-targeting anti-cancer agents, there have also been exciting advances in the field of targeted protein degradation through innovative strategies, such as using proteolysis-targeting chimera, heat shock protein 90 (HSP90)‍-mediated targeting chimera, hydrophobic tag-based protein degradation, and molecular glue. With a focus on the translational potential of cyclin- and CDK-targeting strategies in cancer, this review presents the fundamental roles of cyclins and CDKs in cancer. Furthermore, it summarizes current strategies for the proteasome-dependent targeted degradation of cyclins and CDKs, detailing the underlying mechanisms of action for each approach. A comprehensive overview of the structure and activity of existing CDK degraders is also provided. By examining the structure‍‒‍activity relationships, target profiles, and biological effects of reported cyclin/CDK degraders, this review provides a valuable reference for both CDK pathway-targeted biomedical research and cancer therapeutics.

Objective: To establish a niraparib-resistant ovarian cancer cell line and preliminarily explore its biological characteristics and metabolic signatures. Methods: (1) Using ovarian adenocarcinoma cell line A2780 as parental cells, the niraparib-resistant cell line A2780-NiraR was established by the method of concentration gradient increased induction, and its morphological characteristics were observed using inverted phase-contrast microscope. The half-inhibitory concentration (IC50) of niraparib was determined by cytotoxicity assay. (2) Cell proliferation was determined by cell count kit-8 (CCK-8) assay and direct cell counting assay, cell cycle distribution was analyzed by flow cytometry. (3) The differential metabolites between A2780 and A2780-NiraR cells were detected by non-target metabolomics based on ultra-high performance liquid chromatography-high resolution mass spectrometry (UPLC/HRMS). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was conducted on the above differential metabolites to explore related metabolic pathways. Results: (1) Compared with the parental A2780 cells, A2780-NiraR cells exhibited predominantly short-spindle or oval morphology with reduced cellular projections and indistinct cell borders. The IC50 values of niraparib were 3.17 and 26.19 μmol/L against A2780 cells and A2780-NiraR cells, respectively (F=98.50, P<0.001). (2) A2780-NiraR cells had a slower proliferation rate compared with A2780 cells (F=146.80, P<0.001). The doubling time of A2780-NiraR cells [(37.5±1.9) hours] was significantly longer than that of A2780 cells [(14.5±1.0) hours; t=10.50, P<0.001]. Compared with the parental A2780 cells, A2780-NiraR cells had a significantly lower S phase fraction [(44.5±0.7)% in A2780 cells, (30.2±2.9)% in A2780-NiraR cells; t=4.78, P<0.001] and higher G0/G1 phase fraction [(35.4±1.2)% in A2780 cells, (52.2±3.1)% in A2780-NiraR cells; t=5.10, P<0.001]. (3) The metabolites of A2780 and A2780-NiraR cells were analyzed by non-target metabolomics. Forty-four differential metabolites between A2780 and A2780-NiraR cells were screened using the orthogonal partial least squares-discriminant analysis (OPLS-DA) model, the majority of which were significantly increased, such as pyrrolidone carboxylic acid, L-lysine and 1-pyrroline-4-hydroxy-2-carboxylate. Pathway enrichment analysis indicated that the arginine metabolism, purine metabolism, and pyrimidine metabolism were the most significantly enriched pathways. Conclusion: A2780-NiraR cells have acquired a stable niraparib resistance phenotype, and metabolic pathways including arginine metabolism may serve as potential therapeutic targets for enhancing niraparib efficacy in ovarian cancer.

