CANCER CHEMOTHERAPY AND PHARMACOLOGY癌症化疗与药理学
CANCER CHEMOTHERAPY AND PHARMACOLOGY(英文缩写 CANCER CHEMOTH PHARM),ISSN 0344-5704,eISSN 1432-0843,中文译名:癌症化疗与药理学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.288 | Q3 |
| 2022 | 3.000 | Q3 |
| 2023 | 2.700 | Q2 |
| 2024 | 2.300 | Q3 |
| 2025 | 2.500 | Q3 |
CANCER CHEMOTHERAPY AND PHARMACOLOGY 最新收录文献
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1. Continuous infusion of granulocyte colony-stimulating factor is associated with an advantage in neutrophil recovery in pediatric oncologic disorders.
PMID:日期:2026-10-03The use of intensified chemotherapy has significantly improved overall survival (OS) and relapse-free survival (RFS) in cancer patients. However, it also increases the risk of chemotherapy-induced neutropenia (CIN). Granulocyte colony-stimulating factor (G-CSF) is commonly used to hasten neutrophil recovery, but limited research has focused on the superiority of different routes of G-CSF administration. This was a randomized, prospective, single-institution study. Twenty-eight participants were enrolled and randomly assigned to experimental and control arms in a 1:1 ratio. At the end of the study, 20 cases were eligible for statistical analysis. The primary endpoint was the duration from the onset of neutropenia to steady neutrophil recovery. Secondary endpoints included the safety profile, 7-day emergency return rate, and the occurrence of infectious or febrile events. The mean duration from CIN to neutrophil recovery was 6.2 days in the intravenous drip (IVD) group and 7.6 days in the intravenous injection (IVI) group (P = 0.0068). The mean difference between the two groups was 1.4 days. A significantly lower incidence of febrile neutropenia (FN) was observed in the IVD group compared to the IVI group (15% vs. 50%, P = 0.0407). Adverse effects (AEs) were comparable between the two groups. The IVD route of G-CSF administration leads to faster neutrophil recovery and reduces the risk of FN. All evaluable AEs are comparable between the two groups. These findings suggest that the IVD route may be a preferable option for optimizing supportive care in cancer patients with CIN.
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2. Population pharmacokinetic analysis of pirtobrutinib, a non-covalent BTK inhibitor, in patients with hematological malignancies from the Phase 1/2 BRUIN study.
PMID:日期:2026-09-24This study aimed to characterize the pharmacokinetics (PK) of pirtobrutinib, a highly selective and noncovalent Bruton's tyrosine kinase (BTK) inhibitor, in adult patients with hematological malignancies using data from the Phase 1/2 BRUIN study (NCT03740529). Pirtobrutinib was administered as monotherapy at doses ranging from 25 to 300 mg once daily (QD). PK samples were collected at multiple time points, including intensive sampling on Cycle (C) 1 Day (D) 1, C1D8, C2D1, and C4D1 for Phase 1 dose-escalation, and sparse sampling on C1D8 and C4D1 for Phase 1 dose-expansion and Phase 2. Population PK (popPK) analysis used nonlinear mixed-effects modeling. Overall, 4487 evaluable pirtobrutinib concentrations obtained from 595 patients were included in the popPK analysis. Pirtobrutinib PK was well characterized by a 2-compartment model with linear clearance and 4-transit compartments for absorption. The mean elimination half-life was estimated to be 18.8 h. At the recommended Phase 2 dose (200 mg QD), the steady-state mean maximum drug concentration was 6460ng/mL, the mean minimum was 2260ng/mL, and the mean area under the concentration-time curve was 91300ng*h/mL. Pirtobrutinib disposition was significantly affected by body weight, renal function, and serum albumin, but not by formulation, cancer type, age, sex, race, ethnicity, or mild hepatic impairment. With the proposed starting dose of 200 mg QD, most patients (96%) were expected to exceed 90% BTK inhibition, across the entire dosing interval, indicating extensive and durable engagement of the drug target. No dose adjustments based on body weight, serum albumin or renal function were recommended. NCT03740529.
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3. Association of androgen deprivation therapy and acute kidney injury in patients with prostate cancer: a systematic review and meta-analysis of 72,980 patients.
