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Genomics 2003 Jan;81(1):6-14
Curly bare (cub), a new mouse mutation on chromosome 11 causing skin and hair abnormalities, and a modifier gene (mcub) on chromosome 5.
In the outcrossing of a new recessive mouse mutation causing hair loss, a new wavy-coated phenotype appeared. The two distinct phenotypes were shown to be alternative manifestations of the same gene mutation and attributable to a single modifier locus. The new mutation, curly bare (cub), was mapped to distal Chr 11 and the modifier (mcub) was mapped to Chr 5. When homozygous for the recessive mcub allele, cub/cub mice appear hairless. A single copy of the dominant Mcub allele confers a full, curly coat in cub/cub mice. Reciprocal transfer of full-thickness skin grafts between mutant and control animals showed that the skin phenotype was tissue autonomous. The hairless cub/cub mcub/mcub mice show normal contact sensitivity responses to oxazolone. The similarity of the wavy coat phenotype to those of Tgfa and Egfr mutations and the map positions of cub and mcub suggest candidate genes that interact in the EGF receptor signal transduction pathway.
J Am Acad Dermatol 2002 Dec;47(6):809-18; quiz 818-20
Approach to the adult female patient with diffuse nonscarring alopecia.
Alopecias are traditionally categorized by the presence or absence of scarring and by a diffuse or localized pattern. A common clinical conundrum is that of a woman presenting with the chief complaint of diffuse, nonscarring hair loss. We review the 4 main diagnostic possibilities for this clinical scenario: (1) female pattern hair loss (androgenetic alopecia), (2) acute and chronic telogen effluvium, (3) diffuse alopecia areata, and (4) loose anagen syndrome. We also outline our approach to the individual patient, emphasizing the pertinent history, physical examination, and appropriate diagnostic testing. This approach usually allows the clinician to make a definitive diagnosis or limited differential diagnosis and to offer the patient therapeutic options.
J Invest Dermatol 2002 Aug;119(2):392-402
Gene array profiling and immunomodulation studies define a cell-mediated immune response underlying the pathogenesis of alopecia areata in a mouse model and humans.
Alopecia areata is a suspected autoimmune hair loss disease. In a rodent model, alopecia areata can be induced in normal haired C3H/HeJ mice by transfer of skin grafts from mice with spontaneous alopecia areata. At weeks 2, 4, 6, and 10 after surgery, grafted mice were euthanized, skin collected and processed for histology, and RNA extracted. Age-matched sham-grafted mice, and mice with and without spontaneous alopecia areata, were similarly processed. For comparison, skin biopsies from alopecia areata and androgenetic alopecia affected humans were also collected. Skin mRNA processed to cDNA was analyzed using Affymetrix mouse 11K and human 6800 gene chip(R) array technology. Microarray results indicated 42 known genes upregulated or downregulated during onset of mouse alopecia areata consistent with an inflammatory cell-mediated disease pathogenesis involving antigen presentation, costimulation, and a T helper 1 lymphocyte response. In contrast, 114 genes, many regulating immunoglobulin response, were altered late in disease development. In alopecia areata affected humans, 95 genes were significantly modulated. As confirmation of microarray analysis results, lymph node and spleen cells from alopecia areata affected mice injected into normal haired littermates transferred the alopecia areata phenotype. Alopecia areata onset could be inhibited in skin-grafted mice by modulation with B7.1- and B7.2-specific monoclonal antibodies. In addition, depletion of CD4+ CD8+ expressing cells in chronic alopecia areata affected mice using monoclonal antibodies permitted hair regrowth. The results consistently demonstrated the importance of an immune cell-mediated disease mechanism in alopecia areata pathogenesis and suggested targeting antigen-presenting cells and reactive lymphocytes may be effective in alopecia areata treatment.
Indian J Cancer 2000 Jun-Sep;37(2-3):95-104
Occurrence and severity of alopecia in patients on combination chemotherapy.
The aim of the study was to evaluate the occurrence and severity of alopecia resulting from combination chemotherapy on cancer patients. The study was conducted during the period 1994-1996 on 58 confirmed cases of malignancies attending the Kasturba Medical College Hospital, Mangalore, South India. The treatment regimens followed were standard protocols recommended for those malignancies and which are widely adopted. Specific drug combinations, their dosage and routes and schedules of administration were studied. The influence of 20 different treatment regimens, most of them in combination chemotherapy, were studied. The patients studied were not receiving any other medication which could have caused alopecia as observed in the present study. The pathophysiology of the hair, as influenced by the treatment regimens, were studied by examination of samples of the affected hairs under a Leica compound microscope. Alopecia was the most dominant side effect influencing 35 of the 58 patients undergoing the treatment (60%). The severity of alopecia was assessed by grouping them in four distinct grades. Specific drugs and their combinations causing varying degrees of severity were identified. The initiation of hair loss in different treatment regimens were analysed. It is seen that alopecia is an early manifestation of cutaneous side effects of cancer chemotherapy. In a majority of patients, the manifestation initiated after the first or the second cycle of administration of the rapeutic regimen, indicating a time interval of 1 to 8 weeks after the start of chemotherapy. Single agent drugs, when used alone or in combination with immunomodulator drugs seem to cause much less side effects, including alopecia, when compared to multiple drug regimens. Microscopic examination of the affected hair showed trichorrhexis, fragmentation, decrease in diameter and depigmentation of the hair shaft.
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