Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A monoclonal antikeratin antibody, EKH4, was produced from a hybridoma cell line which was established by fusing P3X63SAg8 mouse myeloma cells with spleen cells of mice immunized with human trichilemmoma cells. Immunoblot analysis showed that EKH4 antibody reacts predominantly with 50 kilodalton keratin polypeptide in normal epidermis. By indirect immunofluorescence and immunoperoxidase techniques, EKH4 antibody reacted with the lower 2-3 cell layers of the epidermis as well as most cells of pilosebaceous follicle of human and animal skin. Tumor cells of human basal cell epitheliomas and squamous cell carcinomas were also stained with this antibody. The staining was much more regular and intense compared with an available monoclonal antikeratin antibody, AE1. In the lesion of epidermal proliferative disorders, such as psoriasis and actinic keratosis, the entire epidermis instead of the lower layers was stained with EKH4 antibody. Normal skin overlying or adjacent to epithelial tumors also showed positive staining in the entire epidermis. By using indirect immunoperoxidase technique, EKH4 also stained alcohol-fixed, paraffin-embedded tissue sections.
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PMID:Monoclonal antikeratin antibody: production, characterization, and immunohistochemical application. 258 61

Follicular hyperkeratosis was observed in a patient with multiple myeloma. This keratosis is considered to be a cutaneous manifestation of multiple myeloma, since similar cases have been observed before. In addition, the patient had cutaneous, ocular, and articular signs and symptoms of cryocrystalglobulinemia, ie, cutaneous vasculitis, blurring, and joint swellings.
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PMID:Follicular hyperkeratosis and cryocrystalglobulinemia syndrome. Occurrence in a patient with multiple myeloma. 400 5

Disulfide (S-S) bonds and sulfhydryl (-SH) groups in skin-limited and systemic amyloidoses in frozen and paraffin-embedded sections were examined with a thiol reagent, N-(7-dimethylamino-4-methyl-3-coumarinyl)-maleimide (DACM). In frozen sections, dermal amyloids of skin-limited amyloidoses contained a large number of S-S bonds but no -SH groups [macular amyloidosis (9 cases), lichen amyloidosis (4), and skin tumor-associated (seborrheic keratosis) amyloidosis (1)]. In contrast, amyloids of systemic amyloidoses contained no S-S bonds or -SH groups [primary and myeloma-associated amyloidoses (1 each)]. The identical results were obtained from paraffin-embedded sections in skin-limited amyloidoses [macular (31), biphasic (4), lichenoid (9) and skin tumor-associated Bowen's disease (3), seborrheic keratosis (2), solar keratosis (2), porokeratosis Mibelli (1), and basal cell epithelioma (1) amyloidoses], systemic amyloidoses [primary (3), myeloma-associated (2), and secondary (2) amyloidoses] and tumefactive amyloidoses of the tongue (2). Furthermore, amyloid-like deposits confirmed by various histochemical stainings were found in the epidermis in 27/67 cases of skin-limited amyloidoses in both frozen and paraffin sections. These intraepidermal amyloid-like deposits contained S-S bonds in all cases (27/27) and -SH groups in 10 of 27 cases. In contrast, an intraepidermal amyloid-like deposit was not observed in any systemic amyloidoses (0/9) or tumefactive amyloidoses of the tongue (2). These results showed that skin-limited amyloidoses could be differentiated from systemic amyloidoses by DACM methods (this appears to depend upon the differences of amino acid composition between skin-limited and systemic amyloidoses) and that paraffin-embedded sections were usable for DACM methods. Present study further suggests that amyloids ion skin-limited amyloidoses are, at least in part, derived from epidermal keratinocytes.
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PMID:Sulfhydryl and disulfide stainings in amyloids of skin-limited and systemic amyloidoses. 619 91

We describe a 72-year-old woman with a 13-year history of a lichenoid dermatitis, who developed multiple, papular keratoacanthoma (KA)-like lesions and few crater-like nodules on the extremities over a period of 6 months before our observation. Her medical history also recorded multiple myeloma diagnosed a few years before. The long-standing dermatosis was diagnosed, clinically, as keratosis lichenoides chronica (KLC), although, histologically, a lichenoid tissue reaction pattern was not evident. On the other hand, histology from papular and nodular lesions of recent onset was consistent with a possible early phase of KA and spinocellular carcinoma, respectively. Oral acitretin induced regression of KA-like lesions and improvement of KLC but had no effects on crater-like nodules, which required surgical excision. KLC is a chronic disorder of keratinization characterized by lichenoid hyperkeratotic papules arranged in a linear pattern, erythematosquamous plaques and seborrhoea-like dermatitis. We emphasize in our case the association between KLC and multiple possible KAs, never previously reported, and speculate that these two rare conditions may represent here a 'continuum' from a pathogenetic point of view.
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PMID:Keratosis lichenoides chronica and eruptive keratoacanthoma-like lesions in a patient with multiple myeloma. 1564 10

