MYC, MYCL, and MYCN as therapeutic targets in lung cancer

Massó-Vallés, Daniel; Beaulieu, Marie-Ève; Soucek, Laura

doi:10.1080/14728222.2020.1723548

Cited by 80 publications

(65 citation statements)

References 139 publications

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“…55 It has also been hypothesized that MYC amplification appears during tumor progression and is connected to CHT resistance. 54,56 Aurora kinase A and B (AURKA and AURKB) are serine/threonine kinases and have a main function in the regulation of mitosis. 57 The overexpression of AURKA promotes cell proliferation.…”

Section: Molecular Subtypesmentioning

confidence: 99%

Molecular profiles of small cell lung cancer subtypes: Therapeutic implications

Schwendenwein

Megyesfalvi

Bárány

et al. 2021

Molecular Therapy - Oncolytics

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Section: Molecular Subtypesmentioning

confidence: 99%

Molecular profiles of small cell lung cancer subtypes: Therapeutic implications

Schwendenwein

Megyesfalvi

Bárány

et al. 2021

Molecular Therapy - Oncolytics

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“…It is also often translocated to one of the immunoglobulin loci in multiple myeloma, Burkitt's lymphoma and diffuse large cell lymphoma, or to T-cell receptor loci in T-cell acute lymphoblastic leukemia [29]. Finally, upstream oncogenic signaling from the Notch, Wnt, TGF-β, Hedgehog, EGFR, ALK, and Hippo pathways also drive aberrant expression of Myc in lung and many other cancers [17,30]. Therefore, even when Myc is not the driver oncogenic lesion, it acts as an integrator of extracellular and intracellular oncogenic signals, an attribute that makes it a 'most wanted' target for the treatment of cancer [31].…”

Section: Myc In Cancermentioning

confidence: 99%

“…In physiological conditions in adult tissues, Myc proteins are not present in quiescent cells but are rapidly induced in response to growth factor stimuli [1]. This switch is tightly regulated at the transcriptional and post-transcriptional level, and both Myc mRNA and protein display a very short half-life [17]. Also, Myc transcription is controlled by multiple extracellular and intracellular signals that funnel through an array of transcription factors, chromatin modifiers and regulatory RNAs that are either recruited to or synthesized at the Myc locus [18].…”

mentioning

confidence: 99%

Blocking Myc to Treat Cancer: Reflecting on Two Decades of Omomyc

Massó-Vallés

Soucek

2020

Cells

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109

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First designed and published in 1998 as a laboratory tool to study Myc perturbation, Omomyc has come a long way in the past 22 years. This dominant negative has contributed to our understanding of Myc biology when expressed, first, in normal and cancer cells, and later in genetically-engineered mice, and has shown remarkable anti-cancer properties in a wide range of tumor types. The recently described therapeutic effect of purified Omomyc mini-protein-following the surprising discovery of its cell-penetrating capacity-constitutes a paradigm shift. Now, much more than a proof of concept, the most characterized Myc inhibitor to date is advancing in its drug development pipeline, pushing Myc inhibition into the clinic.

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“…EGFR and ALK are two of the multitude of currently identified and targetable oncogenic drivers in NSCLC. As a reminder, in lung adenocarcinoma, targetable alterations comprise roughly half of all diseases, and the list of actionable therapeutic targets is constantly growing [ 32 ].…”

Section: Others Oncogenic Driversmentioning

confidence: 99%

Targeted Therapies in Early Stage NSCLC: Hype or Hope?

Friedlaender

Addeo

Russo

et al. 2020

IJMS

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Non-small-cell lung cancer (NSCLC) represents roughly 85% of lung cancers, with an incidence that increases yearly across the world. The introduction in clinical practice of several new and more effective molecules has led to a consistent improvement in survival and quality of life in locally advanced and metastatic NSCLC. In particular, oncogenic drivers have indeed transformed the therapeutic algorithm for NSCLC. Nearly 25% of patients are diagnosed in an early stage when NSCLC is still amenable to radical surgery. In spite of this, five-year survival rates for fully resected early stage remains rather disappointing. Adjuvant chemotherapy has shown a modest survival benefit depending on the stage, but more than half of patients relapse. Given this need for improvement, over the last years different targeted therapies have been evaluated in early-stage NSCLC with no survival benefit in unselected patients. However, the identification of reliable predictive biomarkers to these agents in the metastatic setting, the design of molecularly-oriented studies, and the availability of novel potent and less toxic agents opened the way for a novel era in early stage NSCLC treatment. In this review, we will discuss the current landscape of targeted therapeutic options in early NSCLC.

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MYC, MYCL, and MYCN as therapeutic targets in lung cancer

Cited by 80 publications

References 139 publications

Molecular profiles of small cell lung cancer subtypes: Therapeutic implications

Molecular profiles of small cell lung cancer subtypes: Therapeutic implications

Blocking Myc to Treat Cancer: Reflecting on Two Decades of Omomyc

Targeted Therapies in Early Stage NSCLC: Hype or Hope?

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