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  • 1
    Online Resource
    Online Resource
    Metabolic factors affecting hepatocellular carcinoma in steatohepatitis
    Wiley ; 2019
    In:  Liver International Vol. 39, No. 3 ( 2019-03), p. 531-539
    Details
    In: Liver International, Wiley, Vol. 39, No. 3 ( 2019-03), p. 531-539
    Abstract: With the rising prevalence of alcoholism, obesity and metabolic syndrome, steatohepatitis will become the leading cause of end‐stage liver disease and hepatocellular carcinoma in the United States by 2025. Patients with non‐alcoholic steatohepatitis and alcoholic liver disease have similar clinical and histopathological presentations, whether these similarities persist in non‐alcoholic steatohepatitis and alcoholic liver disease patients with hepatocellular carcinoma remains unknown. Methods A retrospective analysis of the clinical features of adult patients from a large transplant center who underwent liver transplantation for steatohepatitis due to non‐alcoholic steatohepatitis and alcoholic causes (alcoholic liver disease) between 1/1/02 and 1/1/12 was performed. Clinical features, explant histopathology, and clinical outcomes were compared. Results Hepatocellular carcinoma was present in 80 of 317 patients, who underwent liver transplantation for steatohepatitis with equivalent distribution in non‐alcoholic steatohepatitis and alcoholic liver disease patients (24% vs 26%; P  = 0.8). On multivariate analysis, significant predictors of hepatocellular carcinoma included age, ethnicity (Hispanic), and diabetes, but not BMI, hypertension or smoking. A lower risk of hepatocellular carcinoma was associated with a clinical history of hyperlipidemia. Clinical parameters were similar between patients with alcoholic liver disease ‐ hepatocellular carcinoma and non‐alcoholic steatohepatitis‐hepatocellular carcinoma, except sex and presence of metabolic syndrome. non‐alcoholic steatohepatitis‐hepatocellular carcinoma livers retained histopathological features of non‐alcoholic steatohepatitis such as ballooning and Mallory bodies, while alcoholic liver disease‐hepatocellular carcinoma livers did not. There were no significant differences in hepatocellular carcinoma recurrence rates or post‐transplant overall survival. Conclusions We report the largest single‐center study evaluating clinical, histopathological and outcome measures of patients undergoing liver transplantation for steatohepatitis. Older patients, diabetics, and Hispanics may warrant more frequent cancer screening due to increased risk of hepatocellular carcinoma.
    Type of Medium: Online Resource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    URL: Article
    DOI: 10.1111/liv.2019.39.issue-3
    DOI: 10.1111/liv.14002
    Language: English
    Publisher: Wiley
    Publication Date: 2019
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  • 2
    Online Resource
    Online Resource
    Neoadjuvant immunotherapy in resectable non-small cell lung cancer at a checkpoint
    AME Publishing Company ; 2021
    In:  Translational Lung Cancer Research Vol. 10, No. 12 ( 2021-12), p. 4328-4335
    Details
    In: Translational Lung Cancer Research, AME Publishing Company, Vol. 10, No. 12 ( 2021-12), p. 4328-4335
    Type of Medium: Online Resource
    ISSN: 2218-6751 , 2226-4477
    URL: Journal
    URL: Article
    DOI: 10.21037/tlcr
    DOI: 10.21037/tlcr-21-830
    Language: Unknown
    Publisher: AME Publishing Company
    Publication Date: 2021
    detail.hit.zdb_id: 2754335-3
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  • 3
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    Abstract 4985: Notch1 as a key mediator in promoting advanced castration-resistant prostate cancer
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 4985-4985
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 4985-4985
    Abstract: The first line of treatment for men with advanced prostate cancers is androgen deprivation therapy. However, the disease commonly relapses in its lethal metastatic form referred to as castration-resistant prostate cancer (CRPC). CRPC is the primary cause of prostate cancer specific mortality in men. Current therapies including chemotherapeutic agents improve median overall survival by only few months. The mechanisms that distinguish clinically localized indolent tumors from lethal CRPC are unclear. Here we demonstrate that ectopic expression of Notch1 promotes progression to poorly differentiated carcinoma when combined with pathways that are altered in advanced disease but are insufficient to drive aggressive prostate cancer alone. Notch1 driven tumors are resistant to androgen deprivation. Transcriptional profiling reveals that these tumors display features of epithelial to mesenchymal transition, a morphological change associated with tumor aggressiveness and metastasis. Our study provides the first functional evidence that Notch1 signaling axis is a key mediator in promoting advanced prostate cancer and may represent a new therapeutic target for the advanced disease. Note: This abstract was not presented at the meeting. Citation Format: Tanya Stoyanova, Claire Faltermeier, Bryan Smith, Andrew Goldstein, Xi Zhang, Justin Drake, John Lee, Sandra Orellana, Steven Blum, Donghui Cheng, Kenneth Pienta, Jiaoti Huang, Owen Witte. Notch1 as a key mediator in promoting advanced castration-resistant prostate cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4985. doi:10.1158/1538-7445.AM2015-4985
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-4985
