hypopigmentation/tyrosine

This study presents laboratory methods for the quantification of hypopigmentation activity in vitro. Melanin, the major pigment in melanocytes, is synthesized in response to multiple cellular and environmental factors. Melanin protects skin cells from ultraviolet damage, but also has biophysical and

Dasatinib is an oral second-generation multitarget tyrosine-kinase inhibitor (TKI) that is efficacious in treating imatinib-resistant chronic myeloid leukemia (CML) or intolerant cases. Noncutaneous adverse effects with dasatinib are well known in the literature, most commonly cytopenias and fluid

Halogenated dipeptides, 3, 5-di-I-tyrosylalanine (DIYA), have been identified as novel disinfection byproducts (DBPs), following chloramination of authentic water. However, little is known about their toxicity. Zebrafish embryos were used to assess the toxicity of novel iodinated DBPs (I-DBPs).

In our laboratory, a single autosomal recessive mutation in a phenotype similar to ruby-eye (ru/Hps6(ru)) or ruby-eye 2 (ru2/Hps5(ru2)) spontaneously occurred in siblings of C57BL/10JHir (+/+, black) mice in 2006. RT-PCR analysis revealed that this novel mutation, named ru2(d)/Hps5(ru2-d), exhibited

In order to determine the frequency and characterization of hypopigmentation in Prader-Labhart-Willi syndrome (PLWS), clinical, cytogenetic and biochemical findings are reported in 56 PLWS individuals. Forty-eight percent of the individuals with PLWS met the criteria for hypopigmentation.

Dasatinib is a second-generation multi-target tyrosine kinase inhibitor (TKI) that has activity against many imatinib-resistant BCR-ABL mutant forms, Src, and c-Kit tyrosine kinases. While skin hypopigmentation is a well recognized adverse effect of first generation TKIs; it has rarely been reported

Imatinib mesylate (STI 571, Gleevec) is a potent bcr-abl tyrosine kinase inhibitor. It also inhibits c-kit tyrosine kinase. Imatinib mesylate is active in the treatment of cronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GIST). It is considered by some authorities to be the

The pink-eyed dilution phenotype in mice arises from mutations in the p gene; in humans, analogous mutations in the P gene result in oculocutaneous albinism type 2. Although the molecular mechanisms which underlie this phenotype remain obscure, it has been postulated that mutations in p result in

Imatinib mesylate is a tyrosine kinase inhibitor used in the treatment of oncological conditions, including chronic myeloid leukemia and gastrointestinal stromal tumors. The most frequent dermatological side effect reported is pigmentary abnormalities. We report a case series of three Asian Chinese

Gefitinib is a tyrosine kinase inhibitor that targets and inhibits epidermal growth factor receptors. It was initially used to treat non-small cell lung cancer but has increasingly been used for other solid tumors such as those in the breast, colorectal sites, and head and neck, as in our patient.

Signaling by stem cell factor and Kit, its receptor, plays important roles in gametogenesis, hematopoiesis, mast cell development and function, and melanogenesis. Moreover, human and mouse embryonic stem cells express Kit transcripts. Stem cell factor exists as both a soluble and a membrane-bound

Mutations in the P gene of humans and the homologous p-locus of mice, respectively, result in the homologous disorders oculocutaneous albinism type 2 (OCA2) and pink-eyed dilution. Although clearly required for melanin biosynthesis, the specific function of the P gene product, a melanosomal

BACKGROUND Imatinib mesylate is a tyrosine kinase inhibitor that targets the BCR-ABL protein in CML, c-kit (KIT) and platelet-derived growth factor receptors. In clinical trials with imatinib mesylate, common side effects of nausea, emesis, diarrhea, periorbital edema, fluid retention, and

Dermatologic manifestations from therapy with imatinib are well known and frequently include hypopigmentation, and less commonly, hyperpigmentation. There have been few reports of oral hyperpigmentation. We present a case of palatal melanosis related to imatinib therapy for chronic myelogenous