Objective: To investigate the effectiveness and safety of secondary cytoreductive surgery (SCS) in patients with platinum-sensitive recurrent epithelial ovarian cancer who progressed after first-line maintenance therapy with poly adenosine diphosphate ribose polymerase inhibitor (PARPi). Methods: Clinical pathological data and prognostic information were retrospectively collected from 30 ovarian cancer patients who underwent SCS between January 2018 and June 2024. The Kaplan-Meier method was used to analyze the second progression-free survival (PFS2) time and 3-year overall survival (OS) rate. Results: (1) Primary treatment: the median age at diagnosis was 51.3 years. A total of 40% (12/30) patients underwent primary debulking surgery with an expectation of achieving no gross residual disease (R0), while 60% (18/30) received neoadjuvant chemotherapy and interval debulking surgery. Optimal cytoreduction was achieved in 93% (28/30) of patients. BRCA1/2 gene testing was performed in 29 patients (testing rate 97%, 29/30), identifying 11 BRCA-mutated (37%, 11/30) and 18 BRCA wild-type (60%, 18/30) patients. The median duration of PARPi maintenance therapy among the 30 patients was 11.9 months; patients with BRCA gene mutations had a median duration of 19.2 months, while those with BRCA wild-type had a median duration of 10.1 months. (2) Secondary surgery: pathologically confirmed recurrence patterns, single lesion in 9 patients (30%, 9/30), oligo-lesion (2 lesions) in 3 patients (10%, 3/30), and multi-lesion (≥3 lesions) in 18 patients (60%, 18/30). Among the 30 patients, optimal cytoreduction was achieved in 97% (29/30) of SCS patients, with suboptimal cytoreduction in 1 patient (3%, 1/30). Adjuvant chemotherapy included platinum+paclitaxel in 24 (80%, 24/30) patients and platinum+liposomal doxorubicin in 6 (20%, 6/30) patients. PARPi re-treatment was administered to 17 patients (57%, 17/30) after chemotherapy. (3) Efficacy and safety: as of the follow-up cutoff in June 2024, the median follow-up time was 28.0 months. A total of 19 (63%, 19/30) patients experienced the next recurrence. The median PFS2 time after SCS was 18.5 months. Recurrence occurred in 7 BRCA-mutated and 12 BRCA gene wild-type patients. Median PFS2 time was significantly longer in BRCA-mutated patients compared to BRCA wild-type patients (25.7 vs 14.1 months; P=0.028). Three deaths occurred during follow-up, resulting in a 3-year OS rate of 90%. Among the 30 patients, postoperative complications occurred in 4 patients (13%, 4/30). One patient developed a ureteral fistula on 7 days post-SCS requiring ureteral stenting, and one patient was transferred to the intensive care unit on 1 day post-SCS due to hypovolemic shock. No deaths occurred within 30 days after SCS. Conclusion: For platinum-sensitive recurrent ovarian cancer patients progressed after first-line PARPi maintenance therapy who are anticipated to achieve R0 resection, SCS represents a safe and effective second-line treatment option.

Objective: To evaluate the safety and effectiveness of fuzuloparib for the treatment of ovarian epithelial cancer patients in the real world setting. Methods: A retrospective analysis was conducted on the baseline data of 4 620 ovarian cancer patients who had received fuzuloparib monotherapy or combination therapy. Another 224 ovarian cancer patients who were willing to receive fuzuloparib monotherapy or combination therapy were prospectively enrolled, and their baseline characteristics, drug effectiveness, and safety data were analyzed. Results: (1) Among the 4 620 patients in the retrospective cohort, the median age of patients was 60 years; tumor types: 89.8% (4 149/4 620) had ovarian cancer. Among patients with clearly documented information, the vast majority had a histological type of serous carcinoma (82.9%, 3 770/4 546) and International Federation of Gynecology and Obstetrics (FIGO) staging of Ⅲ-Ⅳ (90.9%, 1 537/1 691). (2) Among the 224 patients in the prospective cohort, the median age of patients was 57 years; tumor types: 83.9% (188/224) had ovarian cancer. Among patients with clearly documented records, the predominant pathologic type was serous carcinoma (91.9%, 193/210), and FIGO stage was Ⅲ-Ⅳ in 79.9% (139/174). (3) Among the 224 prospective patients: 84 patients received first-line fluzoparib maintenance therapy, 92 patients received fluzoparib maintenance therapy after platinum-sensitive recurrence, 23 patients received direct fluzoparib treatment after platinum-sensitive recurrence, 19 patients received direct fluzoparib treatment after platinum-resistant recurrence. The median follow-up durations were 8.5, 8.7, 7.9, and 6.7 months, respectively. The median durations of fluzoparib treatment were 6.7, 4.8, 3.1, and 1.9 months, respectively. The median progression-free survival (PFS) times were not reached during follow-up, 12.6 months, not reached during follow-up, and 4.8 months, respectively. The 1-year PFS rates were 84.1%, 55.0%, 69.8%, and 45.5%, respectively. The remaining 6 patients received other fluzoparib regimens. (4) Among the 224 patients in the prospective dataset, 205 had safety data recorded. Of these, 127 patients (62.0%, 127/205) experienced treatment-related adverse events, with common events including anemia (24.4%, 50/205), thrombocytopenia (21.0%, 43/205), and leukopenia (19.5%, 40/205). Among the 205 patients, 43 (21.0%, 43/205) experienced grade 3 or higher treatment-related adverse events, with common events including anemia (8.3%, 17/205) and thrombocytopenia (8.3%, 17/205). Conclusions: The effectiveness of fuzuloparib in clinical application is generally consistent with other drugs in the same class, with good safety. This study provids new clinical evidence for the treatment of ovarian cancer with fuzuloparib.

