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  1. Article ; Online: Development of the PARP inhibitor talazoparib for the treatment of advanced

    Hobbs, Evthokia A / Litton, Jennifer K / Yap, Timothy A

    Expert opinion on pharmacotherapy

    2021  Volume 22, Issue 14, Page(s) 1825–1837

    Abstract: Introduction: BRCA1: Areas covered: In this review, the authors highlight the relevant clinical trials of talazoparib, as well as, safety, tolerability, and quality of life considerations. They also examine putative response and resistance mechanisms, ...

    Abstract Introduction: BRCA1
    Areas covered: In this review, the authors highlight the relevant clinical trials of talazoparib, as well as, safety, tolerability, and quality of life considerations. They also examine putative response and resistance mechanisms, and rational combinatorial therapeutic strategies under development.
    Expert opinion: Talazoparib has been a major advance in the treatment of germline
    MeSH term(s) BRCA1 Protein/genetics ; BRCA2 Protein/genetics ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Female ; Germ-Line Mutation ; Humans ; Phthalazines ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use ; Quality of Life
    Chemical Substances BRCA1 Protein ; BRCA1 protein, human ; BRCA2 Protein ; BRCA2 protein, human ; Phthalazines ; Poly(ADP-ribose) Polymerase Inhibitors ; talazoparib (9QHX048FRV)
    Language English
    Publishing date 2021-07-26
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2001535-5
    ISSN 1744-7666 ; 1465-6566
    ISSN (online) 1744-7666
    ISSN 1465-6566
    DOI 10.1080/14656566.2021.1952181
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5130: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: Prognostic/predictive markers in systemic therapy resistance and metastasis in breast cancer.

    Hobbs, Evthokia A / Chen, Natalie / Kuriakose, Alphi / Bonefas, Elizabeth / Lim, Bora

    Therapeutic advances in medical oncology

    2022  Volume 14, Page(s) 17588359221112698

    Abstract: Breast cancer is a highly heterogeneous group of diseases posing a significant challenge in biomarker-driven research and the development of effective targeted therapies. Especially the treatment of metastatic breast cancer poses even more challenges, as ...

    Abstract Breast cancer is a highly heterogeneous group of diseases posing a significant challenge in biomarker-driven research and the development of effective targeted therapies. Especially the treatment of metastatic breast cancer poses even more challenges, as we still lose more than 42,000 women and men each year in the United States alone. New biological insight helps to improve breast cancer treatment through early detection, adaptation to chemotherapy resistance, and tailoring to find the right size of care. This review focuses on existing and new areas of predictive biomarkers under development to tailor the management of breast cancer and the application of integrative approaches that have resulted in the promising candidate biomarker discovery. Furthermore, we review new methods to detect metastatic progression using imaging, and blood-based assays. We hope to increase the attention and awareness of a new generation of therapeutic development strategies in metastatic breast cancer.
    Language English
    Publishing date 2022-07-16
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2503443-1
    ISSN 1758-8359 ; 1758-8340
    ISSN (online) 1758-8359
    ISSN 1758-8340
    DOI 10.1177/17588359221112698
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Real-World Evaluation of Disease Progression After CDK 4/6 Inhibitor Therapy in Patients With Hormone Receptor-Positive Metastatic Breast Cancer.

    West, Malinda T / Goodyear, Shaun M / Hobbs, Evthokia A / Kaempf, Andy / Kartika, Thomas / Ribkoff, Jessica / Chun, Brie / Mitri, Zahi I

    The oncologist

    2022  Volume 28, Issue 8, Page(s) 682–690

    Abstract: Background: Cyclin-dependent kinase 4/6 inhibitors (CDKi) have changed the landscape for treatment of patients with hormone receptor positive, human epidermal growth factor receptor 2-negative (HR+/HER-) metastatic breast cancer (MBC). However, next- ... ...

    Abstract Background: Cyclin-dependent kinase 4/6 inhibitors (CDKi) have changed the landscape for treatment of patients with hormone receptor positive, human epidermal growth factor receptor 2-negative (HR+/HER-) metastatic breast cancer (MBC). However, next-line treatment strategies after CDKi progression are not yet optimized. We report here the impact of clinical and genomic factors on post-CDKi outcomes in a single institution cohort of HR+/HER2- patients with MBC.
    Methods: We retrospectively reviewed the medical records of patients with HR+/HER2- MBC that received a CDKi between April 1, 2014 and December 1, 2019 at our institution. Data were summarized using descriptive statistics, the Kaplan-Meier method, and regression models.
    Results: We identified 140 patients with HR+/HER2- MBC that received a CDKi. Eighty percent of patients discontinued treatment due to disease progression, with a median progression-free survival (PFS) of 6.0 months (95% CI, 5.0-7.1), whereas those that discontinued CDKi for other reasons had a PFS of 11.3 months (95% CI, 4.6-19.4) (hazard ratio (HR) 2.53, 95% CI, 1.50-4.26 [P = .001]). The 6-month cumulative incidence of post-CDKi progression or death was 51% for the 112 patients who progressed on CDKi. Patients harboring PTEN mutations pre-CDKi treatment had poorer clinical outcomes compared to those with wild-type PTEN.
    Conclusion: This study highlights post-CDKi outcomes and the need for further molecular characterization and novel therapies to improve treatments for patients with HR+/HER2- MBC.
    MeSH term(s) Humans ; Female ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Receptor, ErbB-2/metabolism ; Retrospective Studies ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Protein Kinase Inhibitors/therapeutic use ; Disease Progression
    Chemical Substances Receptor, ErbB-2 (EC 2.7.10.1) ; Protein Kinase Inhibitors
    Language English
    Publishing date 2022-12-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1409038-7
    ISSN 1549-490X ; 1083-7159
    ISSN (online) 1549-490X
    ISSN 1083-7159
    DOI 10.1093/oncolo/oyad035
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4845: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 494: Show issues

