Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0027627 (metastases)
103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Litters of suckling young of the laboratory opossum (Monodelphis domestica) were irradiated with UV light from sunlamps with a spectral emission peak at 302 nm (UVB) to induce melanocytic nevi. Total doses of 0.87-5.0 kJ/m2 were divided equally among up to 14 exposures during the 19 days from birth. Of 358 sucklings exposed, 217 survived to weaning, and 22 (10%) possessed a nevus when shaved and examined at or after weaning. Affected animals were then exposed 3 times/week to 125 J/m2 of UVB for up to 45 weeks to promote progression to malignancy. Nevi of 8 of the 20 chronically-exposed animals progressed to malignant melanoma with metastases to lymph node(s). Cell cultures were prepared from affected nodes to confirm that pigmented nodal cells were metastatic melanomas. One established cell line (TD15L) contained highly pigmented, dendritic, malignant melanoma cells. These cells, injected s.c. as xenogeneic grafts into athymic nude mice, remained viable in the subcutis and were moderately tumorigenic in the dermis. UVR exposure of Monodelphis sucklings is a novel, effective, and proficient way of initiating melanocytic lesions for studies on susceptibility and progression to melanoma, and the cell lines derived from these melanomas will provide promising new reagents for chemotherapy and immunotherapy investigations.
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PMID:Malignant melanoma in ultraviolet irradiated laboratory opossums: initiation in suckling young, metastasis in adults, and xenograft behavior in nude mice. 795 32

Blue nevus is an uncommon pigmented lesion of dermal melanocytes. By convention, two well defined histologic variants, designated as "common" and "cellular", have been recognised. In the last few years, these lesions have attracted much attention due to the recognition of news entities and to its confusion with malignant melanoma. In the present review, we point out the more striking features of new related entities (combined nevus, deep penetrating nevus, compound blue nevus) and establish the differential diagnosis with conflictive lesions such as atypical blue nevus, locally aggressive blue nevus, congenital giant melanocytic nevus with nodular growth and melanocytic dermal tumor of unpredictable outcome. We also review the concept of malignant blue nevus and the significance of lymph node metastases. The blue nevus is an uncommon pigmented lesion consisting of dermal melanocytes that can appear in diverse forms: dendritic, spindle-shaped, oval-shaped, or polyhedral. Although it usually occurs in skin, it has been reported in other locations, such as oral mucosa, sclera, uterine cervix, vagina, prostate, spermatic cord, pulmonary hilus, orbit, conjunctiva, maxillary sinus, breast, and lymph nodes 3,8,42,49. Generally, it occurs in adults as a single, acquired, intensely pigmented lesion, although familial and multiple nevi have been reported 7,39. By convention, there are two well-defined histologic variants, designated as "common" and "cellular", but lesions often manifest intermediate features. In the last few years, blue nevus has attracted much attention due to the recognition of new (clinical and histologic) entities and to its confusion with malignant melanoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blue nevus: classical types and new related entities. A differential diagnostic review. 798 22

The estimated incidence of twin pregnancy consisting of hydatidiform mole and a coexisting fetus is 1 per 22,000-100,000 pregnancies. Since 1965, nine patients with this entity have been treated at the New England Trophoblastic Disease Center (NETDC), Boston. One patient had a partial hydatidiform mole coexisting with a normal placenta and fetus. The other eight patients had twin pregnancies with a complete hydatidiform mole (CHM) and coexisting fetus. We compared the clinical outcomes in these 8 patients and 14 additional published case reports of multiple gestations composed of CHM and coexisting fetuses with a group of 71 patients with singleton CHM treated at NETDC. Twelve of the 22 patients (55%) with CHM and coexisting fetuses developed persistent gestational trophoblastic tumor, requiring chemotherapy. Five of these patients developed metastases requiring multiple cycles of chemotherapy to achieve remission. The presenting symptoms of multiple conception with CHM and coexisting fetuses were similar to those in patients with a singleton conception and complete mole. However, as compared to singleton CHM, patients having a multiple conception with CHM and coexisting fetuses were diagnosed at a later gestational age, had higher preevacuation beta-human chorionic gonadotropin levels and had a greater propensity to develop persistent tumor. These data indicate that patients with multiple conceptions consisting of CHM and coexisting fetuses are at high risk of developing persistent gestational trophoblastic tumor.
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PMID:Clinical features of multiple conception with partial or complete molar pregnancy and coexisting fetuses. 803 69