Objective: To explore the application value of machine learning algorithms in constructing a predictive model for cardiovascular toxicity in breast cancer patients receiving anthracycline-based chemotherapy. Methods: This study was a retrospective cohort study. The female patients with breast cancer who received anthracyclines in the Affiliated Cancer Hospital of Xinjiang Medical University from January 2020 to December 2023 were enrolled. The endpoint event was abnormal electrocardiogram (ECG). According to whether the patients had ECG abnormalities during chemotherapy, they were divided into the ECG abnormal group and the ECG normal group. The dataset was divided into the training set and the test set at a ratio of 8∶2, and logistic regression, random forest, extreme gradient boosting (XGBoost), support vector machine (SVM) and multilayer perceptron (MLP) were used to construct a risk prediction model for cardiovascular toxicity in breast cancer patients, and the receiver operating characteristic curve, calibration curve and clinical decision curve were used to evaluate the model. Results: A total of 731 female patients with breast cancer, aged (51.6±9.4) years, were enrolled. The follow-up time was (130.3±37.1) days. There were 333 cases in the ECG abnormal group and 398 cases in the ECG normal group. Seven factors influencing cardiovascular toxicity were identified, including age, menstrual history, diabetes, combination therapy with trastuzumab, combination therapy with dexrazoxane, creatine kinase isoenzymes, and α-hydroxybutyrate dehydrogenase. In the training set, the area under the curve (AUC) for the logistic regression, random forest, XGBoost, SVM, and MLP models was 0.712, 0.863, 0.774, 0.813, and 0.733, respectively. In the test set, the AUC was 0.671, 0.778, 0.746, 0.771, and 0.705, respectively. Calibration curves and clinical decision curves showed that the random forest model performed the best. Conclusion: Models constructed with machine learning algorithms show promise in predicting cardiovascular toxicity in breast cancer patients receiving anthracycline-based chemotherapy, with the random forest prediction model performing the best.

Doxorubicin is a commonly used antitumor drug for the treatment of various cancers. However, its clinical application is greatly restricted by its severe cardiotoxicity. At present, doxorubicin-induced cardiotoxicity is categorized into acute and chronic forms, depending on the dosage and duration of exposure, which may eventually lead to the occurrence of heart failure. The pathogenesis of doxorubicin cardiotoxicity is associated with oxidative stress, mitochondrial damage, calcium overload, dysregulation of autophagy, and apoptosis. In forensic medical practice, cases of poisoning or even cardiac death caused by doxorubicin showed no obvious changes in cardiac morphology through routine forensic pathological examinations. The paper aims to summarize the research on the mechanisms of action of doxorubicin-induced cardiotoxicity in recent years, analyze and discuss the possible pathways of cardiomyocyte injury caused by doxorubicin, and provide references for research on the mechanisms of doxorubicin-induced cardiotoxicity and forensic application.

Epigallocatechin-3-gallate (EGCG), a bioactive polyphenol abundant in green tea, has garnered significant attention for its diverse therapeutic applications, ranging from antioxidant and anti-inflammatory effects to potential anticancer properties. Despite its immense promise, the practical utilization of EGCG in therapeutic settings as a medication has been hampered by inherent limitations of this drug, including poor bioavailability, instability, and rapid degradation. This review comprehensively explores the current challenges associated with the application of EGCG and evaluates the potential of nanoparticle-based formulations in addressing these limitations. Nanoparticles, with their unique physicochemical properties, offer a platform for the enhanced stability, bioavailability, and targeted delivery of EGCG. Various nanoparticle strategies, including polymeric nanoparticle, micelle, lipid-based nanocarrier, metal nanoparticle, and silica nanoparticle, are currently employed to enhance EGCG stability and pharmacological activity. This review concludes that the particle sizes of most of these formulated nanocarriers fall within 300 nm and their encapsulation efficiency ranges from 51% to 97%. Notably, the pharmacological activities of EGCG-loaded nanoparticles, such as antioxidative, anti-inflammatory, anticancer, and antimicrobial effects, are significantly enhanced compared to those of free EGCG. By critically analyzing the existing literature and highlighting recent advancements, this article provides valuable insights into the promising prospects of nanoparticle-mediated EGCG formulations, paving the way for the development of more effective and clinically viable therapeutic strategies.