In 1994, the field of bone biology was significantly advanced by the discovery that activating mutations in the fibroblast growth factor receptor 3 (FGFR3) receptor tyrosine kinase (TK) account for the common genetic form of dwarfism in humans, achondroplasia (ACH). Other conditions soon followed, with the list of human disorders caused by FGFR3 mutations now reaching at least 10. An array of vastly different diagnoses is caused by similar mutations in FGFR3, including syndromes affecting skeletal development (hypochondroplasia [HCH], ACH, thanatophoric dysplasia [TD]), skin (epidermal nevi, seborrhaeic keratosis, acanthosis nigricans), and cancer (multiple myeloma [MM], prostate and bladder carcinoma, seminoma). Despite many years of research, several aspects of FGFR3 function in disease remain obscure or controversial. As FGFR3-related skeletal dysplasias are caused by growth attenuation of the cartilage, chondrocytes appear to be unique in their response to FGFR3 activation. However, the reasons why FGFR3 inhibits chondrocyte growth while causing excessive cellular proliferation in cancer are not clear. Likewise, the full spectrum of molecular events by which FGFR3 mediates its signaling is just beginning to emerge. This article describes the challenging journey to unravel the mechanisms of FGFR3 function in skeletal dysplasias, the extraordinary cellular manifestations of FGFR3 signaling in chondrocytes, and finally, the progress toward therapy for ACH and cancer.
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PMID:Sixteen years and counting: the current understanding of fibroblast growth factor receptor 3 (FGFR3) signaling in skeletal dysplasias. 2204 36

Cutaneous cryosurgery refers to localized application of freezing temperatures to achieve destruction of skin lesions. It can be used to treat a broad range of benign and premalignant skin conditions, and certain malignant skin conditions, with high cure rates. Cellular destruction is accomplished by delivery of the cryogen via dipstick, probe, or spray techniques. It is widely used in primary care because of its safety, effectiveness, low cost, ease of use, good cosmetic results, and lack of need for anesthesia. Cryosurgery is as effective as alternative therapies for most cases of molluscum contagiosum, dermatofibromas, keloids, and plantar or genital warts. It is a more effective cure for common warts than salicylic acid or observation. Cryosurgery is generally the treatment of choice for actinic keratosis. Contraindications to cryosurgery include cryofibrinogenemia, cryoglobulinemia, Raynaud disease, agammaglobulinemia, and multiple myeloma. Complications from cryosurgery include hypopigmentation and alopecia, and can be avoided by limiting freeze times to less than 30 seconds. Referral to a dermatologist should be considered in cases of diagnostic uncertainty or for treatment of skin cancer, which requires larger amounts of tissue destruction, resulting in higher complication rates.
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PMID:Cutaneous cryosurgery. 2331 84

FGFR3 mutations cause wide spectrum of disorders ranging from skeletal dysplasias (hypochondroplasia, achondroplasia, and thanatophoric dysplasia), benign skin tumors (epidermal nevi, seborrhaeic keratosis, and acanthosis nigricans), and epithelial malignancies (multiple myeloma and prostate and bladder carcinoma). Hypochondroplasia is the most common type of short-limb dwarfism in children resulting from fibroblast growth factor receptor 3 (FGFR3) mutation. Acanthosis nigricans might be seen in severe skeletal dysplasia, including thanatophoric dysplasia and SADDAN syndrome, without a biochemical evidence of hyperinsulinemia. Insulin insensitivity and acanthosis nigricans are uncommonly seen in hypochondroplasia patients with FGFR3 mutations which may represent a new association. We aim to describe the association of hypochondroplasia, acanthosis nigricans, and insulin resistance in a child harboring FGFR3 mutation. To our knowledge, this is the first case report associating the p.N540 with acanthosis nigricans and the second to describe hyperinsulinemia in hypochondroplasia. This finding demonstrates the possible coexistence of insulin insensitivity and acanthosis nigricans in hypochondroplasia patients.
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PMID:Hypochondroplasia, Acanthosis Nigricans, and Insulin Resistance in a Child with FGFR3 Mutation: Is It Just an Association? 2550 98