ArticleMedical molecular morphology2014
An association between nuclear morphology and immunohistochemical expression of p53 and p16INK4A in lung cancer cells.
Article in Medical molecular morphology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 10 citations in OpenAlex.
- p53 Regulates Nuclear Architecture to Reduce Carcinogen Sensitivity and Mutagenic Potential.bioRxiv : the preprint server for biology · 2025Article
- Subcellular Organelle Targeting as a Novel Approach to Combat Tumor Metastasis.Pharmaceutics · 2025Review
- Chondroitin sulfate proteoglycan 4 increases invasion of recessive dystrophic epidermolysis bullosa-associated cutaneous squamous cell carcinoma by modifying transforming growth factor-β signalling.The British journal of dermatology · 2024Article
- Article
- Review
- Nuclear Morphological Abnormalities in Cancer: A Search for Unifying Mechanisms.Results and problems in cell differentiation · 2022Article
- Sizing and shaping the nucleus: mechanisms and significance.Current opinion in cell biology · 2014Review
- Diagnostic Usefulness of p53 Immunostaining in Gastric Cancer and Dysplasia: A Real-world Clinical Experience.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear atypia is one of the most important morphological features used to diagnose malignant neoplasms. The potential molecular alteration that causes nuclear atypia remains unknown. P53 and p16INK4A play crucial roles in cell cycle checkpoints and repairing DNA damage to maintain integrity of the genome. Thus, inactivation of p53 and p16INK4A has been hypothesized to alter the chromatin structure and result in nuclear atypia. This study examined 201 primary lung cancers for the immunohistochemical expression of p53 and p16INK4A, and analyzed potential associations with the essential elements of nuclear atypia, such as nuclear size, circularity of the outline, and the density and granularity of chromatin. Tumors that expressed high levels of p53 had larger nuclei with higher chromatin density and distorted nuclear outlines. Tumors that expressed low levels of p16INK4 had larger nuclei with distorted nuclear outlines. Thus, alterations in p53 and p16INK4A may be the potential cause of nuclear atypia in neoplastic cells.
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.