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Query: UMLS:C0027651 (tumor)
685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aggregates of cells resembling those of cutaneous nevi have been found in the capsules of lymph nodes. Although seemingly rare, this extraordinary lesion could conceivably occur often enough to be more than a pathological curiosity, and should be differentiated from metastatic tumor. Slides from every axillary lymph node dissection for female mammary carcinoma in the years 1964 and 1974 at Memorial Hospital were reviewed, as were slides from 100 consecutive lymph node dissections performed during 1974 in patients with malignant melanoma. Nevus cell aggregates (NCA) were associated with three of 17,504 lymph nodes (0.017%) obtained from 909 mastectomies, or 0.33% of the cases. Among the 100 lymph node dissections for malignant melanoma, NCA were found associated with three of the 2,607 lymph nodes examined (0.12%), or 3.0% of the cases studied. Since NCA occur in association with lymph nodes more often than previously thought, the possibility that they may be a potential source of malignant melanoma in patients without a demonstrable cutaneous or mucosal primary is discussed.
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PMID:Nevus cell aggregates associated with lymph nodes: estimated frequency and clinical significance. 83 30

Antibodies directed against different components of ocular melanoma cells were identified by indirect immunofluorescence in the sera of 12 patients with histologically proven malignant melanoma of the uvea. Antibodies reacing with autologous surface membrane antigens were found only in the sera of the 5 patients with the smallest tumors. The sera from most of the patients with small, large, or extraocular tumor contained antibodies directed against autologous cytoplasmic components while about one-half of the tests for antibodies reacting with allogeneic cytoplasmic antigens were positive. The incidence of positive tests with cytoplasmic antigens, in 67 patients with clinically diagnosed benign uveal nevi and 56 other individuals not showing evidence of proliferative lesions of uveal melanocytes, was 25%.
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PMID:Immunological studies in patients with malignant melanoma of the uvea. 84 36

The morphological substrates of pigmented and depigmented skin as well as the structural characteristics of spontaneously developing melanomas were revealed by clinical, light- and electron microscopic methods in gray horses (Lipizzaner breed) from the Vienna Spanish Riding School. On clinical investigations in a group of 31 older horses (more than 10 years old) 20 exhibited melanomas, whereas 23 younger animals (less than 10 years of age) had no evidence for visuable melanotic tumors. Concomitantly with the progressive graying of the hair a depigmentation of the skin was frequently observed. Light and electron microscopic studies of skin biopsies revealed that in pigmented areas melanin is produced by DOPA-positive melanocytes and stored in form of large single melanosomes within keratinocytes. In depigmented areas melanocytes and melanosomes are completely lacking, but a high number of indeterminated cells is present in the basal layer. Melanotic tumors from the root of the tail, the lips, the perianal region, the sholder and intestinal lymph nodes exhibited either encapsulated nodules or diffusely infiltrating melanomatous structures similar to blue nevi in the dermis. Junctional activity could never be observed. A differentiation between melanin-producing tumor cells and melanophages was difficult in light microscopy but possible according to ultrastructural characteristics.
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PMID:[Comparative investigations of depigmented and melanomatous lesions in gray horses of the lipizzaner breed (author's transl)]. 90 Sep 91

Using microradiograms (x-rays of histological sections) and polarized light, we examined collagenous tissue surrounding junctional nevi, benign juvenile melanomas, Dubreuilh's melanosis and early malignant melanomas similar to junctional nevi. Wherever there were tumor cells and infiltrates the collagenous tissue was reduced or destroyed, but had not usually been pushed aside as claimed in previous accounts. The absence of a connective tissue membrane, comparable to the border-zone beneath the epidermis, argues against a nevus. Mature collagenous bundles are clearly shown up by microradiograms and by pollarized light. The degree of thier destruction does not make it possible to distinguish between nevi and malignant melanomas.
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PMID:[Response of collagenous tissue to pigmented tumors]. 93 45

