JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH实验与临床癌症研究杂志
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH(英文缩写 J EXP CLIN CANC RES),ISSN 0392-9078,eISSN 1756-9966,中文译名:实验与临床癌症研究杂志 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：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH 最新收录文献
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1. Correction: Galectin-3 induces pathogenic immunosuppressive macrophages through interaction with TREM2 in lung cancer.
1. 更正：Galectin-3通过与TREM2相互作用在肺癌中诱导致病性免疫抑制巨噬细胞PMID:日期:2026-10-01该文献暂无摘要。
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2. Retraction Note: Regulation of TRIM24 by miR-511 modulates cell proliferation in gastric cancer.
2. 撤稿声明：miR-511对TRIM24的调控可调节胃癌细胞增殖PMID:日期:2026-10-01该文献暂无摘要。
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3. Retraction Note: SULF2 overexpression positively regulates tumorigenicity of human prostate cancer cells.
3. 撤稿说明：SULF2过表达正向调控人前列腺癌细胞的致瘤性PMID:日期:2026-09-24该文献暂无摘要。
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4. Correction: B7-H3 CAR T cells eradicate intrahepatic cholangiocarcinoma and induce durable response.
4. 更正：B7-H3 CAR T细胞可清除肝内胆管癌并诱导持久缓解PMID:日期:2026-09-19该文献暂无摘要。
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5. Correction: Novel covalent CDK7 inhibitor potently induces apoptosis in acute myeloid leukemia and synergizes with Venetoclax.
5. 更正：新型共价CDK7抑制剂可有效诱导急性髓系白血病细胞凋亡并与Venetoclax产生协同作用PMID:日期:2026-09-18该文献暂无摘要。
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6. Targeting the DNA-repair chromatin-modifier protein SMYD3 as a novel epigenetics-based therapy for gastric cancer.
PMID:日期:2026-09-12SMYD3 is a histone methyltransferase implicated in cancer progression and is overexpressed in several malignancies, including gastric cancer (GC). Building on previous evidence linking SMYD3 to DNA damage repair, we investigated the molecular mechanisms through which SMYD3 regulates double-strand break (DSB) repair in GC and evaluated its therapeutic potential. In silico and in vitro analyses were performed to investigate the interactions between SMYD3 and key homologous recombination (HR) proteins, and to evaluate the ATM-mediated phosphorylation of SMYD3. Functional assays assessed the impact of pharmacological SMYD3 inhibition on HR and non-homologous end joining (NHEJ) repair pathways. Mechanistically, SMYD3 interacted with key HR factors and facilitated chromatin remodeling at damaged sites. ATM phosphorylated SMYD3 at threonine 22, a modification required for HR complex assembly and validated in GC patient samples following neoadjuvant chemotherapy. Inhibition of SMYD3 abolished HR and partially impaired NHEJ. Combined inhibition of SMYD3 and PARP induced synthetic lethality in GC cells, spheroids, and patient-derived organoids, and overcame resistance to olaparib. These findings reveal the ATM-dependent molecular mechanism by which SMYD3 regulates DNA DSB repair, further supporting SMYD3 as a promising therapeutic target for precision oncology strategies in GC.
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7. Correction: Supervillin promotes epithelialmesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38pathway.
7. 更正：Supervillin在缺氧条件下通过激活RhoA/ROCK-ERK/p38通路促进肝细胞癌的上皮-间质转化和转移PMID:日期:2026-09-05该文献暂无摘要。
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8. Correction: Curcumin derivative WZ35 inhibits tumor cell growth via ROS-YAP-JNK signaling.
8. 更正：姜黄素衍生物WZ35通过ROS-YAP-JNK信号抑制肿瘤细胞生长PMID:日期:2026-08-29该文献暂无摘要。
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9. Correction: Suppression of Spry1 reduces HIF1α‑dependent glycolysis and impairs angiogenesis in BRAF‑mutant cutaneous melanoma.
9. 更正：抑制Spry1可降低HIF1α依赖性糖酵解并损害BRAF突变型皮肤黑色素瘤的血管生成PMID:日期:2026-08-21该文献暂无摘要。