Genetic variation and bone mineral density in long‐term adult survivors of childhood cancer

Hoed, Marissa A. H. den; Pluijm, Saskia M F; Stolk, Lisette; Uitterlinden, André G.; Pieters, Rob; Heuvel‐Eibrink, Marry M. van den

doi:10.1002/pbc.26198

Cited by 9 publications

(3 citation statements)

References 40 publications

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“…Evaluation of long-term childhood cancer survivors demonstrated that the GG genotype of rs in the ESR gene (encoding estrogen receptor-?) and the GG genotype of rs599083 in the LRP5 gene were associated with impairment of BMD (475). This study did not show an association with the MTHFR or MTRR polymorphisms.…”

Section: Pathophysiologycontrasting

confidence: 70%

Long-Term Endocrine and Metabolic Consequences of Cancer Treatment: A Systematic Review

Gebauer

Higham

Langer³

et al. 2018

Endocrine Reviews

118

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The number of patients surviving $5 years after initial cancer diagnosis has significantly increased during the last decades due to considerable improvements in the treatment of many cancer entities. A negative consequence of this is that the emergence of long-term sequelae and endocrine disorders account for a high proportion of these. These late effects can occur decades after cancer treatment and affect up to 50% of childhood cancer survivors. Multiple predisposing factors for endocrine late effects have been identified, including radiation, sex, and age at the time of diagnosis. A systematic literature search has been conducted using the PubMed database to offer a detailed overview of the spectrum of late endocrine disorders following oncological treatment. Most data are based on late effects of treatment in former childhood cancer patients for whom specific guidelines and recommendations already exist, whereas current knowledge concerning late effects in adult-onset cancer survivors is much less clear. Endocrine sequelae of cancer therapy include functional alterations in hypothalamic-pituitary, thyroid, parathyroid, adrenal, and gonadal regulation as well as bone and metabolic complications. Surgery, radiotherapy, chemotherapy, and immunotherapy all contribute to these sequelae. Following irradiation, endocrine organs such as the thyroid are also at risk for subsequent malignancies. Although diagnosis and management of functional and neoplastic long-term consequences of cancer therapy are comparable to other causes of endocrine disorders, cancer survivors need individually structured follow-up care in specialized surveillance centers to improve care for this rapidly growing group of patients.

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Section: Pathophysiologycontrasting

confidence: 70%

Long-Term Endocrine and Metabolic Consequences of Cancer Treatment: A Systematic Review

Gebauer

Higham

Langer³

et al. 2018

Endocrine Reviews

118

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“…Furthermore, in 2020, Im and collaborators performed genome-wide association studies of fracture risk after cancer diagnosis in patients from the Childhood Cancer Survivor Study (CCSS), identifying a genetic locus (HAGHL, 16p13.3) for fracture risk [ 6 ]. A few years earlier, it was demonstrated by multivariate analyses that CCS carrying SNPs in the ESR1 (estrogen receptor type 1) or LRP5 (low-density lipoprotein receptor) genes had an impairment in bone mass at an early adult age [ 62 ]. Given these considerations, developing genetic screening strategies could be useful to improve the prediction of bone fracture risk and prevent it in CCS.…”

Section: Physiopathology Of Osteoporosis In Ccs: General Risk Factorsmentioning

confidence: 99%

Osteoporosis in Childhood Cancer Survivors: Physiopathology, Prevention, Therapy and Future Perspectives

Tortora

Paoletta

Marrapodi

et al. 2022

Cancers

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The improvement of chemotherapy, radiotherapy, and surgical interventions, together with hematopoietic stem cell transplantation, increased childhood cancer survival rate in the last decades, reaching 80% in Europe. Nevertheless, anti-cancer treatments are mainly responsible for the onset of long-term side effects in childhood cancer survivors (CCS), including alterations of the endocrine system function and activity. In particular, the most frequent dysfunction in CCS is a metabolic bone disorder characterized by low bone mineral density (BMD) with increased skeletal fragility. BMD loss is also a consequence of a sedentary lifestyle, malnutrition, and cancer itself could affect BMD, thus inducing osteopenia and osteoporosis. In this paper, we provide an overview of possible causes of bone impairment in CCS in order to propose management strategies for early identification and treatment of skeletal fragility in this population.

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“…However, genetic and ethnic determinants of bone mineral density are well recognized, as are the importance of nutritional status and weight-bearing activity (50,51). Using a candidate SNP approach leveraging data from previous GWAS in healthy adult men and women, den Hoed et al (52) found that low bone mineral density was associated with exposure to radiation, in addition to SNPs in the genes encoding estrogen receptor type 1 (ESR1) and low-density lipoprotein receptor 5 (LRP5). However, two smaller studies that also adopted a candidate SNP approach were not able to uncover any statistically significant associations with these and other SNPs related to low bone mineral density (47,53), suggesting the need for further study.…”

Section: Reduced Bone Mineral Densitymentioning

confidence: 99%

Evidence for Genetic Risk Contributing to Long-Term Adverse Treatment Effects in Childhood Cancer Survivors

Gramatges

Bhatia

2018

Annu. Rev. Med.

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Survivors of childhood cancer are at increased risk for therapy-related morbidities and mortality. Although the demographic and clinical factors predicting the risk for long-term effects of cancer therapy are well known, the impact of genetic risk for specific late effects is less clearly defined. Here, we review the extant literature and recent research describing genetic modifiers to risk for the more common late effects of childhood cancer therapy. Results of this research support the need for clinical trials that attempt to further refine risk prediction by incorporating genetic testing into existing algorithms that are primarily based on clinical and demographic factors. Confirmation of genetic predisposition, as defined by reproducibility and prospective validation, would permit therapeutic modification and discussion of individualized survivor care plans even at initial cancer diagnosis.

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Genetic variation and bone mineral density in long‐term adult survivors of childhood cancer

Cited by 9 publications

References 40 publications

Long-Term Endocrine and Metabolic Consequences of Cancer Treatment: A Systematic Review

Long-Term Endocrine and Metabolic Consequences of Cancer Treatment: A Systematic Review

Osteoporosis in Childhood Cancer Survivors: Physiopathology, Prevention, Therapy and Future Perspectives

Evidence for Genetic Risk Contributing to Long-Term Adverse Treatment Effects in Childhood Cancer Survivors

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