Phospholipid extracts of surgical tissue specimens from 18 patients, consisting of normal esophagus, distal esophageal tumor and normal stomach, were analyzed using 31P NMR. The prominent phospholipids detected in these tissues included cardiolipin (CL), phosphatidylethanolamine plasmalogen, phosphatidylethanolamine (PE), phosphatidylserine (PS), sphingomyelin (SPH), phosphatidylinositol (PI), phosphatidylcholine plasmalogen and phosphatidylcholine (PC). Very small quantities of the phospholipids lysophosphatidylcholine, phosphatidic acid, phosphatidylglycerol, and an uncharacterized phospholipid at -0.13 delta also were detected in some of the 54 tissue specimens analyzed. The mean relative concentrations of these phospholipids, in mole percentages of total detected phosphorus, were determined from the acquired spectra and used to differentiate among the three tissue groups. The relative concentrations of the following phospholipids differed significantly (p < 0.001) among the respective tissue groups: normal esophagus vs esophageal tumor, PS, SPH, PI, PC; normal esophagus vs normal stomach, CL, PE, PS, SPH; esophageal tumor vs normal stomach, CL, PE. Membrane phospholipids implicated in modulating the growth and metastases of tumors of epithelial origin can be profiled to discriminate among normal esophagus, distal esophageal tumor and normal stomach using 31P NMR.
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PMID:Esophageal cancer phospholipid characterization by 31P NMR. 834 52

Gestational trophoblastic disease is a term that describes a group of tumors that share several characteristics as follows: (1) they arise in fetal chorion, (2) they produce human chorionic gonadotropin (hCG), and (3) they respond extremely well to chemotherapy. Although rare, they have received a disproportionate amount of attention because they were the first metastatic solid tumor to be cured using chemotherapy. Also, hCG was the first reliable tumor marker. Finally, because they arise in fetal tissue, they have the potential for a strong immune response against paternal antigens in the tumor. This potential for immunologic rejection was thought initially to explain the success of chemotherapy in this disease. The early detection of gestational trophoblastic disease is successful in patients who have had a hydatidiform mole as the pregnancy event that begins the process but unsuccessful in the early detection of the development of choriocarcinoma after a normal term delivery, abortion (spontaneous or elective), or ectopic pregnancy. Surveillance after evacuation of a molar pregnancy (whether complete or a partial mole) consists of regular evaluation of hCG production and the detection of metastatic disease. However, the development of gestational choriocarcinoma after term pregnancy or an abortion (no molar tissue can develop as a consequence of these pregnancies) is detectable only by signs or symptoms of metastatic disease in any of the many organs to which this tissue can spread. Unlike most staging classifications in gynecologic cancers, which are based on histologic findings and tumor location, the classification used in gestational trophoblastic disease stresses other features that are more useful for treatment selection. Both the National Institutes of Health and the World Health Organization classifications emphasize the importance of recognizing factors that predict the likelihood of a tumor responding to chemotherapy. Currently available treatment can cure all patients except those who are in the very high-risk group, which usually is characterized by metastasis to the brain or liver or a history of prior chemotherapy. Even in this category, approximately 80% of patients are curable.
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PMID:Diagnosis and management of gestational trophoblastic disease. 838 9

The term ocular melanoma refers to a heterogeneous group of cancers of melanocytic origin. The precursor of most cases of conjunctival melanoma is known to ophthalmologists as primary acquired melanosis. This condition passes through well-defined stages of tumor progression. Although tumor progression is not obligatory, as a conjunctival melanocytic lesion acquires new biologic properties it is more likely to progress further. Although junctional nevi are seldom encountered beyond childhood and primary acquired melanosis usually develops in middle-aged individuals, these two conditions may be histologically indistinguishable. Most junctional nevi eventually show evidence of differentiation, whereas nearly half of the cases of primary acquired melanosis with atypia progress to melanoma. Therefore, it is possible that aging may modulate the capability of certain clonal proliferations to differentiate. Uveal melanocytes normally reside in mesenchyme, so that the traditional histologic criterion for establishing the diagnosis of most melanomas--breach of an epithelial basement membrane--does not apply. Because uveal melanomas are not easily accessible to incisional biopsy (without disruption of vision), only two points in the spectrum of tumor progression are defined clinically: nevus and melanoma. Experimental evidence suggests that a spectrum of atypical melanocytic proliferations separates benign nevi from melanomas capable of generating metastases. Unlike conjunctival melanomas that spread first to regional lymph nodes, choroidal and ciliary body melanomas preferentially spread first to the liver and are examples of organ-specific metastases.
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PMID:Tumor progression in ocular melanomas. 844 Sep 16

A study of 57 cutaneous melanocytic tumors from 53 horses revealed 4 distinct clinical syndromes: melanocytic nevus, dermal melanoma, dermal melanomatosis, and anaplastic malignant melanoma. Melanocytic nevus and anaplastic melanoma each had histopathologic features that distinguished them from dermal melanoma and dermal melanomatosis. Dermal melanoma and dermal melanomatosis were histologically similar but could be differentiated by their clinical features. Melanocytic nevi were diagnosed in 29 horses with an average age of 5 years; they were solitary, superficial masses that occurred in both grey and nongrey horses, and in which surgical excision was generally curative. Dermal melanomas were diagnosed in 20 horses with an average age of 13 years; all horses of known coat color were grey. Eight horses with an average age of 7 years had 1 or 2 discrete dermal melanomas. Follow-up information was available for 6 horses; metastases occurred in 2 horses, and surgical excision was apparently curative in 4 horses. Dermal melanomatosis was diagnosed in 12 grey horses with an average age of 17 years; all 6 of these horses evaluated had internal metastases. In 2 aged nongrey horses with anaplastic malignant melanoma, the tumors metastasized within 1 year of diagnosis. Two tumors with features of both melanocytic nevus and dermal melanoma remained unclassified.
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PMID:Equine melanocytic tumors: a retrospective study of 53 horses (1988 to 1991). 853 Nov 73

