Evidence map›Paper›PMID 41884741›Full record

ArticleIndian journal of dermatology

Genetic Insight into Gorlin-Goltz Syndrome.

M Madhu

Abstract read
In one paragraph

Article in Indian journal of dermatology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

M MadhuFrom the Department of Dermatology, SSIMS and RC, Davangere, Karnataka, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gorlin-Goltz syndrome, also called Basal cell nevus syndrome (BCNS), Nevoid basal cell carcinoma syndrome (NBCCS), or Basal nevus cell carcinoma syndrome (BNCCS) is a rare, inherited, autosomal dominant genodermatoses, with variable expression and complete penetrance, characterized by the occurrence of multiple basal cell carcinomas (BCCs) at a young age, palmoplantar pits, keratocystic odontogenic tumors, intracranial ectopic calcifications, facial dysmorphism, and ocular and skeletal anomalies. It occurs due to a defective hedgehog cell signaling pathway, caused by heterozygous germ-line mutations in either Patched 1 (PTCH1), Suppressor of fused (SUFU), Smoothened (SMO), or Patched 2 (PTCH2) genes, leading to tumorigenesis and various developmental anomalies. Because of variable phenotypic expression, the syndrome is difficult to diagnose and is often diagnosed late, increasing the risk of morbidity and rarely mortality in the patients. The gene mutated also determines the phenotypic expression of the syndrome. Detection of the gene mutated plays an important role in, antenatal diagnosis, confirming the diagnosis when in doubt clinically and predictive diagnosis in family members of the affected individuals, which helps us to diagnose the syndrome early, hence screen for various clinical manifestations at the appropriate age according to the gene that is mutated and initiate early treatment to reduce morbidity and mortality.

Indexed as

Basal cell carcinomasBasal cell nevus syndromefacial dysmorphismgenodermatosesGorlin-Goltz syndromekeratocystic odontogenic tumorsNevoid basal cell carcinoma syndromePalmo-plantar pitsSonic hedgehog cell signaling pathwaytumorigenesis

Identifiers

PMID41884741
PMCPMC13012755

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Registered trials

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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.