GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Comparison of the clinicopathologic features and prognosis of bilateral versus unilateral multifocal papillary thyroid cancer: An updated study with more than 2000 consecutive patients
    Wiley ; 2016
    In:  Cancer Vol. 122, No. 2 ( 2016-01-15), p. 198-206
    Details
    In: Cancer, Wiley, Vol. 122, No. 2 ( 2016-01-15), p. 198-206
    Abstract: This study provides initial evidence that bilateral papillary thyroid cancers (PTCs) are more aggressive than unilateral‐multifocal PTCs. The poorer outcome of patients with bilateral PTCs may be caused in part by their high incidence of lymph node metastasis.
    Type of Medium: Online Resource
    ISSN: 0008-543X , 1097-0142
    URL: Issue
    URL: Article
    DOI: 10.1002/cncr.v122.2
    DOI: 10.1002/cncr.29689
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 1479932-7
    detail.hit.zdb_id: 2599218-1
    detail.hit.zdb_id: 2594979-2
    detail.hit.zdb_id: 1429-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    BRAF inhibition promotes ER stress-mediated cell death in uveal melanoma
    AEPress, s.r.o. ; 2022
    In:  Neoplasma Vol. 69, No. 05 ( 2022), p. 1070-1078
    Details
    In: Neoplasma, AEPress, s.r.o., Vol. 69, No. 05 ( 2022), p. 1070-1078
    Type of Medium: Online Resource
    ISSN: 1338-4317
    URL: Article
    DOI: 10.4149/neo_2022_220428N462
    Language: Unknown
    Publisher: AEPress, s.r.o.
    Publication Date: 2022
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    FOXK2 promotes ovarian cancer stemness by regulating the unfolded protein response pathway
    American Society for Clinical Investigation ; 2022
    In:  Journal of Clinical Investigation Vol. 132, No. 10 ( 2022-5-16)
    Details
    In: Journal of Clinical Investigation, American Society for Clinical Investigation, Vol. 132, No. 10 ( 2022-5-16)
    Type of Medium: Online Resource
    ISSN: 1558-8238
    URL: Article
    URL: Article
    DOI: 10.1172/JCI151591
    DOI: 10.1172/JCI151591DS1
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 2022
    detail.hit.zdb_id: 2018375-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    IL-6 mediates platinum-induced enrichment of ovarian cancer stem cells
    American Society for Clinical Investigation ; 2018
    In:  JCI Insight Vol. 3, No. 23 ( 2018-12-6)
    Details
    In: JCI Insight, American Society for Clinical Investigation, Vol. 3, No. 23 ( 2018-12-6)
    Type of Medium: Online Resource
    ISSN: 2379-3708
    URL: Article
    URL: Article
    DOI: 10.1172/jci.insight.122360
    DOI: 10.1172/jci.insight.122360DS1
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 2018
    detail.hit.zdb_id: 2874757-4
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    The Ratio of Toxic-to-Nontoxic miRNAs Predicts Platinum Sensitivity in Ovarian Cancer
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Research Vol. 81, No. 15 ( 2021-08-01), p. 3985-4000
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 15 ( 2021-08-01), p. 3985-4000
    Abstract: Ovarian cancer remains one of the deadliest gynecologic malignancies affecting women, and development of resistance to platinum remains a major barrier to achieving a cure. Multiple mechanisms have been identified to confer platinum resistance. Numerous miRNAs have been linked to platinum sensitivity and resistance in ovarian cancer. miRNA activity occurs mainly when the guide strand of the miRNA, with its seed sequence at position 2–7/8, is loaded into the RNA-induced silencing complex (RISC) and targets complementary short seed matches in the 3′ untranslated region of mRNAs. Toxic 6mer seeds, which target genes critical for cancer cell survival, have been found in tumor-suppressive miRNAs. Many siRNAs and short hairpin RNAs (shRNA) can also kill cancer cells via toxic seeds, the most toxic of which carry G-rich 6mer seed sequences. We showed here that treatment of ovarian cancer cells with platinum led to increased RISC-bound miRNAs carrying toxic 6mer seeds and decreased miRNAs with nontoxic seeds. Platinum-tolerant cells did not exhibit this toxicity shift but retained sensitivity to cell death mediated by siRNAs carrying toxic 6mer seeds. Analysis of RISC-bound miRNAs in tumors from patients with ovarian cancer revealed that the ratio between miRNAs with toxic versus nontoxic seeds was predictive of treatment outcome. Application of the 6mer seed toxicity concept to cancer relevant miRNAs provides a new framework for understanding and predicting cancer therapy responses. Significance: These findings demonstrate that the balance of miRNAs that carry toxic and nontoxic 6mer seeds contributes to platinum resistance in ovarian cancer.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-21-0953
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    The Novel, Small-Molecule DNA Methylation Inhibitor SGI-110 as an Ovarian Cancer Chemosensitizer
    American Association for Cancer Research (AACR) ; 2014
    In:  Clinical Cancer Research Vol. 20, No. 24 ( 2014-12-15), p. 6504-6516
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 20, No. 24 ( 2014-12-15), p. 6504-6516