To investigate the effects of methylenetetrahydrofolate reductase (MTHFR) rs1801133 and γ-glutamyl hydrolase (GGH) rs11545078 gene polymorphisms on plasma concentrations and toxicity following high-dose methotrexate (MTX) therapy in children with acute lymphoblastic leukemia (ALL).

To observe the effect of wheat-grain moxibustion plus chemotherapy on the activities of phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling and expressions of Caspase-3 and Caspase-9 in mice with breast cancer, so as to explore its mechanisms underlying suppression of tumor growth.

To investigate the effect of wrist-ankle acupuncture on the α7 nicotinic acetylcholine receptor (α7nAChR)/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway in the spinal dorsal horn of mice with chemotherapy-induced neuropathic pain (CINP), and to explore the mechanisms by which low-intensity wrist-ankle electroacupuncture alleviates pain hypersensitivity in CINP mice.

The tumor microenvironment (TME) is a critical determinant of tumor initiation, progression, and therapeutic response, and serves as the basis for designing precise delivery strategies. Its marked heterogeneity underscores the need for a more comprehensive understanding of its composition and function. In addition to the extensively studied classical TME, emerging evidence highlights the significant roles of the tumor mechanical microenvironment and the tumor microbial microenvironment in modulating treatment efficacy. These non-classical dimensions not only independently influence tumor behavior but also interact dynamically with classical TME components. Mechanical cues within the TME, including matrix stiffness and solid stress, significantly affect drug distribution and treatment efficacy, suggesting that mechanical remodeling represents a potential strategy to enhance therapeutic outcomes. Concurrently, tumor-associated microbiota and their metabolites participate in immune regulation and metabolic reprogramming, contributing to tumor development and offering novel therapeutic targets. Moreover, recent advances have broadened our understanding on the multilayered regulatory landscape of the TME through the investigation of previously underappreciated factors such as neural regulation, metabolic niche dynamics, spatiotemporal heterogeneity, and epigenetic modulation. This review systematically summarizes the characteristics of these diverse TME dimensions and highlights recent progress in targeted delivery strategies, to facilitate the development of more personalized and effective anticancer therapies.

To investigate the clinical features of thyroid dysfunction in lung cancer patients treated with programmed cell death receptor-1 (PD-1) or programmed cell death receptor-ligand 1 (PD-L1) and their value for predicting therapeutic efficacy.

Totally implantable venous access ports (TIVAP) are widely applied in cancer patients, primarily those requiring long-term intravenous infusion. Given the absence of clinical practice guidelines designed specifically for the use of TIVAP in cancer patients, the National Cancer Center, the Professional Committee of Interventional Oncology of Chinese Anti-Cancer Association, the Professional Committee on Minimally Invasive Intervention of World Association of Chinese Oncology, the Professional Committee of Intervention of Beijing Association of Oncology, and cancer prevention and control institutions from various provinces and cities have jointly established a guideline compilation committee comprising multidisciplinary experts. Drawing upon the latest research findings, this guideline has been formulated. It comprehensively covers the clinical application indications, preoperative preparation, intraoperative procedures, postoperative care, usage and maintenance, removal techniques, complication management, and quality control indicators related to TIVAP use in cancer patients. The recommendations were graded using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system to ensure that the TIVAP technology can be used to serve cancer patients with greater safety and efficiency in clinical practice, thereby enhancing overall medical quality and patient satisfaction.

