Disease relevance of Growth Disorders

• Thus, TGF-betaRII agonists and antagonists may provide useful therapeutic tools for human hair growth disorders based on premature or retarded catagen development (effluvium, alopecia, hirsutism) [1].
• A number of rare diseases (including Sotos syndrome) of unknown aetiology, which occur mainly sporadically and with features of growth disorder and developmental delay, may be caused by imprinted genes and therefore be associated with UPD [2].
• The growth disorders associated with homocystinuria, including arteriosclerosis and accelerated growth, are believed to result from increased conversion of methionine to homocysteine thiolactone and homocysteic acid [3].
• Bloom's syndrome (BS) is an autosomal recessive growth disorder associated with chromosomal breaks and rearrangements [4].
• CONCLUSION: Abnormal p53 expression in the epithelium of primary and recurrent pterygium specimens suggests that pterygium is a growth disorder rather than a degeneration [5].

High impact information on Growth Disorders

• Mulibrey nanism is a rare growth disorder of prenatal onset caused by mutations in the TRIM37 gene, which encodes a RING-B-box-coiled-coil protein [6].
• Finally, we consider human growth disorders that may involve defects in STAT5-dependent signal transduction [7].
• One of the most studied imprinted genes encodes insulin-like growth factor 2, and aberrant imprinting and DNA methylation of this gene is associated with the growth disorders Beckwith-Wiedemann and Silver-Russell syndromes and many human cancers [8].
• Owing to its location in 7p11.2-p12, GRB10 has been considered a candidate gene for the imprinted growth disorder, the Silver-Russell syndrome (SRS), but its predominantly biallelic expression argues against involvement in the syndrome [9].
• In addition, germline PTEN mutations are associated with several dominant growth disorders [10].

Chemical compound and disease context of Growth Disorders

• As a result, disorders of either growth hormone or sex steroid hormone production may result in clinical growth disorders during puberty [11].
• LPS-mediated lung injury in neonatal rats induced both gelatinase B overactivity and alveolar growth disorders, although no causal link between these two effects was demonstrated [12].
• Growth disorders and homocysteine metabolism [3].
• However, an alteration in the balance of other factors, such as platelet-derived growth factor and angiotensin (Ang) II, could contribute to the growth disorder [13].

Biological context of Growth Disorders

• Familial adenomatous polyposis (FAP) is a genetic disease created by an abnormality of chromosome number five resulting in a generalized cellular growth disorder [14].
• This includes several clinical situations, such as growth disorders, where serum IGFBP-3 is a highly specific screening tool for growth hormone deficiency, various malignancies in which serum IGFBP-2 levels are elevated, and disorders of carbohydrate metabolism that display an inverse relationship between serum IGFBP-1 and insulin secretion [15].

Anatomical context of Growth Disorders

• Thus, dysregulated Ihh/PTHrP feedback loop activity may be a key mechanism that underlies growth disorders in childhood thyroid disease [16].
• The evaluation of GHR on circulating B lymphocytes may prove to be a useful means of evaluating GH-GHR interactions in subjects with growth disorders [17].

Gene context of Growth Disorders

• A precise understanding of the actions of SOCS proteins in GH signalling may offer new opportunities for therapeutic intervention in growth disorders and other conditions involving GH action [18].
• This suggests that the growth disorders in this group of children might be due to a defect in a DNA region regulating expression of the GHR and IGF1 genes or genes involved in their regulation [19].
• Thus, TrkB agonists and antagonists deserve exploration as novel hair growth-modulatory drugs for the management of common hair growth disorders [20].
• Of the growth disorders that involve excessive growth, many could be attributable to overexpression of IGF2 [21].
• These findings strongly support TRPV1 as a significant novel player in human hair growth control, underscore the physiological importance of TRPV1 in human skin beyond nociception, and identify TRPV1 as a promising, novel target for pharmacological manipulations of epithelial growth disorders [22].

Analytical, diagnostic and therapeutic context of Growth Disorders

• This work investigated in rats whether passive immunization against the endogenous GHRF in the early postnatal period led to permanent alterations of somatotropic function, similar to those observed in several human growth disorders, e.g. constitutional growth delay (CGD) [23].
• In order to evaluate the potential use of IGF monitoring in children treated with GH, a cross-sectional study has been carried in 215 children and adolescents (134 with GH deficiency (GHD), 54 with Turner syndrome (TS) and 27 with non-GHD growth disorders) treated with GH for 0.2-13.7 years [24].

References