    Abstract: Purpose: To investigate SGI-110 as a “chemosensitizer” in ovarian cancer and to assess its effects on tumor suppressor genes (TSG) and chemoresponsiveness-associated genes silenced by DNA methylation in ovarian cancer. Experimental Design: Several ovarian cancer cell lines were used for in vitro and in vivo platinum resensitization studies. Changes in DNA methylation and expression levels of TSG and other cancer-related genes in response to SGI-110 were measured by pyrosequencing and RT-PCR. Results: We demonstrate in vitro that SGI-110 resensitized a range of platinum-resistant ovarian cancer cells to cisplatin (CDDP) and induced significant demethylation and reexpression of TSG, differentiation-associated genes, and putative drivers of ovarian cancer cisplatin resistance. In vivo, SGI-110 alone or in combination with CDDP was well tolerated and induced antitumor effects in ovarian cancer xenografts. Pyrosequencing analyses confirmed that SGI-110 caused both global (LINE1) and gene-specific hypomethylation in vivo, including TSGs (RASSF1A), proposed drivers of ovarian cancer cisplatin resistance (MLH1 and ZIC1), differentiation-associated genes (HOXA10 and HOXA11), and transcription factors (STAT5B). Furthermore, DNA damage induced by CDDP in ovarian cancer cells was increased by SGI-110, as measured by inductively coupled plasma-mass spectrometry analysis of DNA adduct formation and repair of cisplatin-induced DNA damage. Conclusions: These results strongly support further investigation of hypomethylating strategies in platinum-resistant ovarian cancer. Specifically, SGI-110 in combination with conventional and/or targeted therapeutics warrants further development in this setting. Clin Cancer Res; 20(24); 6504–16. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-14-1553
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Abstract 6063: FOXK2 promotes stemness in ovarian cancer by regulating unfolded protein response signaling
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 12_Supplement ( 2022-06-15), p. 6063-6063
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 12_Supplement ( 2022-06-15), p. 6063-6063
    Abstract: Introduction: Cancer stem cells (CSCs), a rare cell population within tumors that possesses self-renewal and tumor initiation capacity, have been implicated in cancer relapse and resistance to chemotherapy. In ovarian cancer (OC), CSCs are characterized by a high expression of aldehyde dehydrogenase (ALDH). Understanding the regulatory programs promoting stemness could identify new treatments. We identified FOXK2 as a key transcription factor (TF) that promotes stemness in OC. Methods: We generated FOXK2 knockdown OC models by stable transduction of shRNA targeting this TF and measured the population of ALDH+ CSCs, expression of stemness-associated genes, and in vivo tumor initiation capacities. Transcriptomic and ChIP-seq analyses were used to identify key FOXK2 targets. CRISPR-dCas9 genome editing was used to verify the regulatory function of FOXK2. Rescue experiments validated the roles of a newly discovered target gene of FOXK2. Results: Through gene expression analyses in CSCs vs. non-CSCs, we identified FOXK2 as a highly expressed stemness-specific TF in OC. Genetic depletion of FOXK2 diminished stemness features and reduced in vivo tumor initiation capacity. Through ChIP-sequencing we discovered that FOXK2 directly regulates IRE1α (ERN1 gene) expression, a key sensor for the unfolded protein response (UPR). ChIP-sequencing analysis further revealed that FOXK2 binds to an intronic regulatory element of ERN1. Blocking FOXK2 from binding to this enhancer by using a CRISPR/dCas9 diminished IRE1α transcription. At the molecular level, FOXK2-driven upregulation of IRE1α led to alternative XBP1 mRNA splicing and activation of stemness pathways, while genetic or pharmacological blockade of IRE1α inhibited CSCs in OC models. Conclusion: Our data establish a new function for FOXK2 as a key transcriptional regulator of CSCs and a mediator of the UPR, providing insight into potentially targetable new pathways in ovarian CSCs. Citation Format: Yaqi Zhang, Yinu Wang, Guangyuan Zhao, Edward J. Tanner, Mazhar Adli, Daniela E. Matei. FOXK2 promotes stemness in ovarian cancer by regulating unfolded protein response signaling [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 6063.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2022-6063
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Abstract 5359: M6A regulated NNMT mediates resistance to platinum in ovarian cancer
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 12_Supplement ( 2022-06-15), p. 5359-5359
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 12_Supplement ( 2022-06-15), p. 5359-5359
