Evidence map›Paper›PMID 31853800›Full record

ArticleMolecular and cellular biochemistry2020

Substance P receptor blocker, aprepitant, inhibited cutaneous and other neurogenic inflammation side effects of the EGFR1-TKI, erlotinib.

Joanna J Chmielinska, Jay H Kramer, I-Tong Mak, Christopher F Spurney, William B Weglicki

Abstract read
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Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 22% of its field
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

9 citing papers in PubMed, 16 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Joanna J ChmielinskaDepartment of Biochemistry and Molecular Medicine, The George Washington University School of Medicine and Health Sciences, 439A Ross Hall, 2300 I St., N.W., Washington, DC, 20037, USA. phyjch@gwu.edu.ORCID http://orcid.org/0000-0002-5057-8797
Jay H KramerDepartment of Biochemistry and Molecular Medicine, The George Washington University School of Medicine and Health Sciences, 442 Ross Hall, 2300 I St., N.W., Washington, DC, 20037, USA. phyjhk@gwu.edu.
I-Tong MakDepartment of Biochemistry and Molecular Medicine, The George Washington University School of Medicine and Health Sciences, 441 Ross Hall, 2300 I St., N.W., Washington, DC, 20037, USA. itmak@gwu.edu.
Christopher F SpurneyDepartment of Pediatrics, The Children's National Medical Center, Washington, DC, 20010, USA.
William B WeglickiDepartment of Biochemistry and Molecular Medicine, The George Washington University School of Medicine and Health Sciences, Washington, DC, 20037, USA.
George Washington University · USChildren's National · US

Funding

GWU George Washington University McCormick Genomic & Proteomic Center 2018Hoth Biopharmaceutical Inc, Nevada, USA. Contract
6 · The paper itself

Abstract

Cutaneous changes like rash and hair loss, as well as other neurogenic inflammation side effects, occur frequently during anticancer treatment with the epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI), erlotinib. These adverse events may be so severe that they impair the patient's compliance with the treatment or even cause its discontinuation. In the current preclinical study, rats (9.2 weeks) were treated with erlotinib (10 mg/kg/day) ± aprepitant (2 mg/kg/day) for 12 weeks. Visual changes in the development of facial skin lesions/hair loss and SP-receptor expression (immunohistochemically) in facial skin tissue were assessed; also changes in plasma magnesium, 8-isoprostane, substance P (SP), neutrophil superoxide production, and cardiac function (echocardiography) were measured. Erlotinib lowered plasma magnesium 14%, elevated SP 65%, caused 3.7-fold higher basal superoxide production, 2.5-fold higher 8-isoprostane levels, 11.6% lower cardiac systolic, and 10.9% lower diastolic function. Facial dermatological changes (alopecia, skin reddening, scabbing, nose crusting) occurred by 4 weeks (± + to ++) in erlotinib-treated rats, and progressively worsened (±++ to +++) by week 12. Facial skin SP-receptor upregulation (78% higher) occurred in epidermal and hair follicle cells. All adverse effects were substantially and significantly mitigated by aprepitant, including a 62% lowering of skin SP-receptors (p < 0.05). Elevated SP levels mediated the side effects of erlotinib treatment, but aprepitant's significant prevention of the systemic and cutaneous adverse events indicates a novel potential therapy against the side effects of this anticancer treatment.

Indexed as

Drug EruptionsNervous System DiseasesAnimalsAprepitantErlotinib HydrochlorideMaleNeurokinin-1 Receptor AntagonistsRatsRats, Sprague-DawleyAprepitantErlotinib HydrochlorideNeurokinin-1 Receptor AntagonistsCardiac dysfunctionCirculating substance PEGFR tyrosine kinase inhibitor erlotinibHypomagnesemiaNeutrophil activationSkin substance P receptors, progressive skin rash/hair lossSubstance P receptor blocker, aprepitantTotal plasma 8-isoprostane

Identifiers

PMID31853800
OpenAlexW2996208952

What OpenQuestion holds

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Read underepoch 390

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.