3. 雄激素剥夺治疗与前列腺癌患者急性肾损伤的关联：一项纳入72,980例患者的系统评价和荟萃分析PMID:日期:2026-09-24Androgen deprivation therapy (ADT) has been associated with increased cardiovascular and renal risks in prostate cancer patients. We performed a systematic review and meta-analysis of the currently available evidence to evaluate the rates of acute kidney injury (AKI) in prostate cancer patients under ADT. PubMed, Embase, and the Cochrane Central Register of Controlled Trials were searched from inception to October 2024. Eligible observational studies comparing prostate cancer patients receiving ADT with those not receiving ADT were included. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using a random-effects model. Heterogeneity was assessed using I², τ², and 95% prediction intervals. Risk of bias and certainty of evidence were evaluated using the Newcastle-Ottawa Scale and GRADE framework, respectively. Statistical analyses were performed using R software version 4.3.1, and the study was reported according to PRISMA and MOOSE recommendations. Four studies involving 72,980 patients were included. ADT was significantly associated with AKI occurrence when compared with the non-ADT control group (OR 1.34; 95% CI 1.29-1.40; p < 0.001; I2 = 68%). In a subgroup analysis, GnRH agonists demonstrated positive association with AKI risk (OR 1.49; 95% CI 1.02-2.17; p = 0.038; I2 83.1%). In contrast, orchiectomy was not associated with AKI (OR 1.1; 95% CI 0.85-1.42; p = 0.488; I2 = 0%). GnRH agonist ADT, compared to other ADT modalities, demonstrated negative association with AKI (OR 0.77; 95% CI 0.61-0.98; p = 0.035; I2 = 0%). The analysis of orchiectomy against GnRH agonist therapy suggests lower AKI rate in orchiectomized patients (OR 0.77; 95% CI 0.66-0.91; p = 0.001; I2 = 0%). ADT was associated with higher odds of AKI among patients with prostate cancer. The association was particularly evident among patients receiving GnRH agonist-based therapy. However, the findings should be interpreted in light of the observational nature of the available evidence and the methodological limitations related to the synthesis of effect estimates reported using different statistical approaches.
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4. Crossing the toxicity threshold: a repeated landmark analysis of early toxicities and treatment modification during first-line CDK4/6 inhibitor therapy.
PMID:日期:2026-09-24Whether early treatment-related toxicities during cyclin-dependent kinase 4/6 inhibitor (CDK4/6i) therapy reflect treatment activity or simply longer treatment exposure remains unclear. Previous studies have largely evaluated toxicities cumulatively, potentially introducing immortal time bias into toxicity-outcome associations. We evaluated the prognostic significance of early toxicities and treatment modifications using repeated landmark analyses in patients receiving first-line CDK4/6i therapy for HR+/HER2- metastatic breast cancer. This retrospective study included 404 patients receiving first-line CDK4/6i plus endocrine therapy. Repeated landmark analyses at 8, 12, and 24 weeks evaluated associations of early toxicities and treatment modifications with subsequent progression-free survival (PFS) and overall survival (OS). During treatment, any-grade neutropenia occurred in 88.1% of patients, hepatotoxicity in 22.5%, QTc prolongation in 17.6%, and dose modification in 37.4%. At both the 8- and 12-week landmarks, grade 1-2 neutropenia was consistently associated with improved PFS and OS in multivariable analyses (all p<0.05; 8-week PFS: 33.2 vs. 22.1 months; OS: 90.6 vs. 40.8 months). Grade 3-4 neutropenia showed less consistent associations with survival but remained associated with improved OS at 12 weeks. Dose modification was independently associated with shorter PFS at the 12- and 24-week landmarks (all p<0.05). Associations between neutropenia and survival were attenuated at the 24-week landmark. Grade 1-2 neutropenia was the most consistent toxicity-based predictor of favorable survival and may represent a potential clinical marker of treatment activity. Associations with grade 3-4 neutropenia were less consistent. Dose modification was associated with shorter PFS, whereas hepatotoxicity and QTc prolongation showed no consistent independent prognostic associations.
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6. CNS distribution and preclinical activity of the PI3K/AKT inhibitors inavolisib and ipatasertib in pediatric-type diffuse high-grade gliomas.
