Search engine for discovering works of Art, research articles, and books related to Art and Culture
ShareThis
Javascript must be enabled to continue!

Abstract 4761: Investigation of the role of N-MYC in lung neuroendocrine carcinoma

View through CrossRef
Abstract Small cell lung cancer and large cell neuroendocrine carcinoma are classified as high-grade neuroendocrine tumors of the lung, representing extremely aggressive, life-threatening cancers with limited treatment options among various lung cancers. In these cancers, amplification of MYC family transcription factors: c-MYC, L-MYC and N-MYC is found to be mutually exclusive and overall account for ∼20%. In addition, recent studies have reported that L-MYC and c-MYC control lineage plasticity across molecular subtypes of small cell lung cancer defined by lineage-specific transcription factors such as ASCL-1 and NEUROD-1. Compared with L-MYC and c-MYC, the role of N-MYC, a lineage factor highly expressed in several tumors derived from neural cell lineages and a subset of neuroendocrine lung cancers, have not been described clearly. In this study, we aimed to investigate the role of N-MYC as a lineage-specific factors in neuroendocrine lung cancers. First, we investigated N-MYC binding profiles in N-MYC-high neuroendocrine lung cancer cell lines and found that genes related to neural cell differentiation were enriched in genes near N-MYC bound regions. Next, examination of genome-wide Myc-accessible regions in neuroendocrine lung cancer cell lines revealed that a fraction of peaks that overlapped between N-MYC- and c-MYC-classified cells, suggesting common functional binding of N-MYC and c-MYC. When we overexpressed N-MYC in L-MYC- or c-MYC-classified cells, expression profiles of the neuroendocrine lineage factors did not change, which was different from the previous findings on the relationships between L-MYC and c-MYC. Our findings suggest that N-MYC regulates distinct transcriptional program among the MYC family members although N-MYC and c-MYC share common binding profile. Citation Format: Hiroki Yamamoto, Takashi Sato, Yuri Yagami, Ryosuke Inoue, Hiromi Matsuo, Hideo Watanabe, Naoki Katsuhiko. Investigation of the role of N-MYC in lung neuroendocrine carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 4761.
Title: Abstract 4761: Investigation of the role of N-MYC in lung neuroendocrine carcinoma
Description:
Abstract Small cell lung cancer and large cell neuroendocrine carcinoma are classified as high-grade neuroendocrine tumors of the lung, representing extremely aggressive, life-threatening cancers with limited treatment options among various lung cancers.
In these cancers, amplification of MYC family transcription factors: c-MYC, L-MYC and N-MYC is found to be mutually exclusive and overall account for ∼20%.
In addition, recent studies have reported that L-MYC and c-MYC control lineage plasticity across molecular subtypes of small cell lung cancer defined by lineage-specific transcription factors such as ASCL-1 and NEUROD-1.
Compared with L-MYC and c-MYC, the role of N-MYC, a lineage factor highly expressed in several tumors derived from neural cell lineages and a subset of neuroendocrine lung cancers, have not been described clearly.
In this study, we aimed to investigate the role of N-MYC as a lineage-specific factors in neuroendocrine lung cancers.
First, we investigated N-MYC binding profiles in N-MYC-high neuroendocrine lung cancer cell lines and found that genes related to neural cell differentiation were enriched in genes near N-MYC bound regions.
Next, examination of genome-wide Myc-accessible regions in neuroendocrine lung cancer cell lines revealed that a fraction of peaks that overlapped between N-MYC- and c-MYC-classified cells, suggesting common functional binding of N-MYC and c-MYC.
When we overexpressed N-MYC in L-MYC- or c-MYC-classified cells, expression profiles of the neuroendocrine lineage factors did not change, which was different from the previous findings on the relationships between L-MYC and c-MYC.
Our findings suggest that N-MYC regulates distinct transcriptional program among the MYC family members although N-MYC and c-MYC share common binding profile.
Citation Format: Hiroki Yamamoto, Takashi Sato, Yuri Yagami, Ryosuke Inoue, Hiromi Matsuo, Hideo Watanabe, Naoki Katsuhiko.
Investigation of the role of N-MYC in lung neuroendocrine carcinoma [abstract].
In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA.
Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 4761.

Related Results

Complex Collision Tumors: A Systematic Review
Complex Collision Tumors: A Systematic Review
Abstract Introduction: A collision tumor consists of two distinct neoplastic components located within the same organ, separated by stromal tissue, without histological intermixing...
<i>MYC</i> rearrangement but not extra <i>MYC</i> copies is an independent prognostic factor in patients with mantle cell lymphoma
<i>MYC</i> rearrangement but not extra <i>MYC</i> copies is an independent prognostic factor in patients with mantle cell lymphoma
Mantle cell lymphoma (MCL) with MYC rearrangement (MYC-R) is rare and little is known about the importance of MYC extra copies (EC) in the absence of MYC-R in MCL patients. This st...
Improving immunotherapy in high-grade B-cell lymphoma
Improving immunotherapy in high-grade B-cell lymphoma
MYC is a transcription factor that upon deregulation acts as an oncogene. Cancer patients with MYC overexpression face significant worse outcomes to treatment with (immuno)chemothe...
Breast Carcinoma within Fibroadenoma: A Systematic Review
Breast Carcinoma within Fibroadenoma: A Systematic Review
Abstract Introduction Fibroadenoma is the most common benign breast lesion; however, it carries a potential risk of malignant transformation. This systematic review provides an ove...
Abstract 1457: NELFE regulates chromatin accessibility to affect MYC induced transcription
Abstract 1457: NELFE regulates chromatin accessibility to affect MYC induced transcription
Abstract Liver cancer incidence rates have more than tripled in the last 40 years and is projected to increase more than 40% in the next decade. Although progress ha...
Abstract 1872: Targeting MYC-driven medulloblastoma using inhibitors of glutamine metabolism.
Abstract 1872: Targeting MYC-driven medulloblastoma using inhibitors of glutamine metabolism.
Abstract Medulloblastoma is the most common malignant brain tumor in children. Currently, treatment consists of surgical resection, chemotherapy, and whole brain and...

Back to Top