Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (6)
  • Open Access

    ARTICLE

    New insights into ATR inhibition in muscle invasive bladder cancer: The role of apolipoprotein B mRNA editing catalytic subunit 3B

    HYUNHO KIM1, UIJU CHO2, SOOK HEE HONG3, HYUNG SOON PARK1, IN-HO KIM3, HO JUNG AN1, BYOUNG YONG SHIM1, JIN HYOUNG KANG3,*

    Oncology Research, Vol.32, No.6, pp. 1021-1030, 2024, DOI:10.32604/or.2024.048919 - 23 May 2024

    Abstract Background: Apolipoprotein B mRNA editing catalytic polypeptide (APOBEC), an endogenous mutator, induces DNA damage and activates the ataxia telangiectasia and Rad3-related (ATR)-checkpoint kinase 1 (Chk1) pathway. Although cisplatin-based therapy is the mainstay for muscle-invasive bladder cancer (MIBC), it has a poor survival rate. Therefore, this study aimed to evaluate the efficacy of an ATR inhibitor combined with cisplatin in the treatment of APOBEC catalytic subunit 3B (APOBEC3B) expressing MIBC. Methods: Immunohistochemical staining was performed to analyze an association between APOBEC3B and ATR in patients with MIBC. The APOBEC3B expression in MIBC cell lines was assessed… More >

  • Open Access

    ARTICLE

    cGAS regulates the DNA damage response to maintain proliferative signaling in gastric cancer cells

    BIN LIU1,2,#, HAIPENG LIU3,#, FEIFEI REN1,2, HANGFAN LIU1, IHTISHAM BUKHARI1, YUMING FU4, WANQING WU4, MINGHAI ZHAO5, SHAOGONG ZHU6, HUI MO1, FAZHAN LI1,2, MICHAEL B. ZHENG7, YOUCAI TANG1,2, PENGYUAN ZHENG1,2,*, YANG MI1,2,*

    Oncology Research, Vol.29, No.2, pp. 87-103, 2021, DOI:10.32604/or.2022.03529 - 13 July 2022

    Abstract The activation of some oncogenes promote cancer cell proliferation and growth, facilitate cancer progression and metastasis by induce DNA replication stress, even genome instability. Activation of the cyclic GMP-AMP synthase (cGAS) mediates classical DNA sensing, is involved in genome instability, and is linked to various tumor development or therapy. However, the function of cGAS in gastric cancer remains elusive. In this study, the TCGA database and retrospective immunohistochemical analyses revealed substantially high cGAS expression in gastric cancer tissues and cell lines. By employing cGAS high-expression gastric cancer cell lines, including AGS and MKN45, ectopic silencing… More >

  • Open Access

    RETRACTION

    Retraction notice to “High Blood miR-802 Is Associated With Poor Prognosis in HCC Patients by Regulating DNA Damage Response 1 (REDD 1)-Mediated Function of T Cells” [Oncology Research 27(9) (2019) 1025-1034]

    Chao Jiang*, Xueyan Liu, Meng Wang*, Guoyue Lv*, Guangyi Wang*

    Oncology Research, Vol.28, No.7-8, pp. 833-833, 2020, DOI:10.3727/096504018X16233193839045

    Abstract This article has no abstract. More >

  • Open Access

    ARTICLE

    High Blood miR-802 Is Associated With Poor Prognosis in HCC Patients by Regulating DNA Damage Response 1 (REDD1)-Mediated Function of T Cells

    Chao Jiang*, Xueyan Liu, Meng Wang*, Guoyue Lv*, Guangyi Wang*

    Oncology Research, Vol.27, No.9, pp. 1025-1034, 2019, DOI:10.3727/096504018X15456687424096

    Abstract miR-802 has been reported to be dysregulated in multiple tumors and contribute to tumor progression. However, its role in HCC was still largely unknown. The aim of this study is to investigate the function and mechanism of miR-802 in HCC progression. The results showed that miR-802 was upregulated in the peripheral blood and tumor tissue of HCC patients, and high levels of blood miR-802 predicted poor prognosis. miR-802 had no effect on the proliferation and migration of HCC cell lines. Interestingly, the levels of CD8/CD28 and regulated in development and DNA damage response 1 (REDD1) More >

  • Open Access

    CORRECTION

    The Inhibitory Effects of HYDAMTIQ, a Novel PARP Inhibitor, on Growth in Human Tumor Cell Lines With Defective DNA Damage Response Pathways

    Enrico Mini*, Ida Landini*, Laura Lucarini, Andrea Lapucci*, Cristina Napoli, Gabriele Perrone*, Renato Tassi*, Emanuela Masini, Flavio Moroni, Stefania Nobili

    Oncology Research, Vol.26, No.2, pp. 333-334, 2018, DOI:10.3727/096504018X15187172557369

    Abstract The poly(ADP-ribose) polymerase (PARP) enzymes play a key role in the regulation of cellular processes (e.g., DNA damage repair, genomic stability). It has been shown that PARP inhibitors (PARPIs) are selectively cytotoxic against cells having dysfunctions in genes involved in DNA repair mechanisms (synthetic lethality). Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. The aim of this study was to evaluate the inhibitory effects of a novel PARPI, HYDAMTIQ, on growth in human tumor cell lines characterized by different features with regard… More >

  • Open Access

    ARTICLE

    The Inhibitory Effects of HYDAMTIQ, a Novel PARP Inhibitor, on Growth in Human Tumor Cell Lines With Defective DNA Damage Response Pathways

    Enrico Mini*, Ida Landini*, Laura Lucarini, Andrea Lapucci*, Cristina Napoli, Gabriele Perrone*, Renato Tassi*, Emanuela Masini, Flavio Moroni, Stefania Nobili

    Oncology Research, Vol.25, No.9, pp. 1441-1451, 2017, DOI:10.3727/096504017X14926854178616

    Abstract The poly(ADP-ribose) polymerase (PARP) enzymes play a key role in the regulation of cellular processes (e.g., DNA damage repair, genomic stability). It has been shown that PARP inhibitors (PARPIs) are selectively cytotoxic against cells having dysfunctions in genes involved in DNA repair mechanisms (synthetic lethality). Drug-induced PARP inhibition potentiates the activity of anticancer drugs such as 5-fluorouracil in enhancing DNA damage, whose repair involves PARP-1 activity. The aim of this study was to evaluate the inhibitory effects of a novel PARPI, HYDAMTIQ, on growth in human tumor cell lines characterized by different features with regard… More >

Displaying 1-10 on page 1 of 6. Per Page