Evidence map›Paper›PMID 38328478›Full record

ArticleJournal of the Endocrine Society2024

Humanin Treatment Protects Against Venetoclax-Induced Bone Growth Retardation in

Lilly Velentza, Malin Wickström, Per Kogner, Claes Ohlsson, Farasat Zaman, Lars Sävendahl

Abstract read
In one paragraph

Article in Journal of the Endocrine Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

6 authors.

Lilly VelentzaDivision of Pediatric Endocrinology, Department of Women's and Children's Health, Karolinska Institutet, 171 65 Stockholm, Sweden.ORCID https://orcid.org/0000-0003-3211-1664
Malin WickströmDivision of Pediatric Oncology and Surgery, Department of Women's and Children's Health, Karolinska Institutet, 171 65 Stockholm, Sweden.
Per KognerDivision of Pediatric Oncology and Surgery, Department of Women's and Children's Health, Karolinska Institutet, 171 65 Stockholm, Sweden.
Claes OhlssonCentre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, 413 45 Gothenburg, Sweden.ORCID https://orcid.org/0000-0002-9633-2805
Farasat ZamanDivision of Pediatric Endocrinology, Department of Women's and Children's Health, Karolinska Institutet, 171 65 Stockholm, Sweden.
Lars SävendahlDivision of Pediatric Endocrinology, Department of Women's and Children's Health, Karolinska Institutet, 171 65 Stockholm, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Context: Recent preclinical studies reported that the BCL-2 inhibitor venetoclax can impair bone growth. A strategy to prevent such a side effect of this promising anticancer drug is highly desired. Earlier Objective: We hypothesized that co-treatment with the humanin analog HNG may prevent venetoclax-induced bone growth impairment. Methods: Results: Venetoclax suppressed metatarsal bone growth and when combined with HNG, bone growth was rescued and all histological parameters affected by venetoclax monotherapy were normalized. Mechanistic studies showed that HNG downregulated the pro-apoptotic proteins Bax and p53 in cultured metatarsals and human growth plate tissues, respectively. The study in a neuroblastoma mouse model confirmed a growth-suppressive effect of venetoclax treatment. In this short-term

Indexed as

growthhumaninmetatarsalsneuroblastomavenetoclax

Identifiers

PMID38328478
PMCPMC10848303

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.