PMID:日期:2026-09-17Pediatric-type diffuse high-grade gliomas (pHGG) are aggressive, largely incurable malignancies often characterized by PI3K/AKT pathway activation. This study investigated whether the PI3K inhibitor inavolisib and the AKT inhibitor ipatasertib could achieve therapeutic concentrations in the central nervous system (CNS) and demonstrate efficacy against PIK3CA-mutated pHGG. A panel of 12 pHGG cell lines with diverse PI3K/AKT genetic aberrations was screened for sensitivity to inavolisib and ipatasertib. Pharmacokinetic (PK) modeling was performed in mice to determine brain-to-plasma exposure ratios following oral administration (50 mg/kg inavolisib and 100 mg/kg ipatasertib). Finally, the in vivo efficacy of both inhibitors was evaluated using intracranial PIK3CA-mutated pHGG xenograft models, with survival and cerebrospinal fluid (CSF) circulating tumor DNA (ctDNA) levels as primary endpoints. All 12 cell lines exhibited PI3K/AKT alterations. The PIK3CA H1047R-mutated line (HSJD-DIPG-007) was the most sensitive in vitro (IC = 0.016 µM for inavolisib; 0.52 µM for ipatasertib). PK modeling revealed geometric mean brain-to-plasma ratios of 0.07 for inavolisib and 0.20 for ipatasertib, with model-predicted maximum brain concentrations of 0.69 µM and 0.93 µM, respectively. In vivo, inavolisib significantly extended survival (P = 0.0070) and increased CSF ctDNA release (P = 0.0317). In contrast, ipatasertib did not demonstrate significant in vivo activity. These findings highlight the therapeutic potential of inavolisib for treating PIK3CA-mutated pHGG. Despite the blood-brain barrier, inavolisib achieved sufficient CNS exposure to prolong survival in preclinical models, whereas ipatasertib efficacy did not translate from in vitro to in vivo settings.
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7. Outcomes of locally produced donor-derived anti-CD19 chimeric antigen receptor T-cells in relapsed or refractory B-cell acute lymphoblastic leukemia patients.
PMID:日期:2026-09-17Donor-derived anti-CD19 chimeric antigen receptor T-cell (CAR T-cell) therapy has emerged as one of the most promising treatments for relapsed/refractory (R/R) B-cell acute lymphoblastic leukemia (B-ALL). In this retrospective study, we evaluated the safety and efficacy of donor-derived anti-CD19 CAR T cells manufactured at our local GMP-compliant production facility. Eleven patients with R/R B-ALL received donor-derived anti-CD19 CAR T-cell therapy. Seven of the eleven patients had previously undergone allogeneic hematopoietic stem cell transplantation (allo-HSCT). All eleven patients achieved minimal residual disease (MRD) negativity by day 28 post-infusion. Three patients developed grade 1 cytokine release syndrome (CRS), and one patient developed grade 2 CRS. No case of immune effector cell-associated neurotoxicity syndrome (ICANS) was observed. The patient who experienced grade 2 CRS also developed grade 2 graft-versus-host disease (GVHD. At the median follow-up time of 47 months (range, 6-104 months), eight patients remained alive and MRD-negative. Three patients died: one from bone marrow (BM) relapse, one from concurrent BM and central nervous system (CNS) relapses, and one from candidemia. The 5-year overall survival and event-free survival rates were both 70%. In this retrospective study, donor-derived anti-CD19 CAR T-cells produced in a GMP-compliant environment demonstrated a favorable safety profile and high efficacy in treating patients with R/R B-ALL. Larger studies are warranted to confirm these findings.
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8. Main pulmonary artery enlargement during bevacizumab therapy in KRAS-mutant metastatic colon cancer.
PMID:日期:2026-09-17Bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor (VEGF), is a cornerstone of metastatic colorectal cancer treatment. While systemic hypertension is a recognized complication of VEGF pathway inhibition, the effects of bevacizumab on the pulmonary vasculature remain poorly characterized, and the only longitudinal CT data to date derive from hepatocellular carcinoma patients receiving atezolizumab plus bevacizumab. In this exploratory study, we investigated whether serial thoracic computed tomography (CT) demonstrates progressive enlargement of the main pulmonary artery (mPA) during bevacizumab-based chemotherapy in colon cancer. In this retrospective single-center study, 150 patients with KRAS-mutant colon cancer treated with bevacizumab between 2017 and 2025 were screened. Patients with a minimum of 3 months of bevacizumab exposure and at least two follow-up thoracic CT scans were included. The mPA diameter, ascending aorta (AAo) diameter, and mPA/AAo ratio were measured at baseline (T0) and at approximately 3 (T1), 6 (T2), and 9 (T3) months. The primary analysis employed a linear mixed-effects model (LMM) with a patient-level random intercept. Adjusted models, paired secondary analyses, and exploratory overall survival (OS) analyses were also performed. All analyses were conducted in R. Seventy-four patients met inclusion criteria (median age 62.8 years; 71.6% male). The mPA increased significantly from 23.7 ± 3.3 mm at T0 to 25.9 ± 3.3 mm at T3. In the unadjusted LMM, the mPA increased by + 0.94 mm at T1 (p < 0.001), + 1.45 mm at T2 (p < 0.001), and + 2.22 mm at T3 (p < 0.001) relative to baseline. The linear trend estimate was + 0.72 mm per 3-month interval (95% CI: 0.61-0.83; p < 0.001). Time effects remained significant after covariate adjustment. The mPA/AAo ratio also increased over time (p < 0.001 at all timepoints). No cases of probable pulmonary hypertension (mPA ≥ 33 mm) were identified at any assessment. Exploratory Cox regression showed no significant association between early mPA change and OS (HR 0.92; 95% CI: 0.70-1.19; p = 0.508). Progression-free survival could not be analyzed because the dataset lacked a progression variable. Sensitivity analyses consistently confirmed the robustness of the longitudinal mPA increase. Serial thoracic CT imaging demonstrated a statistically significant but small, progressive increase in mPA diameter during bevacizumab-based chemotherapy in this selected cohort. The change remained within the normal range, no patient crossed the threshold for probable pulmonary hypertension, and no association with OS was observed. In the absence of a non-bevacizumab comparator and of hemodynamic correlation, these changes cannot be attributed to bevacizumab; whether they carry clinical significance requires prospective validation with hemodynamic and echocardiographic correlation.
