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Relevant bibliographies by topics / Notch1, Pin1, Breast Cancer, gamma-secretase

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Journal articles
Dissertations / Theses

Academic literature on the topic 'Notch1, Pin1, Breast Cancer, gamma-secretase'

Author: Grafiati

Published: 11 March 2023

Last updated: 31 July 2025

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Journal articles on the topic "Notch1, Pin1, Breast Cancer, gamma-secretase"

1

Broner, Esther Channah, Genia Alpert, Udi Gluschnaider, et al. "AL101 mediated tumor inhibition in notch-altered TNBC PDX models." Journal of Clinical Oncology 37, no. 15_suppl (2019): 1064. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.1064.

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1064 Background: The Notch pathway is activated during mammary gland development and has been implicated as a key driver in breast cancer. There is an urgent need to identify new therapeutic strategies for triple-negative breast cancer (TNBC), a sub-type associated with poor prognosis and no available targeted therapies. Notch gain of function (GOF) genetic alterations are potential tumor drivers found in ~10% of TNBC. This motivated the development of Notch inhibitors, including AL101 a pan-Notch, gamma secretase inhibitor (J Clin Oncol 36, 2018 abstract 2515). AL101 is currently being evalua

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2

Hossain, Fokhrul, Soroor Heidari, Yong Ran, et al. "Abstract P5-06-05: Targeting Triple-Negative Breast Cancer with a Novel Adeno-Associated Virus-mediated Therapy." Clinical Cancer Research 31, no. 12_Supplement (2025): P5–06–05—P5–06–05. https://doi.org/10.1158/1557-3265.sabcs24-p5-06-05.

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Abstract Triple-negative breast cancer (TNBC) is a group of aggressive breast cancers with a higher mortality rate. TNBC poses a major clinical challenge for several reasons: 1) molecular heterogeneity among patients, 2) intra-tumoral heterogeneity, 3) phenotypic plasticity, and 4) failure of the immune system to eliminate malignant clones. Unfortunately, there are very limited therapies for TNBC, making it a critical medical need to develop a targeted therapy. Notch signaling has emerged as an important factor in TNBC. There is strong evidence for the involvement of Notch signaling in TNBC. R

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3

Piya, Sujan, Seemana Bhattacharya, Hong Mu, et al. "Disruption of NOTCH1-MYC-CD44 Axis Targets Leukemia Initiating Cells (LIC) in T-ALL." Blood 132, Supplement 1 (2018): 890. http://dx.doi.org/10.1182/blood-2018-99-115692.

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Abstract Background: Persistence of leukemia initiating cells (LIC) in T acute lymphoblastic leukemia (T-ALL) results in relapse in 20- 25% of pediatric and over 50% of adult patients1. LIC are characterized by high CD44 expression and low reactive oxygen species (ROS) levels 2, 3. T-ALL LIC maintain low ROS by cystine/glutamate anti-porter complex of which CD44 is a key component 2, 4. CD44 also interacts with microenvironmental components; hyaluronic acid, osteopontin, fibronectin etc. NOTCH1 transcriptionally upregulates CD44/MYC by binding the upstream 'super-enhancer' sites. BRD4, a membe

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4

Hossain, Fokhrul, Claudia Sorrentino, Ayse Bilyeu, et al. "Non‐cannonical notch signaling pathways regulate breast cancer stem‐like cells function in triple negative breast cancer." FASEB Journal 31, S1 (2017). http://dx.doi.org/10.1096/fasebj.31.1_supplement.671.6.

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Triple negative breast cancer (TNBC) is a heterogeneous group of clinically aggressive form of breast cancers, characterized by lack of expression of estrogen receptor α (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2).TNBC patients have high risk of recurrence and metastasis, and current treatment options remain limited. Cancer stem‐like cells (CSCs) have been linked to cancer initiation, progression and chemotherapy resistance. Therefore CSC‐targeted therapies are keenly sought. There is strong evidence for the involvement of Notch signaling in TNBC. Notch

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5

Fournier, Morgane, Joaquim Javary, Vincent Roh, Nadine Fournier, and Freddy Radtke. "Reciprocal inhibition of NOTCH and SOX2 shapes tumor cell plasticity and therapeutic escape in triple-negative breast cancer." EMBO Molecular Medicine, October 30, 2024. http://dx.doi.org/10.1038/s44321-024-00161-8.

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AbstractCancer cell plasticity contributes significantly to the failure of chemo- and targeted therapies in triple-negative breast cancer (TNBC). Molecular mechanisms of therapy-induced tumor cell plasticity and associated resistance are largely unknown. Using a genome-wide CRISPR-Cas9 screen, we investigated escape mechanisms of NOTCH-driven TNBC treated with a gamma-secretase inhibitor (GSI) and identified SOX2 as a target of resistance to Notch inhibition. We describe a novel reciprocal inhibitory feedback mechanism between Notch signaling and SOX2. Specifically, Notch signaling inhibits SO

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Dissertations / Theses on the topic "Notch1, Pin1, Breast Cancer, gamma-secretase"

1

Tiberi, Luca. "Human notch1 and pin1 unveil a molecular circuitry involved in tumorigenesis." Doctoral thesis, Università degli studi di Trieste, 2008. http://hdl.handle.net/10077/2623.

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2006/2007<br>Cancers arise as somatic cells mutate and escape the control of cell cycle, survival or death. These processes are normally regulated by several signalling pathways and recently several studies highlight the potential importance of the Notch1 signaling pathway in human cancer. Notch activation has been involved in several mouse models of mammary carcinogenesis and recently also in human breast cancer. Importantly loss of Numb, a negative regulator of Notch1, has been observed in about 50% of breast carcinomas (Pece et al., 2004). Expression of Notch1 and Ras correlates in breast

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