    Abstract: Background: Ovarian cancer (OC) remains one of the deadliest malignancies. Development of resistance to platinum (Pt) is a major clinical problem and understanding its underpinnings will help find new approaches to overcome it. Fat mass and obesity associated protein (FTO) is a N6-methyladenosine (m6A) demethylase and plays an important role regulating how the messenger RNA is processed translating into functional proteins. We recently showed that m6A modifications induced by FTO play a suppressive role in tumorigenicity and survival of OC stem cells. Here we hypothesized that RNA modifications caused by FTO regulate the response of OC cells to Pt. Methods: To study the mechanisms related to FTO implicated in response to Pt; we used OC cells in which FTO was knocked down (KD) via shRNA or overexpressed (OE). Additionally, Pt-resistant (Pt-R) OC cells were obtained through repeated (3-4) exposures to Pt. Cell viability assay determined the IC50 (half maximal inhibitory concentration) to Pt. Pt response in vivo was assessed in FTO expressing vs. FTO KD xenografts. Induction of DNA damage was assessed by immunofluorescence (IF) for γ-H2AX. Apoptosis was evaluated by Annexin V staining in the IncuCyte system. To identify potential targets of FTO-mediated m6A modifications in Pt induced response, RNA-seq and MeRIP-seq were integrated. Results: FTO was significantly downregulated in Pt-R vs. sensitive OC cells. Forced expression of FTO increased sensitivity to Pt in vitro and in vivo, while FTO KD increased Pt resistance (p & lt;0.05). A catalytic mutant FTO did not appreciably alter responsiveness to Pt. Increased γ-H2AX foci and increased apoptosis were observed after exposure to Pt in FTO OE vs. control cells. Through integrated RNA-seq and MeRIP-seq, we identified and validated several potential targets involved in response to Pt including IER5, IER5, ST3Gal, and the enzyme nicotinamide N-methyltransferase (NNMT). NNMT was upregulated and significantly hypomethylated in FTO OE cells and was downregulated in Pt resistant cells. Treatment with an NNMT inhibitor rescued the FTO induced sensitivity to Pt in OC cells demonstrating that its function is necessary in the response to Pt. Conclusions: We identified a new function of FTO-dependent m6A RNA modifications in regulating response to Pt through NNMT, a novel RNA methylated target. Activating FTO could improve response to Pt in OC. Citation Format: Hao Huang, Guangyuan Zhao, Andres Felipe Valdivia, Horacio Cardenas, Yinu Wang, Daniela Daniela Matei. M6A regulated NNMT mediates resistance to platinum in ovarian cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5359.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2022-5359
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Abstract A80: Targeting ovarian cancer stem cell by Dot1L inhibition
    American Association for Cancer Research (AACR) ; 2020
    In:  Clinical Cancer Research Vol. 26, No. 13_Supplement ( 2020-07-01), p. A80-A80
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 26, No. 13_Supplement ( 2020-07-01), p. A80-A80
    Abstract: Cancer stem cells (CSCs) are a specific population of cancer cells that are responsible for tumor initiation, chemoresistance, and metastasis. Previously, our lab has demonstrated ovarian cancer cells with high aldehyde dehydrogenase (ALDH) activities have multiple stem cell-like characteristics, including self-renewal, high clonogenicity, and chemoresistance. Here we identify that H3K79 methyltransferase DOT1L (disruptor of telomeric silencing-1-like) is a critical factor in self-renewal and tumor initiation capabilities of ovarian cancer stem cells (OCSCs). Firstly, we found that DOT1L have higher expression in ALDH(+)/CD133(+) OCSCs compared to double negative cells. Ovarian cancer cells with DOT1L-knockdown have reduced CSC fractions in flow cytometry analysis. Besides, knockdown of DOT1L expression impairs clonogenicity characteristics of CSCs, according to in vitro colony-forming assay and spheroid formation assay results. In order to effectively inhibit the enzymatic activity of DOT1L, we applied specific DOT1L inhibitor (DOT1Li) EPZ5676 to specifically target OCSCs and confirmed that the treatment of DOT1Li was able to block H3K79 methylation in ovarian cancer cells, and effectively represses the expression of stemness-associated transcriptional factors. Results from RNA-seq analysis and gene set enrichment assay have indicated that multiple stem-related pathways are repressed in DOT1Li-treated OCSCs. Furthermore, DOT1Li treatment not only shows inhibitory effects on colony forming in vitro but also delays tumor initiation in vivo compared to control treatment, which validates the effects of DOT1Li on CSCs inhibition. Based on our result, we infer that DOT1L is critical for self-renewal and tumor initiation abilities in ovarian cancer stem cells, and DOT1L inhibition by specific inhibitor provides a potential therapeutic strategy to target CSCs in ovarian cancer treatment. Citation Format: Yaqi Zhang, Yinu Wang, Guangyuan Zhao, Daniela Matei. Targeting ovarian cancer stem cell by Dot1L inhibition [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research; 2019 Sep 13-16, 2019; Atlanta, GA. Philadelphia (PA): AACR; Clin Cancer Res 2020;26(13_Suppl):Abstract nr A80.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1557-3265.OVCA19-A80
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    BRAF V600E-dependent role of autophagy in uveal melanoma
    Springer Science and Business Media LLC ; 2017
    In:  Journal of Cancer Research and Clinical Oncology Vol. 143, No. 3 ( 2017-3), p. 447-455
    Details
    In: Journal of Cancer Research and Clinical Oncology, Springer Science and Business Media LLC, Vol. 143, No. 3 ( 2017-3), p. 447-455
    Type of Medium: Online Resource
    ISSN: 0171-5216 , 1432-1335
    URL: Article
    DOI: 10.1007/s00432-016-2317-y
    RVK:
    XA 52301
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 1459285-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...