Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparison of time-dependent localization patterns between lower, asymmetrical (AIPCS2a) and higher, symmetrical (AIPCS4) sulfonates of aluminum phthalocyanines in human malignant melanoma LOX transplanted to athymic nude mice from 1 to 120 hr after i.v. administration was made by means of laser scanning fluorescence microscopy. The lipophilic AIPCS2a was distributed mainly in tumor cells, while the hydrophilic AIPCS4 localized only in the vascular stroma of the tumor tissue. Concomitantly, comparative observations on the killing mechanism of photodynamic effects after treatment with a much lower i.v. dose of AIPCS2a and AIPCS4 plus laser light on the human tumor LOX were also made by morphological studies. Light and electron microscopy showed that there was a direct, extensive, photo-damaging action on all organelles and nuclear structure in the tumor cells after PDT with AIPCS2a; whereas the photo-induced injury to the tumor tissue after treatment with AIPCS4 and light was largely the consequence of initial functional vasogenic response and ultimate damage to vascular structure. These findings correlate well with the different localization patterns of the 2 dyes observed in human tumor tissues.
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PMID:Aluminum phthalocyanines with asymmetrical lower sulfonation and with symmetrical higher sulfonation: a comparison of localizing and photosensitizing mechanism in human tumor LOX xenografts. 221 Aug 87

The recognition of atypical or dysplastic nevomelanocytic nevi potentially provides clinicians with another means of identifying individuals at increased risk for cutaneous malignant melanoma. However, a great deal of controversy still surrounds these lesions, their significance, and the clinical and histologic criteria needed for their diagnosis at present. In general, dysplastic nevi tend to be asymmetrical and larger (greater than 5 mm) than ordinary acquired nevi, have a macular component, irregular and ill-defined borders, and haphazard (variegate) coloration. A clinical diagnosis of dysplastic nevi must be confirmed by histopathology, since not all clinically atypical nevi are dysplastic. While precise histopathologic criteria for dysplastic nevi are lacking, most authorities agree that an abnormal nevomelanocytic proliferative pattern as manifested by increased numbers of basilar melanocytes and/or abnormal junctional nevomelanocytic nesting in the setting of lentiginous epidermal hyperplasia, variable degrees of nevomelanocytic nuclear atypia, and a lymphocytic host response are consistent with a histologic diagnosis of dysplastic nevi. Current data for individuals with dysplastic nevi and a family history of cutaneous malignant melanoma (at least two family members with cutaneous malignant melanoma) indicate a relative risk for cutaneous malignant melanoma about 148 times that of the general population. In comparison, cutaneous malignant melanoma risk seems lower for individuals with familial dysplastic nevi (but without familial cutaneous malignant melanoma) and "sporadic" dysplastic nevi. With respect to progression to melanoma, probably the vast majority of dysplastic nevi remain stable or possibly regress. Management of individuals with histologically confirmed dysplastic nevi involves periodic skin examinations. Regional overview and life-size photography are helpful in following these patients. Patients should also be instructed in the examination of their own skin. While a definite relationship between sun exposure and dysplastic nevi remains unproved, the use of sunscreens and avoidance of unnecessary sun exposure are advised. Examination of family members for atypical melanocytic lesions is also recommended.
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PMID:The dysplastic nevus: recognition and management. 327 48

In 4-8% of all melanoma patients, a lymph node metastasis develops as the first manifestation of the disease, whereas a primary lesion cannot be found. The latter may have been surgically removed already years ago, may be located at an occult place or - as it is especially characteristic for melanoma - may have vanished spontaneously due to a specific immunological mechanism. Such spontaneous tumour regression, which, for instance, becomes recognisable by the development of a halonaevus or an asymmetrical vitiligo, does not imply an improvement of the individual prognosis. However, present knowledge suggests that in patients with unknown primary lesion neither an adjuvant chemotherapy nor immunotherapy can be recommended, if the metastasis has been surgically removed completely. Additional radiotherapy does also not appear to be indicated. Only a short-interval follow-up remains important.
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PMID:[Melanoma metastasis in the neck region with unknown primary tumor]. 670 Mar 27

A 60-year-old woman with superficial spreading melanoma in situ, measuring 2.5 mm in diameter, was examined. She had noticed a very small pigmented lesion 1.2 mm in diameter on her left lower leg in April of 1989. By April of 1990, it had grown to 2.5 mm in diameter. Its edge was irregular, and its color was variegated black to brown. Skin surface markings had disappeared in the center portion. Histopathologically, the lesion was asymmetrical. Atypical large cells nested in the lower epidermis and were scattered singly in the mid and upper epidermis, as seen in Paget's disease. At the periphery of the lesion, single large tumor cells were scattered in the mid epidermis. The tumor cells reacted to monoclonal anti-melanoma antibody HMB-45.
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PMID:A case of superficial spreading melanoma in situ 2.5 mm in diameter. 840 26

