Premature physeal closure following 13‐<i>cis</i>‐retinoic acid and prolonged fenretinide administration in neuroblastoma

Steineck, Angela; MacKenzie, J. D.; Twist, Clare J.

doi:10.1002/pbc.26124

Cited by 17 publications

(13 citation statements)

References 18 publications

(24 reference statements)

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“…Excessive RA, such as in pharmacologic treatment with retinoids, can result in skeletal abnormalities as well. 27 …”

Section: Retinoic Acid Signallingmentioning

confidence: 99%

The growth plate: a physiologic overview

Ağırdil

2020

EFORT Open Reviews

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The growth plate is the cartilaginous portion of long bones where the longitudinal growth of the bone takes place. Its structure comprises chondrocytes suspended in a collagen matrix that go through several stages of maturation until they finally die, and are replaced by osteoblasts, osteoclasts, and lamellar bone. The process of endochondral ossification is coordinated by chondrocytes and a variety of humoral factors including growth hormone, parathyroid hormone, oestrogen, growth factors, cytokines, and various signalling pathways. Chondrocytes progress from a resting state to enter the phases of proliferation and hypertrophy. Under the influence of oestrogen, the proliferation of chondrocytes decreases as the resting chondrocytes are consumed. During the terminal phase of differentiation, cartilage is replaced by blood vessels and organized bone tissue, and once chondrocytes have died, the longitudinal growth of the bone ceases and the growth plate closes. The highly complex regulatory signals involved in this process are genetically determined, and genetic perturbations in any of the associated genes can result in abnormalities of bone growth. Hundreds of chondrodysplasias have been described, pointing to the complexity of the humoral control systems involved in endochondral ossification. While our knowledge of the mechanisms behind the various bone growth control systems is improving, a deeper understanding of the underlying processes could aid clinicians to better understand bone health and bone growth abnormalities. This review describes the current clinical research into the physiology of the growth plate. Cite this article: EFORT Open Rev 2020;5:498-507. DOI: 10.1302/2058-5241.5.190088

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“…Excessive RA, such as in pharmacologic treatment with retinoids, can result in skeletal abnormalities as well. 27 …”

Section: Retinoic Acid Signallingmentioning

confidence: 99%

The growth plate: a physiologic overview

Ağırdil

2020

EFORT Open Reviews

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“…Consensus recommendations are listed in Table 6. 74,75 and fibrodysplasia ossificans progressiva 76 as well as from animal models. 65 Many observational studies during treatment, as well as prospective studies, have substantiated the role of systemic retinoids in accelerating the development of DISH-like hyperostotic changes involving the tendon and ligaments of the spine and peripheral joints (osteophytes, tendon and ligament calcification, and hyperostosis).…”

Section: II Bmentioning

confidence: 99%

Perspective and Consensus Opinion: Good Practices for Using Organotypic Skin and Epidermal Equivalents in Experimental Dermatology Research

Bogaard

Ilić

Dubrac

et al. 2021

Journal of Investigative Dermatology

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“…Additional studies with larger cohorts may be better able to resolve the etiology of the thoracic growth deficiency, as it may be caused by direct influences (eg, thoracic or spinal radiation) or indirect influences (eg, neurohormonal imbalance). It should be noted that while some treatment modalities that historically contributed to thoracic growth deficiency may be omitted in contemporary treatment regimens (eg, craniospinal irradiation in the treatment of ALL), other therapeutic agents are only now being found to have significant skeletal toxicity (eg, cis‐retinoic acid), which could propagate thoracic growth deficiency in future childhood cancer survivors.…”

Section: Discussionmentioning

confidence: 99%

Thoracic growth deficiency in childhood cancer survivors may cause overestimation of lung disease

Dean

McDonough

Josephson

et al. 2019

Pediatric Pulmonology

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Introduction Survivors of childhood cancers undergo routine pulmonary function testing as they are at an increased lifetime risk for significant lung disease. However, this population also demonstrates growth abnormalities that could influence the interpretation of these tests, as reference equations are based on standing height. We aim to determine the impact of the relative thoracic growth deficiency in childhood cancer survivors on the interpretation of pulmonary function testing. Methods Standing height and upper segment length (USL) in childhood cancer survivors undergoing pulmonary function testing at a single academic center were compared to age‐matched historical standards. Additionally, pulmonary function tests were compared to reference values generated from standing height and doubled USL. Results Data were obtained from 107 cancer survivors. While the subjects demonstrated an overall 6.8% lower standing height vs historical standards, they also demonstrated relative thoracic growth abnormality with a further 9.9% decrement in the ratio USL to standing height. The use of doubled upper segment length as a surrogate measure for standing height in pulmonary function reference equations decreased the number of patients with restrictive lung disease as indicated by spirometry. Conclusions Childhood cancer survivors have disproportionately worse thoracic growth deficiency vs appendicular growth deficiency. As a result, their USL is disproportionately short for their standing height, which is most commonly used in pulmonary function testing reference equations. This leads to an increased likelihood in these patients meeting pulmonary function test criteria for restrictive lung disease.

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Premature physeal closure following 13‐cis‐retinoic acid and prolonged fenretinide administration in neuroblastoma

Cited by 17 publications

References 18 publications

The growth plate: a physiologic overview

The growth plate: a physiologic overview

Perspective and Consensus Opinion: Good Practices for Using Organotypic Skin and Epidermal Equivalents in Experimental Dermatology Research

Thoracic growth deficiency in childhood cancer survivors may cause overestimation of lung disease

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