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  4. Article: Impact of TP53 mutations in Triple Negative Breast Cancer.

    Mitri, Zahi I / Abuhadra, Nour / Goodyear, Shaun M / Hobbs, Evthokia A / Kaempf, Andy / Thompson, Alastair M / Moulder, Stacy L

    NPJ precision oncology

    2022  Volume 6, Issue 1, Page(s) 64

    Abstract: Identifying triple negative breast cancer (TNBC) patients expected to have poor outcomes provides an opportunity to enhance clinical management. We applied an Evolutionary Action Score to functionally characterize TP53 mutations (EAp53) in 96 TNBC ... ...

    Abstract Identifying triple negative breast cancer (TNBC) patients expected to have poor outcomes provides an opportunity to enhance clinical management. We applied an Evolutionary Action Score to functionally characterize TP53 mutations (EAp53) in 96 TNBC patients and observed that EAp53 stratification may identify TP53 mutations associated with worse outcomes. These findings merit further exploration in larger TNBC cohorts and in patients treated with neoadjuvant chemotherapy regimens.
    Language English
    Publishing date 2022-09-09
    Publishing country England
    Document type Journal Article
    ISSN 2397-768X
    ISSN 2397-768X
    DOI 10.1038/s41698-022-00303-6
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  5. Article ; Online: Nicotine does not enhance tumorigenesis in mutant K-ras-driven mouse models of lung cancer.

    Maier, Colleen R / Hollander, M Christine / Hobbs, Evthokia A / Dogan, Irem / Linnoila, R Ilona / Dennis, Phillip A

    Cancer prevention research (Philadelphia, Pa.)

    2011  Volume 4, Issue 11, Page(s) 1743–1751

    Abstract: Smoking is the leading cause of preventable cancer deaths in the United States. Nicotine replacement therapies (NRT) have been developed to aid in smoking cessation, which decreases lung cancer incidence. However, the safety of NRT is controversial ... ...

    Abstract Smoking is the leading cause of preventable cancer deaths in the United States. Nicotine replacement therapies (NRT) have been developed to aid in smoking cessation, which decreases lung cancer incidence. However, the safety of NRT is controversial because numerous preclinical studies have shown that nicotine enhances tumor cell growth in vitro and in vivo. We modeled NRT in mice to determine the effects of physiologic levels of nicotine on lung tumor formation, tumor growth, or metastasis. Nicotine administered in drinking water did not enhance lung tumorigenesis after treatment with the tobacco carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Tumors that develop in this model have mutations in K-ras, which is commonly observed in smoking-related, human lung adenocarcinomas. In a transgenic model of mutant K-ras-driven lung cancer, nicotine did not increase tumor number or size and did not affect overall survival. Likewise, in a syngeneic model using lung cancer cell lines derived from NNK-treated mice, oral nicotine did not enhance tumor growth or metastasis. These data show that nicotine does not enhance lung tumorigenesis when given to achieve levels comparable with those of NRT, suggesting that nicotine has a dose threshold, below which it has no appreciable effect. These studies are consistent with epidemiologic data showing that NRT does not enhance lung cancer risk in former smokers.
    MeSH term(s) Adenocarcinoma/drug therapy ; Adenocarcinoma/etiology ; Adenocarcinoma/pathology ; Animals ; Carcinogens/toxicity ; Cell Transformation, Neoplastic/pathology ; Cells, Cultured ; Disease Models, Animal ; Drinking Water ; Female ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/etiology ; Lung Neoplasms/pathology ; Male ; Mice ; Mice, Inbred A ; Mice, Inbred C57BL ; Mutation/genetics ; Nicotine/administration & dosage ; Nitrosamines/toxicity ; Proto-Oncogene Proteins p21(ras)/genetics
    Chemical Substances Carcinogens ; Drinking Water ; Nitrosamines ; Nicotine (6M3C89ZY6R) ; 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (7S395EDO61) ; Hras protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2011-10-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2434717-6
    ISSN 1940-6215 ; 1940-6207
    ISSN (online) 1940-6215
    ISSN 1940-6207
    DOI 10.1158/1940-6207.CAPR-11-0365
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6766: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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