Cancer Gene Therapy

Journal Information
ISSN / EISSN : 0929-1903 / 1476-5500
Current Publisher: Springer Science and Business Media LLC (10.1038)
Former Publisher:
Total articles ≅ 2,255
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Latest articles in this journal

, Benjamin G. Vincent, Alissa M. Weaver,
Cancer Gene Therapy pp 1-14; doi:10.1038/s41417-021-00345-1

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Wanchun Yang, Qiuyun Yuan, Shuxin Zhang, Mingrong Zuo, Tengfei Li, Junhong Li, Xingwang Zhou, Mao Li, Wentao Feng, Xiaoqiang Xia, et al.
Cancer Gene Therapy; doi:10.1038/s41417-021-00353-1

The publisher has not yet granted permission to display this abstract.
Evgeniya Denisova, Dana Westphal, , Friedegund Meier, , Julia Reifenberger, Arno Rütten, Alexander Schulz, Mildred Sergon, Mirjana Ziemer, et al.
Cancer Gene Therapy pp 1-12; doi:10.1038/s41417-021-00347-z

Malignant sweat gland tumours are rare, with the most common form being Eccrine porocarcinoma (EP). To investigate the mutational landscape of EP, we performed whole-exome sequencing (WES) on 14 formalin-fixed paraffin-embedded samples of matched primary EP and healthy surrounding tissue. Mutational profiling revealed a high overall median mutation rate. This was attributed to signatures of mutational processes related to ultraviolet (UV) exposure, APOBEC enzyme dysregulation, and defective homologous double-strand break repair. All of these processes cause genomic instability and are implicated in carcinogenesis. Recurrent driving somatic alterations were detected in the EP candidate drivers TP53, FAT2, CACNA1S, and KMT2D. The analyses also identified copy number alterations and recurrent gains and losses in several chromosomal regions including that containing BRCA2, as well as deleterious alterations in multiple HRR components. In accordance with this reduced or even a complete loss of BRCA2 protein expression was detected in 50% of the investigated EP tumours. Our results implicate crucial oncogenic driver pathways and suggest that defective homologous double-strand break repair and the p53 pathway are involved in EP aetiology. Targeting of the p53 axis and PARP inhibition, and/or immunotherapy may represent promising treatment strategies.
Feng Zeng, Mingkang Yao, Yun Wang, Wei Zheng, Shengshan Liu, Zeyu Hou, XiaoMing Cheng, Suhong Sun, Taolang Li, Hongyuan Zhao, et al.
Cancer Gene Therapy pp 1-13; doi:10.1038/s41417-021-00348-y

MicroRNAs (miRNA) have been shown to be associated with tumor diagnosis, prognosis, and therapeutic response. MiR-328-3p plays a significant role in breast cancer growth; however, its actual function and how it modulates specific biological functions is poorly understood. Here, miR-328-3p was significantly downregulated in breast cancer, especially in patients with metastasis. Mitochondrial carnitine palmitoyl transferase 1a (CPT1A) is a downstream target gene in the miR-328-3p-regulated pathway. Furthermore, the miR-328-3p/CPT1A/fatty acid β-oxidation/stemness axis was shown responsible for breast cancer metastasis. Collectively, this study revealed that miR-328-3p is a potential therapeutic target for the treatment of breast cancer patients with metastasis, and also a model for the miRNA-fatty acid β-oxidation-stemness axis, which may assist inunderstanding the cancer stem cell signaling functions of miRNA.
Yang Bai, Chenchen Ren, Baojin Wang, Jingge Xue, Feiyan Li, Jiaxi Liu, Li Yang
Cancer Gene Therapy pp 1-15; doi:10.1038/s41417-021-00306-8

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Yan Wang, Changkun Lin, Yang Liu
Published: 21 May 2021
Cancer Gene Therapy pp 1-13; doi:10.1038/s41417-021-00342-4

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Cong-Kai Luo, Pei-Hsuan Chou, Shang-Kok Ng, Wen-Yen Lin,
Cancer Gene Therapy pp 1-15; doi:10.1038/s41417-021-00346-0

The publisher has not yet granted permission to display this abstract.
Wenqiang Zhang, Ruiyu Liu, Lin Zhang, Chao Wang, Ziyan Dong, Jiasheng Feng, Mayao Luo, Yifan Zhang, Zhuofan Xu, Shidong Lv, et al.
Cancer Gene Therapy pp 1-12; doi:10.1038/s41417-021-00335-3

Clear cell renal cell carcinoma (ccRCC) is the most common type of renal cancer affecting many people worldwide. Although the 5-year survival rate is 65% in localized disease, after metastasis, the survival rate is <10%. Emerging evidence has shown that microRNAs (miRNAs) play a crucial regulatory role in the progression of ccRCC. Here, we show that miR-335, an anti-onco-miRNA, is downregulation in tumor tissue and inhibited ccRCC cell proliferation, invasion, and migration. Our studies further identify the H3K9me1/2 histone demethylase KDM3A as a new miR-335-regulated gene. We show that KDM3A is overexpressed in ccRCC, and its upregulation contributes to the carcinogenesis and metastasis of ccRCC. Moreover, with the overexpression of KDM3A, YAP1 was increased and identified as a direct downstream target of KDM3A. Enrichment of KDM3A demethylase on YAP1 promoter was confirmed by CHIP-qPCR and YAP1 was also found involved in the cell growth and metastasis inhibitory of miR-335. Together, our study establishes a new miR-335/KDM3A/YAP1 regulation axis, which provided new insight and potential targeting of the metastasized ccRCC.
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