Halo reactions to melanocytic nevi are a well-recognized phenomenon. In contrast, halo reactions to Spitz's nevi have been reported only infrequently. Halo reactions may cause misdiagnosis of an otherwise benign nevus as melanoma because inflammatory cells sometimes obscure the architectural features of the underlying nevus, and may induce cytologic atypia. For Spitz's nevus where the distinction between malignancy and benignancy is already challenging, halo reactions compound the problem. We describe 17 examples of Spitz's nevus with halo reaction, and compare their immunohistochemical features with those of "ordinary" halo nevi. Only 2 of 17 lesions demonstrated clinically apparent halos. Clinical follow-up was available for 12 of 17 cases. None of the 12 has persisted at the biopsy site or metastasized after an average 3.6-year follow-up period. Junctional, compound, intradermal, and combined types of Spitz's nevi were represented. All were characterized by symmetrical lymphocytic infiltrates which permeated the full thickness of the nevus, including junctional nests. Combined Spitz's nevi constituted more than one-half of examples in this series (9/17 cases). The combined Spitz's nevus included a combination of Spitz's nevus with either an ordinary (common, banal) nevus or a superficial congenital type nevus. In these combined Spitz's nevi, the lymphocytic response was often directed exclusively to the Spitz's nevic component. Important distinguishing features from malignant melanoma arising in a pre-existing nevus included symmetry and lateral circumscription of the spitzoid component, no large expansile-appearing aggregates of melanocytes, a decrease in size of nests with increasing dermal depth, a lack of mitotic figures among melanocytes at the base, and a symmetrical and diffusely permeative lymphocytic response. Although the combined Spitz's nevus with halo reaction sometimes appeared asymmetrical at scanning magnification, each component of the combination was symmetrical, when examined independently. Probably because of reactive atypia, nuclear maturation with progressive descent into the dermis was sometimes absent. There were no obvious differences in immunohistochemical staining patterns among 4 Spitz's nevi with halo reaction, 5 regressing melanomas, and 5 benign halo nevi when stained with antibodies to S100, HMB-45, OPD4, CD8, TIA-1, CD1a, CD68, and Ki-67.
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PMID:Spitz's nevi with halo reaction: a histopathologic study of 17 cases. 944 88

It is highly desirable to identify malignant melanoma, a common cancer, at an early stage. One important clinical feature of this cancer is asymmetrical skin lesions. In this paper, we propose an adaptive fuzzy approach that uses symmetric distance (SD) to measure lesions with fuzzy borders. The use of a number of SD variations and the adoption of a backpropagation neural network enhances the discriminative power of the approach. Digitized images from the Lesion Clinic in Vancouver, Canada, demonstrate the accurate classification of asymmetric lesions at around 80%.
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PMID:Determining the asymmetry of skin lesion with fuzzy borders. 1556 81

WNT/planar cell polarity (PCP) signaling pathway controls tissue polarity and cell movement through the activation of RHOA, c-Jun N-terminal kinase (JNK), and nemo-like kinase (NLK) signaling cascades. PCP is induced in Drosophila by the asymmetrical localization of Frizzled-Dishevelled-Diego-Starry night (Flamingo) complex and Van Gogh (Strabismus)-Prickle complex. Here, WNT/PCP signaling pathway implicated in human carcinogenesis is reviewed. Human WNT5A, WNT5B, and WNT11 are representative non-canonical WNTs transducing PCP signals through FZD3 or FZD6 receptors, and ROR1, ROR2 or PTK7 co-receptors. Human VANGL1, VANGL2 (Van Gogh homologs), CELSR1, CELSR2, CELSR3 (Starry night homologs), DVL1, DVL2, DVL3 (Dishevelled homologs), PRICKLE1, PRICKLE2 (Prickle homologs), and ANKRD6 (Diego homolog) are core PCP signaling molecules. MAGI3 assembles FZD, VANGL, PTEN, and adhesion molecules. Dishevelled-dependent WNT/PCP signals are transduced to the RHOA signaling cascade through Formin homology proteins DAAM1 and DAAM2, and to the JNK signaling cascade through MAPKKKs and MAPKK4/7. Dishevelled-independent WNT/ PCP signals are transduced to the NLK signaling cascade through MAP3K7 (TAK1). ANKRD6, NKD1 and NKD2 induce class switch from the WNT/GSK3beta signaling pathway to the WNT/PCP signaling pathway. WNT5A is up-regulated in various types of human cancer, such as gastric cancer, lung cancer, and melanoma. FZD3/FZD6 receptor and ROR2 co-receptor transduce WNT5A signal in gastric cancer. Aberrant activation of WNT/PCP signaling pathway in human cancer leads to more malignant phenotypes, such as abnormal tissue polarity, invasion, and metastasis. cDNA-PCR, microarray or ELISA reflecting aberrant activation of WNT/PCP signaling pathway could be developed as novel cancer prognostics. Single nucleotide polymorphism (SNP) and copy number polymorphism (CNP) of WNT/PCP signaling molecules mentioned above are suitable for use in screening of cancer predisposition, especially for gastric cancer. Antibody, RNAi, or small molecule compounds to regulate the function of WNT/PCP signaling molecules mentioned above are good candidates for development as novel cancer therapeutics.
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PMID:WNT/PCP signaling pathway and human cancer (review). 1627 60