From 1969-1974 1000 unselected enucleated globes have been examined histopathologically. 277 derive from the University Eye Hospital in Hamburg, 723 from various Eye Hospitals in northern and southern Germany. They originate from 589 men and 408 women, three times the sex was unknown. 86 globes had to be removed from children less than 15 years old. 6 groups of etiologies have been distinguished: trauma (308), histologically confirmed neoplastic disease (281), ocular manifestations of systemic diseases (diabetes mellitus, occlusions of central retinal vessels presumably following generalized vascular disease etc.: 128), "operative ocular disease" (164), primary inflammatory disease (71), miscellaneous (malformations, high myopia, pseudo-glioma and pseudo-melanoma: 48). The etiology "operative ocular disease" consists of 67 primary glaucomas (57 adults, 10 buphthalmus), 41 idiopathic cataracts (7 of these congenital) and 3 primary corneal dystrophies, as well as 53 cases of primary retinal detachment. Among the 281 neoplastic diseases, there are 238 primary intraocular malignant melanomas of the uvea, 18 retinoblastomas, 4 primary reticulumcellsarcomas of the retina, 2 choroidal nevi, 10 intraocular metastases and 9 orbital tumors. 16 enucleations among the 1000 enucleations have been performed for pseudo-gliomas (5 x Coats disease, 5 x persistent primary hyperplastic vitreous, 2 x retrolental fibroplasia, others 4 x). The manifestations of systemic disease are consisting of 68 central retinal vein-occlusions, 30 complications of diabetes mellitus and 10 central retinal artery occlusions as well as 20 other generalized diseases. A primary inflammatory disease led to enucleation 50 times due to an intraocular process, 5 times due to scleritis and 18 times as a consequence of keratitis (including 13 times herpes simplex). As the final clinical cause for enucleation the following categories have been elaborated: secondary glaucomas (416), clinical diagnosis of "tumor" (275), atrophy and phthisis bulbi (118), inflammation (112), acute trauma to 4 weeks after the accident (72), others (7). In conclusion the central role of rubeosis iridis leading to secondary angle closure glaucoma is emphasized. This process presents a challenge to ophthalmologic research. Finally the significance of early surgery for primary angle closure glaucomas and for complete restoration of the anterior chamber after trauma and any intraocular procedure is stressed.
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PMID:[Etiology and final clinical cause for 1000 enucleations. (A clinico-pathologic study) (author's transl)]. 95 59

Nevus flammeus (cutaneous hemangioma, port-wine stain) may develop proliferative hamartomatous changes and go on to form monstrous deforming tumors. Excision is feasible, and it may be best to do it early. The mentally retarded, institutionalized patient can also benefit from the reconstruction. In 3 cases it was possible to preserve function of the muscles of facial expression, because of the superficial location of the tumor. Techniques to decrease blood loss are of variable value during the operative procedure.
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PMID:Excision of massive hemangioneurofibroma of the face. 95 19

This report describes 12 patients with the Wiedemann-Beckwith syndrome (WBS), including 6 familial cases from 2 families. The clinical manifestations do not allow for a differentiation between familial and sporadic cases. Consistent morphologic features include organomegaly, cytomegaly and nucleomegaly. The pathogenetic process may involve few or many organs and tissues and may represent a nuclear/mitotic dysfunction. Clinically, the manifestations are hyperplasia, hypoplasia, dysplasia, neoplasia and defects in differentiation. Secondary functional disturbances are at times prominent. The differential diagnosis of the WBS includes 1) the Wilm's tumor (WT)-aniridia syndrome: 2) the "tumor-hypertrophy syndrome" which includes WT, adenocortical tumors or hepatoblastoma; 3) the WT-pseudohermaphroditism syndrome; and 4) the "tumor-nevus syndrome" with or without malformations (particularly duplications) of the urinary tract. The latter two conditions are apparently not associated with hemihypertrophy. Familial occurrence suggests that some cases of the WBS may be due to delayed mutation. Carriers of the premutated allele appear to belong to two classes: those with a high risk of producing affected offspring and those who transmit the premutated allele but have no affected offspring.
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PMID:Studies of malformation syndromes of man XXIX: the Wiedemann-Beckwith syndrome. Clinical, genetic and pathogenetic studies of 12 cases. 97 81