Objective: To explore the effect of miR-3591-3p targeting P53 on cisplatin resistance of ovarian cancer (OC) SKOV3/DDP cells. Methods: Target prediction and dual luciferase assay were used to validate miR-3591-3p targeting P53. SKOV3/DDP cells were divided into control group, DDP group, miR-3591-3p knockdown group (anti-miR-3591-3p), miR-3591-3p knockdown control group (anti-miR-NC), cisplatin+miR-3591-3p knockdown group (DDP+anti-miR-3591-3p), cisplatin+control group (DDP+anti-miR-NC), cisplatin+miR-3591-3p knockdown+P53 knockdown group (DDP+anti-miR-3591-3p+sh-P53), cisplatin+miR-3591-3p knockdown+P53 knockdown control group (DDP+anti-miR-3591-3p+sh-NC). CCK-8 assay was used to detect cell survival rate and IC50 value; Flow cytometry were used to detect cell cycle and apoptosis; RT-qPCR was used to detect miR-3591-3p and P53 mRNA levels in cells; Western blot was used to detect P53, P-gp, MRP1, Ki-67, CyclinD1, Bcl-2, and Bax protein levels in cells. Nude mice were divided into control group, DDP group, miR-3591-3p knockdown group (anti-miR-3591-3p), miR-3591-3p knockdown control group (anti-miR-NC), and cisplatin+miR-3591-3p knockdown group (DDP+anti-miR-3591-3p). Subcutaneous injection of SKOV3/DDP cells was used to prepare transplanted tumor model. Tumor volume, mass, miR-3591-3p, P53 mRNA and protein levels in tumor tissue were detected. Results: MiR-3591-3p and P53 had binding sites. After overexpression of miR-3591-3p, wild-type P53 luciferase activity was decreased (P＜0.05); However, there was no significant difference in the luciferase activity of mutant P53 (P＞0.05). After DDP treatment or knockdown of miR-3591-3p expression, miR-3591-3p level in cells was decreased, the mRNA and protein levels of P53 were increased; the cell survival rate and IC50 value were decreased [DDP group 24, 36, 48 h IC50 (21.26±2.95)mg/L,(17.38±1.93)mg/L and (13.76±1.46)mg/L, control group (41.06±4.39)mg/L, (36.15±3.46)mg/L and(29.87±1.39)mg/L; anti-miR-3591-3p group 24,36,48 h IC50 (19.96±2.19)mg/L, (17.62±3.52)mg/L and (13.05±1.53)mg/L,anti-miR-NC group (43.37±3.83)mg/L, (40.47±2.82)mg/L and (31.41±0.73)mg/L], the proportion of S phase was decreased, the proportion of G0/G1 phase and cell apoptosis rate [DDP group (27.00±2.00)%, Control group (3.33±1.53)%; anti-miR-3591-3p group (28.98±3.14)%, anti-miR-NC group (4.05±1.96)%] were increased; P-gp, MRP1, Ki-67, CyclinD1, Bcl-2 protein levels were decreased, while Bax protein level was increased (all P＜0.05). Knocking down miR-3591-3p could enhance the impact of DDP on the above indicators (all P＜0.05). Knocking down P53 expression could inhibit the impact of miR-3591-3p deletion on the above indicators (all P＜0.05). After DDP treatment or knockdown of miR-3591-3p, the tumor volume and weight of nude mice were decreased [DDP group 14,21,28 d volume (284.26±24.51)mm3,(563.21±44.17)mm3 and (741.32±72.01)mm3,control group (384.25±41.25)mm3, (840.32±71.27)mm3 and (1 242.47±100.54)mm3; anti-miR-3591-3p group 14,21,28 d volume (274.47±27.77)mm3, (584.68±61.14)mm3 and (815.24±73.19)mm3, anti-miR-NC group (355.47±46.84)mm3, (804.24±79.54)mm3 and (1 350.47±108.37)mm3; DDP group weight (0.85±0.15)g,control group (1.34±0.12)g; anti-miR-3591-3p group (0.88±0.14)g, anti-miR-NC group (1.34±0.10)g],miR-3591-3p level in tumor tissue was decreased, and the mRNA and protein levels of P53 were increased (all P＜0.05); Knocking down miR-3591-3p could enhance the effect of DDP on the above indicators (all P＜0.05). Conclusion: MiR-3591-3p targeting P53 enhances cisplatin resistance in SKOV3/DDP cells.