A 62-year-old male Turkish patient had a pigmented lesion on the sole with a 10-year history. It was an asymmetrical macular lesion with an irregular border and irregular brown pigmentation and had a diameter of 1.2 cm x 1.7 cm. Dermoscopy revealed a parallel ridge pattern and an abrupt cut-off of pigmentation on the upper edge. Histologically lentiginous hyperplasia decorated by innocent melanocytes and scattered melanocytic proliferation with slight to moderate cytological atypia were seen. Atypical melanocytes were very scattered and it was insufficient to call it a melanoma in situ. A second finding was a microvascular proliferation located in the papillary dermis. There was no sign of regression such as fibrous tissue or host reaction. Atypical melanosis of the foot has rarely been reported in the published work, which are from Japan and Korea. This case is presented to emphasize the significance of this rare entity which has recently been reported to be a very early phase of acral melanoma.
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PMID:Atypical melanosis of the foot showing a dermoscopic feature of the parallel ridge pattern. 1720 3

The efficacy of the histological criteria currently used in the diagnosis of melanoma is still to be defined. We performed a quantitative analysis of 72 conventional (non-Spitzoid, nondesmoplastic) melanomas and 73 conventional melanocytic naevi, used as controls, for 13 histological diagnostic parameters (dimension >6 mm, asymmetry, poor circumscription, irregular and confluent nests, single melanocytes predominating, absence of maturation, suprabasal melanocytes, asymmetrical melanin, melanin in deep cells, cytological atypia, mitoses, necrosis and dermal lymphocytic infiltrate). Differences in the distribution of selected parameters between the two groups were investigated by Fisher's exact test; for each parameter sensitivity and specificity were calculated. Results showed that all parameters, except poor circumscription, seemed to be significantly associated with melanoma (P<0.05). Cytological atypia, dermal lymphocytic infiltrate, asymmetry, dimension >6 mm and absence of maturation showed a high sensitivity (>90%); absence of maturation, mitoses, necrosis, asymmetrical melanin, suprabasal melanocytes and melanin in deep cells showed a high specificity (>90%); irregular-confluent nests and single melanocytes predominating were poorly sensitive and poorly specific. In melanomas < or =2 mm, two additional parameters were sensitive (> or =90%): suprabasal melanocytes and single melanocytes predominating. We conclude that not all parameters showed to have the same diagnostic value. Absence of maturation and, limited to melanomas < or =2 mm, suprabasal melanocytes were the most discriminating (sensitive and specific) histological features. Cytological atypia, dimension >6 mm, suprabasal melanocytes and mitoses were additional reliable diagnostic features, showing a relatively high sensitivity and a relatively high specificity. Other useful features were dermal lymphocytic infiltrate and asymmetry (sensitive) and necrosis, asymmetrical melanin and melanin in deep cells (specific).
Melanoma Res 2008 Aug
PMID:Sensitivity and specificity of histological criteria in the diagnosis of conventional cutaneous melanoma. 1862 9

We describe the clinicopathologic features of a 69-year-old man affected with acute onset Churg-Strauss syndrome with major peripheral nerve involvement. At admission the patient presented a one-week history of distal upper-limb asymmetrical paresthesias. Asthma had been present since the age of 55 and treated with leukotriene receptor antagonists (LTAs, Montelukast) for a few years. Multiple pulmonary infiltrates had been diagnosed during follow-up for melanoma. During hospitalization he showed rapidly progressive weakness worsening within a few hours; cerebrospinal fluid analysis, cervical MRI, head CT scan, nerve conduction studies and peripheral nerve and skeletal muscle biopsies were performed. Blood analysis showed leukocytosis and marked eosinophilia; p-ANCA were positive. Sural nerve biopsy showed a marked loss of myelinated fibers, thrombosed vessels surrounded by mononuclear and eosinophilic cells, necrotizing and hyaline degeneration. Eosinophilic infiltrates were shown in May-Grunwald-Giemsa stained sections. The eosinophils mostly occupied the outer zone of the adventitia at the margin of the active lesion. Perivascular cellular infiltrates within the epineurium were immunoreactive for T-lymphocytes and macrophages. Strong HLA-DR immunostaining was present in the perineurium and membrane attack complex deposition was present in a few endoneurial capillaries. Muscle biopsy showed neurogenic changes and one vessel surrounded by mononuclear cells. After a few days of corticosteroid therapy leukocytosis and eosinophilia normalized and the patient's clinical features stabilized.
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PMID:Severe acute multineuropathy in Churg-Strauss syndrome in a patient with a history of melanoma. 1935 44


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