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
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    Abstract A64: Mechanistic insights into the misregulation of p27 in HER2-positive breast cancers
    American Association for Cancer Research (AACR) ; 2009
    In:  Molecular Cancer Therapeutics Vol. 8, No. 12_Supplement ( 2009-12-10), p. A64-A64
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 8, No. 12_Supplement ( 2009-12-10), p. A64-A64
    Abstract: Although it is often stated that low amounts of the cell cycle inhibitory protein p27 are predictive of a poor outcome in breast cancers, this is an oversimplifcation of the data. Typically, tumor cells exhibit decreased expression of p27 in the nucleus, while preserving or even increasing the pool of p27 in the cytoplasm. Whereas nuclear p27 is tumor suppressive by inhibiting cell proliferation, newer evidence suggests that cytoplasmic p27 has an oncogenic action: it interacts with the GTPase RhoA to promote cellular migration and motility. Thus, cytoplasmic p27 may be an indicator of tumor cell invasiveness and metastatic potential. Understanding the mechanism of p27 mislocalization in breast cancers may offer insight into pathways of oncogenic transformation, and provide new markers for predicting clinical responses to specific therapies. Toward this goal, we developed antibodies that reliably detect cytoplasmic p27, and also identified a subset of breast cancers positive for the growth factor receptor HER2 that exhibited increased amounts of cytoplasmic p27. In parallel experiments we discovered an E3 ubiquitin ligase, Trim62 that regulates p27 stability, and found that it is overexpressed in HER2+ breast cancers. siRNA knock down of Trim62 in HER2+ breast cancer cell lines not only induced cell cycle arrest but also caused p27 to relocate entirely to the nucleus. We compared knock down of Trim62 to that of the well-characterized p27 regulator, the F box protein Skp2. Unlike Trim62, Skp2 inhibition had no detectable effect on p27 in these cells. As pharmacological inhibition of HER2 has also been shown to increase nuclear p27 protein levels, we investigated the role of Trim62 in modulating the response of breast cancer cells to anti-HER2 therapeutics. Like Trim62 siRNA, the HER2/EGFR inhibitor, Lapatinib increased p27 amounts, and this increase in p27 was located exclusively in the nucleus. Furthermore, we showed that knockdown of Trim62 increased cellular sensitivity to Lapatinib. Overexpression of Trim62 had the opposite effect. Collectively, our results suggest Trim62 underlies the misregulation of p27 in HER2+ breast cancer cell lines. By modulating p27 expression and cellular localization, Trim62 may mediate the antiproliferative effect of HER2 antagonists in breast cancer cells. Moreover, Trim62 could be a potential biomarker to predict biological response of breast cancer cells to anti-HER2 therapeutics such as Lapatinib. Citation Information: Mol Cancer Ther 2009;8(12 Suppl):A64.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-09-A64
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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  • 5
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    Online Resource
    Activation of Notch1 synergizes with multiple pathways in promoting castration-resistant prostate cancer
    Proceedings of the National Academy of Sciences ; 2016
    In:  Proceedings of the National Academy of Sciences Vol. 113, No. 42 ( 2016-10-18)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 113, No. 42 ( 2016-10-18)
    Abstract: Metastatic castration-resistant prostate cancer (CRPC) is the primary cause of prostate cancer-specific mortality. Defining new mechanisms that can predict recurrence and drive lethal CRPC is critical. Here, we demonstrate that localized high-risk prostate cancer and metastatic CRPC, but not benign prostate tissues or low/intermediate-risk prostate cancer, express high levels of nuclear Notch homolog 1, translocation-associated (Notch1) receptor intracellular domain. Chronic activation of Notch1 synergizes with multiple oncogenic pathways altered in early disease to promote the development of prostate adenocarcinoma. These tumors display features of epithelial-to-mesenchymal transition, a cellular state associated with increased tumor aggressiveness. Consistent with its activation in clinical CRPC, tumors driven by Notch1 intracellular domain in combination with multiple pathways altered in prostate cancer are metastatic and resistant to androgen deprivation. Our study provides functional evidence that the Notch1 signaling axis synergizes with alternative pathways in promoting metastatic CRPC and may represent a new therapeutic target for advanced prostate cancer.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1614529113
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2016
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 6
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    Functional screen identifies kinases driving prostate cancer visceral and bone metastasis
    Proceedings of the National Academy of Sciences ; 2016
    In:  Proceedings of the National Academy of Sciences Vol. 113, No. 2 ( 2016-01-12)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 113, No. 2 ( 2016-01-12)