A multistep genetic model of tumorigenesis, based on genetic alterations in benign and primary malignant lesions, has been proposed for neoplasms such as colonic carcinoma. However, evidence for a similar genetic progression in melanoma has relied heavily on findings in cultured lesions or metastases. We have investigated every autosomal arm for loss of heterozygosity in 41 primary cutaneous melanomas and 32 benign melanocytic nevi, and have investigated several chromosome arms that show loss in melanoma in 27 Spitz nevi (a nevus with histological similarities to melanoma). Loss of heterozygosity in primary melanoma was identified most frequently on chromosomes 9p (46%) at loci near the p16INK4 gene, 10q (31%), 6q (31%), and 18q (22%); loss of these chromosome arms were related to the progression of the melanoma. Only two benign melanocytic nevi (both of which showed atypical features on histology) demonstrated genetic alterations, including p9 loss in one case. In addition, two Spitz nevi contained interstitial deletions on chromosome 9p. Our findings show that loss of heterozygosity of 9p is not confined to melanoma, but that other uncultured melanocytic lesions can also display loss of this chromosome arm, and that other genetic changes (e.g., loss of 10q, 6q, and 18q) may be important in conveying the malignant phenotype to melanoma.
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PMID:Allelotypes of primary cutaneous melanoma and benign melanocytic nevi. 856 76

The expression of intercellular adhesion molecule 1 (ICAM-1), a molecule pivotal in many inflammatory and immune paracrine interactions, has been highly correlated with malignant melanoma (MM) progression. Because numerous parallels exist between tissues of neural crest origin and the immune system in the regulation of postmitotic cell survival, ICAM-1 expression was studied in MM and compared with that of B-cell lymphoma/leukemia 2 protein (bcl-2 oncoprotein), an important regulator in prolonging lymphoid cell survival by blocking programmed cell death. Frozen sections from 33 cases were studied by immunoperoxidase techniques: 14 primary MM (five in situ), nine metastatic MM (one epidermotropic), four melanocytic nevi, and six normal skin controls. The percentages of the cells that stained and their intensities (0-4+) were graded. Both ICAM-1 (90%, 3-4+) and bcl-2 (95%, 2-4+) were strongly expressed in all nine metastases, including the epidermotropic disease extension. Bcl-2 strongly decorated the tumor cells in all 14 cases of primary MM (80%, 2-4+); in the five in situ MM, bcl-2 stained the atypical melanocytes at the dermal-epidermal junction (DEJ) and throughout the epidermis (75%, 1-2+). In contrast, ICAM-1 was negative in the in situ MM. ICAM-1 expression became strong (85%, 2-4+) in the dermal component of early invasive disease. Both ICAM-1 and bcl-2 were expressed in melanocytic nevi, decreasing in intensity deep within the dermis as the nevus cells senesced ("matured"). Only bcl-2 was expressed in the normal melanocytes of the six skin controls. These data show that bcl-2 is constitutively expressed in normal melanocytes and melanocytic nevi and persists in the transformed cells of early and late MM. ICAM-1 is expressed only after dermal involvement occurs, both in melanocytic nevi and in invasive MM; it persists in metastatic disease. The coexpression of bcl-2 and ICAM-1 demonstrates another similarity between the immune and neural crest systems, but it does not define or necessarily imply any functional interaction between the two proteins. The intercellular relationship of these two molecules, if any, remains to be investigated.
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PMID:Intercellular adhesion molecule 1 (ICAM-1) and bcl-2 are differentially expressed in early evolving malignant melanoma. 859 46

Alterations in the tumor-suppressor gene p53 are common in many types of human malignancies, but the potential role of p53 in the pathogenesis of cutaneous melanoma is controversial. The gene product, p53 protein, is normally present in very small amounts in noncancerous tissues. Missense mutations lead to accumulation of mutant p53 in the cells, which makes it detectable immunohistochemically in many cancers. Formalin-fixed, paraffin-embedded sections of 14 primary invasive melanomas, 3 cutaneous melanoma metastases, and 10 predominantly intradermal melanocytic nevi were reacted with a panel of three anti-p53 monoclonal antibodies (mAbs) (PAb240, PAb1801, and DO7) and a mAb against Ki-67 (MIB-1), a marker of cellular proliferation. p53 was not detected in morphologically normal epidermal melanocytes or nevus cells. A single primary invasive melanoma, having a very high index of proliferation (Ki-67 expression in > 50% of cells), had diffuse nuclear labeling with all three anti-p53 mAbs used. Abnormalities of p53 expression occur rarely in cutaneous melanomas, but overexpression of p53 may occur in a subset of melanomas with a high index of proliferation.
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PMID:p53 expression is rare in cutaneous melanomas. 860 Jul 97


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