For patients with advanced non-small cell lung cancer (NSCLC) harboring sensitive epidermal growth factor receptor (EGFR) mutations, guidelines prioritize the use of third-generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs), which offer higher objective response rate (ORR), longer progression-free survival (PFS), and better quality of life. However, due to the low proportion of elderly patients enrolled in clinical trials, the existing evidence is insufficient to fully guide clinical practice. This review examines the efficacy and safety differences of third-generation EGFR-TKIs as monotherapy or in combination in the elderly NSCLC by integrating subgroup analyses or pre-specified research objectives from prospective and retrospective studies. The results show that third-generation EGFR-TKIs have comparable efficacy in elderly patients to younger populations and are well-tolerated. Although combination therapies may extend survival time, the associated increased toxicity necessitates careful risk-benefit assessment.
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Lung cancer is the cancer with the highest incidence and mortality rate worldwide. In addition to the diversified treatment and prolonged lifespan in view of the development of medical technology, the side effect of medicine should not be ignored. Drug-induced interstitial lung disease (DI-ILD) is also commonly encountered during this process, and ILD triggered by the treatment of lung cancer characterized by the inflammation and scarring of lung tissue after the antitumor treatment in lung cancer leads to a poor prognosis and high mortality. The diagnosis and treatment of ILD caused by anti-lung cancer agents remains challenging in clinical settings and requires joint efforts from multidisciplinary team (MDT). This review systematically updates the epidemiology, molecular pathogenesis, genomics/genetics study, diagnosis and treatment of ILD related to anti-lung cancer agents. By the integration of the latest evidences, the paper offers clinical work references for early diagnosis of ILD related to anti-lung cancer agents to enhance the survival and quality of life of the lung cancer patients.
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The application of small molecule targeted drugs for lung cancer has significantly improved the survival of lung cancer patients. However, these drugs have a wide variety of types, fast development and market launch of new drugs, complex adverse reactions, and are mostly used at home, which increases the risk of irrational drug use. At the same time, insufficient monitoring of efficacy and safety is also prone to occur, ultimately affecting treatment outcomes. This consensus focuses on 43 small molecule targeted drugs or combinations for lung cancer, providing standardized recommendations for rational drug use and monitoring of efficacy/adverse reactions in clinical practice. The recommendations are regarding drug selection, dosage adjustment, efficacy monitoring, adverse reaction monitoring, and improvement of patient compliance. This consensus aims to improve the rational use and efficacy/safety monitoring quality of small molecule targeted drugs for lung cancer, ensure the effectiveness and safety of drug treatment, prolong the survival of lung cancer patients and improve their quality of life.
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Peritoneal metastasis is a common form of distant metastasis in patients with colorectal cancer, and it is typically associated with a poor prognosis. The development of peritoneal metastasis involves complex molecular mechanisms and multifactorial regulation of the tumor microenvironment. Due to the presence of the blood-peritoneal barrier, only a small amount of systemic medication reaches the peritoneal cavity, resulting in limited efficacy against peritoneal metastasis. Intraperitoneal administration shows significant therapeutic advantages as it can directly target the tumor microenvironment, maintain high local drug concentrations, and reduce systemic toxicity. Intraperitoneal chemotherapy, especially hyperthermic intraperitoneal chemotherapy, has become a cornerstone therapeutic strategy in the clinical treatment of peritoneal metastasis. When selecting chemotherapy drugs and drug combinations, pharmacokinetic properties, efficacy, and safety must be comprehensively considered to optimize the treatment outcomes. In addition, the unique microenvironment of the peritoneal cavity provides new treatment approaches for biological treatment strategies, including antitoxins, vaccines, immune checkpoint inhibitors, etc. Techniques such as pressurized intraperitoneal aerosol chemotherapy and novel drug delivery systems demonstrate potential for enhanced efficacy, offering promising alternatives to improve patient outcomes. This article will review peritoneal barrier characteristics, intraperitoneal drug transport, intraperitoneal chemotherapy, and intraperitoneal biological therapies, thereby establishing a theoretical framework for precision therapy in colorectal cancer peritoneal metastasis.

Pressurized intraperitoneal aerosol chemotherapy (PIPAC) is an emerging therapeutic modality for peritoneal carcinomatosis. This review aims to evaluate the safety, efficacy, and current clinical application of PIPAC in the treatment of peritoneal metastases originating from gastrointestinal malignancies. This review outlines the technical principles, historical development, procedural steps, commonly used drugs, and administration protocols of PIPAC; analyses the current clinical application status of PIPAC technology; discusses the current challenges and future directions of PIPAC; suggests that PIPAC technology still needs to conduct more high-quality and large-sample clinical trials to further establish the safety and efficacy of PIPAC, optimize its indications and formulate standardized operation specifications. In the future, multi-centre cooperation, multi-disciplinary cooperation, precision medicine strategies and new drug research and development will promote the clinical transformation and standardized application of PIPAC technology.