    Abstract: Mutationally activated kinases play an important role in the progression and metastasis of many cancers. Despite numerous oncogenic alterations implicated in metastatic prostate cancer, mutations of kinases are rare. Several lines of evidence suggest that nonmutated kinases and their pathways are involved in prostate cancer progression, but few kinases have been mechanistically linked to metastasis. Using a mass spectrometry-based phosphoproteomics dataset in concert with gene expression analysis, we selected over 100 kinases potentially implicated in human metastatic prostate cancer for functional evaluation. A primary in vivo screen based on overexpression of candidate kinases in murine prostate cells identified 20 wild-type kinases that promote metastasis. We queried these 20 kinases in a secondary in vivo screen using human prostate cells. Strikingly, all three RAF family members, MERTK, and NTRK2 drove the formation of bone and visceral metastasis confirmed by positron-emission tomography combined with computed tomography imaging and histology. Immunohistochemistry of tissue microarrays indicated that these kinases are highly expressed in human metastatic castration-resistant prostate cancer tissues. Our functional studies reveal the strong capability of select wild-type protein kinases to drive critical steps of the metastatic cascade, and implicate these kinases in possible therapeutic intervention.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1521674112
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2016
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 7
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    Online Resource
    EPID-10. EVOLVING SURVIVAL TRENDS IN INFANTS WITH BRAIN TUMORS: A LONGITUDINAL POPULATION BASED STUDY
    Oxford University Press (OUP) ; 2018
    In:  Neuro-Oncology Vol. 20, No. suppl_2 ( 2018-06-22), p. i82-i82
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 20, No. suppl_2 ( 2018-06-22), p. i82-i82
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noy059.243
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 2094060-9
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  • 8
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    Online Resource
    Abstract 5183: Identification and characterization of wild type kinases driving prostate cancer metastasis
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 5183-5183
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 5183-5183
    Abstract: Despite numerous oncogenic alterations implicated in metastatic prostate cancer, mutations or DNA amplifications of kinases are rare. We previously demonstrated that 1) expression of wild type (wt) Src in combination with the androgen receptor synergizes to produce aggressive prostate adenocarcinoma, 2) tyrosine phosphorylation increases with prostate cancer stage, and 3) the phosphoproteomic profile of metastatic prostate cancer is different from localized disease. However, the question still remains as to whether wt kinases can drive prostate cancer metastasis and should be regarded as therapeutic targets. To identify wt kinases driving prostate cancer metastasis, we performed phospho-tyrosine, threonine and serine peptide enrichment and quantitative mass spectrometry on metastatic prostate cancer tissues obtained at rapid autopsy. Analysis of this phosphoproteomic dataset combined with bioinformatic analyses of genomic datasets identified ∼140 kinases differentially expressed or activated in prostate cancer metastases. To determine which of these kinases function to promote prostate cancer metastasis, we developed an in vitro and in vivo metastasis screen. Out of 140 kinases, 20 kinases promote resistance to anoikis in vitro and metastatic colonization in vivo. Positive kinases include Src, Lyn, and EGFR which have been previously reported to be important in prostate cancer metastasis and thus provide strength to the validity of our screen. In addition we identified kinases with uncharacterized roles in prostate cancer metastasis and of particular interest, several of these kinases promote bone metastasis. We expect our findings will improve our understanding of the mechanistic role of kinase activation in prostate cancer and identify promising new therapeutic targets for metastatic disease. Citation Format: Claire Faltermeier, Justin Drake, Peter Clark, Bryan Smith, Colleen Mathis, Yang Zong, Carmen Volpe, Owen Witte. Identification and characterization of wild type kinases driving prostate cancer metastasis. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 5183. doi:10.1158/1538-7445.AM2015-5183
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-5183
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    A Surgical Perspective on Targeted Therapy of Hepatocellular Carcinoma
    MDPI AG ; 2015
    In:  Diseases Vol. 3, No. 4 ( 2015-09-29), p. 221-252
    Details
    In: Diseases, MDPI AG, Vol. 3, No. 4 ( 2015-09-29), p. 221-252
    Type of Medium: Online Resource
    ISSN: 2079-9721
    URL: Article
    DOI: 10.3390/diseases3040221
    Language: English
    Publisher: MDPI AG
    Publication Date: 2015
    detail.hit.zdb_id: 2720869-2
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  • 10
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    Phosphoproteome Integration Reveals Patient-Specific Networks in Prostate Cancer
    Elsevier BV ; 2016
    In:  Cell Vol. 166, No. 4 ( 2016-08), p. 1041-1054
    Details
    In: Cell, Elsevier BV, Vol. 166, No. 4 ( 2016-08), p. 1041-1054
    Type of Medium: Online Resource
    ISSN: 0092-8674
    URL: Article
    DOI: 10.1016/j.cell.2016.07.007
    RVK:
    XA 36269
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2016
    detail.hit.zdb_id: 187009-9
    detail.hit.zdb_id: 2001951-8
    SSG: 12
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