ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016
Targeting MDM2 for Treatment of Adenoid Cystic Carcinoma.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- MDM2 Inhibition with Alrizomadlin (APG-115) in TP53 wild-type salivary gland cancers: a phase I clinical trial.Nature communications · 2026Trial
- Adenoid cystic carcinoma in an 86-year-old male patient: A rare case report.Radiology case reports · 2025Article
- Characterization of uniquely tumorigenic cancer stem cells in salivary gland adenoid cystic carcinoma.Frontiers in oral health · 2025Article
- Establishment and characterization of cMYB-expressing human salivary adenoid cystic carcinoma cell lines (UM-HACC-14, UM-HACC-6) and matching patient-derived xenograft model (UM-PDX-HACC-14).Oral surgery, oral medicine, oral pathology and oral radiology · 2024Article
- MDM2 Inhibitors for Cancer Therapy: The Past, Present, and Future.Pharmacological reviews · 2024Review
- Bmi-1: A master regulator of head and neck cancer stemness.Frontiers in oral health · 2023Review
- Improving Reporter Gene Assay Methodology for Evaluating the Ability of Compounds to Restore P53 Activity.International journal of molecular sciences · 2022Article
- p53 Inhibits Bmi-1-driven Self-Renewal and Defines Salivary Gland Cancer Stemness.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Systemic therapies for salivary gland adenoid cystic carcinoma.American journal of cancer research · 2021Review
- Transcriptome analyses identify hub genes and potential mechanisms in adenoid cystic carcinoma.Medicine · 2020Observational
- UM-HACC-2A: MYB-NFIB fusion-positive human adenoid cystic carcinoma cell line.Oral oncology · 2018Article
- p53 and Cell Fate: Sensitizing Head and Neck Cancer Stem Cells to Chemotherapy.Critical reviews in oncogenesis · 2018Review
- Radiosensitization of Adenoid Cystic Carcinoma with MDM2 Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Unlocking the chromatin of adenoid cystic carcinomas using HDAC inhibitors sensitize cancer stem cells to cisplatin and induces tumor senescence.Stem cell research · 2017Article
- Therapeutic Inhibition of the MDM2-p53 Interaction Prevents Recurrence of Adenoid Cystic Carcinomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
purposeThere are no effective treatment options for patients with advanced adenoid cystic carcinoma (ACC). Here, we evaluated the effect of a new small molecule inhibitor of the MDM2-p53 interaction (MI-773) in preclinical models of ACC. EXPERIMENTAL
designTo evaluate the anti-tumor effect of MI-773, we administered it to mice harboring three different patient-derived xenograft (PDX) models of ACC expressing functional p53. The effect of MI-773 on MDM2, p53, phospho-p53, and p21 was examined by Western blots in 5 low passage primary human ACC cell lines and in MI-773-treated PDX tumors.
resultsSingle-agent MI-773 caused tumor regression in the 3 PDX models of ACC studied here. For example, we observed a tumor growth inhibition index of 127% in UM-PDX-HACC-5 tumors that was associated with an increase in the fraction of apoptotic cells (P = 0.015). The number of p53-positive cells was increased in MI-773-treated PDX tumors (P < 0.001), with a correspondent shift in p53 localization from the nucleus to the cytoplasm. Western blots demonstrated that MI-773 potently induced expression of p53 and its downstream targets p21, MDM2, and induced phosphorylation of p53 (serine 392) in low passage primary human ACC cells. Notably, MI-773 induced a dose-dependent increase in the fraction of apoptotic ACC cells and in the fraction of cells in the G1 phase of cell cycle (P < 0.05).
conclusionsCollectively, these data demonstrate that therapeutic inhibition of the MDM2-p53 interaction with MI-773 activates downstream effectors of apoptosis and causes robust tumor regression in preclinical models of ACC. Clin Cancer Res; 22(14); 3550-9. ©2016 AACR.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.