Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer
A key step during onset of most cases of non-small cell lung cancer (NSCLC) is the loss of the tumor suppressor p16INK4a (best known as p16), commonly due to promoter hypermethylation. We recently reported a novel regulatory pathway involving E6-associated protein and cell division control protein 6...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2017-09-01
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| Series: | Molecular & Cellular Oncology |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/23723556.2017.1299273 |
| _version_ | 1797677165870841856 |
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| author | C. Gamell T. Gulati B. Solomon S. Haupt Y. Haupt |
| author_facet | C. Gamell T. Gulati B. Solomon S. Haupt Y. Haupt |
| author_sort | C. Gamell |
| collection | DOAJ |
| description | A key step during onset of most cases of non-small cell lung cancer (NSCLC) is the loss of the tumor suppressor p16INK4a (best known as p16), commonly due to promoter hypermethylation. We recently reported a novel regulatory pathway involving E6-associated protein and cell division control protein 6, which provides a methylation-independent mechanism for p16 silencing in patients with a particularly aggressive form of NSCLC. |
| first_indexed | 2024-03-11T22:41:07Z |
| format | Article |
| id | doaj.art-ba7b8c2aa8a949628cc75bc76a55cfea |
| institution | Directory Open Access Journal |
| issn | 2372-3556 |
| language | English |
| last_indexed | 2024-03-11T22:41:07Z |
| publishDate | 2017-09-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Molecular & Cellular Oncology |
| spelling | doaj.art-ba7b8c2aa8a949628cc75bc76a55cfea2023-09-22T09:10:58ZengTaylor & Francis GroupMolecular & Cellular Oncology2372-35562017-09-014510.1080/23723556.2017.12992731299273Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancerC. Gamell0T. Gulati1B. Solomon2S. Haupt3Y. Haupt4The University of MelbourneThe University of MelbourneThe University of MelbourneThe University of MelbourneThe University of MelbourneA key step during onset of most cases of non-small cell lung cancer (NSCLC) is the loss of the tumor suppressor p16INK4a (best known as p16), commonly due to promoter hypermethylation. We recently reported a novel regulatory pathway involving E6-associated protein and cell division control protein 6, which provides a methylation-independent mechanism for p16 silencing in patients with a particularly aggressive form of NSCLC.http://dx.doi.org/10.1080/23723556.2017.1299273cdc6e6apink4/arfnsclcp16tumor suppression |
| spellingShingle | C. Gamell T. Gulati B. Solomon S. Haupt Y. Haupt Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer Molecular & Cellular Oncology cdc6 e6ap ink4/arf nsclc p16 tumor suppression |
| title | Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer |
| title_full | Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer |
| title_fullStr | Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer |
| title_full_unstemmed | Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer |
| title_short | Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer |
| title_sort | uncovering a novel pathway for p16 silencing therapeutic implications for lung cancer |
| topic | cdc6 e6ap ink4/arf nsclc p16 tumor suppression |
| url | http://dx.doi.org/10.1080/23723556.2017.1299273 |
| work_keys_str_mv | AT cgamell uncoveringanovelpathwayforp16silencingtherapeuticimplicationsforlungcancer AT tgulati uncoveringanovelpathwayforp16silencingtherapeuticimplicationsforlungcancer AT bsolomon uncoveringanovelpathwayforp16silencingtherapeuticimplicationsforlungcancer AT shaupt uncoveringanovelpathwayforp16silencingtherapeuticimplicationsforlungcancer AT yhaupt uncoveringanovelpathwayforp16silencingtherapeuticimplicationsforlungcancer |