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9. Risk factors associated with febrile neutropenia in patients with esophageal cancer receiving 5-fluorouracil plus cisplatin combination chemoradiotherapy.
PMID:日期:2026-09-17To identify risk factors for febrile neutropenia (FN) in patients with esophageal cancer receiving the first cycle of definitive chemoradiotherapy with 5-fluorouracil plus cisplatin and concurrent radiotherapy (FP+R therapy). We conducted a retrospective single-center cohort study of patients who started FP+R at Oita University Hospital between April 2011 and June 2023. The primary outcome was FN onset in cycle 1. Univariate tests and multivariable logistic regression [forced entry: age, C-reactive protein (CRP), prognostic nutritional index (PNI), dysphagia] were used to evaluate association with FN development. Receiver operating characteristic (ROC) analysis was conducted to evaluate the predictive performance of baseline CRP for FN. Among 120 patients studied, grade ≥ 3 neutropenia occurred in 37 (30.8%) and FN in 14 (11.7%) during the first cycle. In multivariable analysis, higher baseline CRP was independently associated with increased FN risk [odds ratio (OR) 1.790; 95% confidence interval (CI) 1.120-2.850; p = 0.014], whereas dysphagia showed a non-significant association (OR 2.890; p = 0.145). Age and PNI were not independent predictors. ROC analysis for baseline CRP yielded area under the ROC curve of 0.699 (95% CI 0.520-0.877; p = 0.021) with optimal cut-off value of 0.68 mg/dL (sensitivity 61.54%; specificity 70.65%). Baseline systemic inflammation, indicated by elevated CRP, is an independent risk factor for FN development during FP+R therapy. Despite the regimen having an intermediate FN risk, patients with elevated pre-treatment CRP may need closer monitoring. This biomarker may help clinicians perform a more comprehensive risk assessment alongside conventional patient-specific factors.
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10. Modulating PI3K/Akt/mTOR-driven autophagy in liver cancer. The role of phytochemicals.
PMID:日期:2026-09-17Hepatocellular carcinoma is one of the major cancer related causes of mortality all over the world that is mainly caused by successive activation of PI3K/Akt/mTOR signalling axis and subsequent regulation of autophagy by the medium. This review analyses the molecular picture of PI3K/Akt/mTOR pathway in liver cancer, such as PTEN, receptor tyrosine kinase, Akt isoform, mTOR complex, GSK 3Β, CREB, FOXO protein, MDM2 p53 axis, NF kB, and lipid metabolic controller. The dual role of autophagy as a tumour suppressive and tumour promoting process is particularly focused on in regard to the therapeutic resistance to agents like sorafenib. The review summarizes preclinical evidence demonstrating that major classes of phytochemicals, including polyphenols, flavonoids, alkaloids, and terpenoids, target key regulatory components of the PI3K/Akt/mTOR mediated autophagy network. These substances regulate the ULK1 activation, AMPK signalling, reactive oxygen species processes and autophagy crosstalk to apoptosis, and hepatocellular carcinoma model metabolic remodelling. The in vitro and in vivo studies done using the mechanism of action reinforce the idea that phytochemicals are multi target regulators that can restore cytoprotective and cytotoxic autophagy. Finally, the existing challenges in translational research, such as pharmacokinetic issues, biomarker voids, tumour heterogeneity, and resistance, are critically evaluated to set priorities of introducing phytochemicals into the liver cancer treatment in a precision-based fashion.