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People with Laron syndrome have also recently been shown to be of much less risk to develop cancer.
In 1966, he described the type of dwarfism later called Laron syndrome.
People with Laron syndrome have strikingly low rates of cancer and diabetes.
The principal feature of Laron syndrome is abnormally short stature (dwarfism).
People suffering from a rare condition known as Laron syndrome have a mutation in the gene that makes the receptor for growth hormone.
Laron syndrome is characterized by short stature and delayed bone age, as well as high levels of circulating growth hormone.
Recent publications have proposed that Homo floresiensis represented a population with widespread Laron syndrome.
Interestingly, Laron Syndrome patients experienced a lower incidence of cancer mortality and diabetes compared to their non-dwarf kin.
The essential role of IGF-1: Lessons from the long-term study and treatment of children and adults with Laron syndrome.
Normal serum levels of growth hormone Binding Protein 3 may rule out growth hormone insensitivities, like those seen in Laron syndrome.
Patients with Laron Syndrome possess one of three genotypes for the growth hormone receptor gene (GHR).
Since then, severe resistance to GH, characterized by grossly impaired growth despite normal levels of GH in serum, has been termed Laron syndrome.
In one of these studies, 99 individuals with Laron Syndrome (a rare form of Dwarfism) were monitored alongside their non-dwarf kin for a period of ten years.
Patients with Laron syndrome, with resultant deficient IGF, demonstrate varying degrees of alopecia and structural defects in hair follicles when examined microscopically.
The next year, a team including Laron himself published a paper arguing that the morphological features of H. floresiensis are essentially indistinguishable from those of Laron syndrome.
IGF-1 deficient humans, who are categorized as having Laron syndrome, or Laron's dwarfism, are treated with recombinant IGF-1.
Laron syndrome, or Laron-type dwarfism, is an autosomal recessive disorder characterized by an insensitivity to growth hormone (GH), caused by a variant of the growth hormone receptor.
Critics of the hypothesis have however pointed out that despite the low stature, people suffering from Laron syndrome look nothing like the Homo floresiensis remains, particularly in the anatomy of the cranial vault.
The well known Laron syndrome, or Laron-type dwarfism described by him in 1966, together with A. Pertzelan and S. Mannheimer, related to a growth hormone receptor mutation is named after him.
The team said that to determine whether the H. floresiensis individuals had Laron syndrome would require testing their DNA for the presence of the defective genes, if samples of that DNA ever become available.
The anatomist Gary D. Richards introduced a new skeptical hypothesis in June 2006: that the skeletons from Flores might be the remains of people who suffered from Laron syndrome, a genetic disorder first reported in 1966.
Associated abnormalities vary and may include facial dysmorphism, upslanting palpebral fissures, hypertelorism, cleft palate, genital anomalies, mild developmental delay, ureterocele, smooth muscle hamartoma, nevus lipomatosus, Laron syndrome (dwarfism with high growth hormone and low somatomedin activity), and other defects.
A second form of the disorder known as Laron syndrome type II (LTD2) shows typical clinical features of the Laron syndrome but is due to a defect in the biochemical processing of growth hormone after the hormone has been bound on the cell surface.