Two cases of tubular apocrine adenoma were studied by light, histochemical, and electron microscopic methods. This benign apocrine hamartoma must be considered in the classification of appendage tumors, particularly those associated with organoid epithelial nevus, and may be confused with metastatic adenocarcinoma. The tumor is characterized by dermal and subcutaneous lobular masses of tubular structures. Connection to the epidermis by one or more ductlike structures is observed. The tubules contain typical apocrine epithelial cells, some with hyaline or clear cell differentiation. The tumor cells have apocrine differentiation by histochemistry and ultrastructure. The localization to the scalp and the nodular, lobulated appearance and the apocrine structures indicate that this tumor is similar to nevus syringocystadenoma papilliferum and must be diffentiated from it.
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PMID:Tubular apocrine adenoma. 99

A retrospective study of bioptic material was used to design the following outline of a histological classification of epithelial skin tumours tentatively compared with handbooks published by the WHO (1) and AFIP (2): I. Tumour-like changes: 1. senile verruca (mixed, acanthotic, melanoacanthotic, hyperkeratonic, reticular, inverted). 2. Virus verrucosities (v. vulgaris, v. plana, c. accuminatum, molluscom contagiosum). 3. Hamartogenic verrucosities (naevus verrucosus, n. comedonicus, fibroepithelial papilloma. 4. Genetically undefined verrucosities (acanthosis nigricans, light cell acanthoma, verrucous dyskeratosis). 5. Cysts (atheroma, epidermoid cyst, dermoid cyst, others). 6. Unclassified. II. Precanceroses: 1. Pseudoepitheliomatous hyperplasis, 2. keratosis senilis, 3. Radiation dermatosis, 4. Unclassified. III. Epithelial tumours A. From surface epithelium 1. Spinocellular carcinoma (basic type, anaplastic, adenoid, sarcomatoid, clear cell carcinoma, intraepidermal). 2. Basocellular carcinoma: a) varieties derived from surface epithelium (intraepithelial, superficial, solid, cystic, invasive), b) varieties with adenoid features (cylindromatous, fibroepithelia), c) varieties with trichoepithelial features (keratinizing, pigment-type, clear cell type), d) naevus varieties (basocellular naevi). 3. Spinobasocellular carcinoma. 4. Unclassifiable. B. Sweat gland tumours: 1. syringocystadenoma papilliferum, 2. hidradenoma papillare, 3. nodular hidradenoma (eccrine spiradenoma, eccrine acrospiroma, myxochondroepithelioma, myoepithelioma, mucinous epithelioma), 4. syringoma, 5. eccrine cylindroma, 6. hidrocystoma, 7. eccrine poroma, 8. carcinomas (so called extramammary Paget carcinoma), 9. unclassifiable. C. Sebaceous gland tumours: 1. adenoma sebaceum, 2. carcinoma sebaceum, 3. quasi tumours (naevus sebaceus, Pringle's hamartoma, steatocystoma multiplex, hyperplasia), 4. unclassifiable. D. Trichoepithelial tumours: 1. trichofolliculoma, 2. follicular poroma, 3. keratoacanthoma, 4. tricholemoma, 5. pilomatrixoma, 6. trichogenic adnexal tumour, 7. trichoepithelioma, 8l unclassifiable.
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PMID:[Epithelial tumor-like changes, precancerous conditions and skin neoplasms (standardization study)]. 100 15

It is strongly recommended that any pigmented lesion which cannot be diagnosed with certainty as benign should be excised and pathologically examined. In addition, any mole which is removed, no matter for what purpose, whether it is suspected of having malignant or premalignant changes or for cosmetic and functional purposes, should always be pathologically examined. If the lesion is suspected of showing malignant change, then if technically possible it should be completely excised. If the location is such, or if it is a sufficiently large lesion, that a simple complete excision cannot be performed at that time, then it is justifiable and good medical practice to do an incisional biopsy. However, if the pathological report shows that the tumor is malignant then the necessary radical surgery should be performed within 7 to 10 days of the initial biopsy. Under these circumstances, incisional biopsy does not adversely affect the prognosis. Under these circumstances, the incisional biopsy prevents unnecessary radical and sometimes mutilating surgery being performed for the treatment of a benign pigmented tumor.
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PMID:Moles that cause concern. 104 89


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