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)

We have examined the expression of the cellular apoptosis susceptibility protein, a nuclear transport factor that plays a role in apoptosis and cell proliferation, in benign and malignant melanocytic lesions. Tissue samples of 55 formalin-fixed, paraffin-embedded melanoma (primary n=32, metastatic n=23) and of 27 control cases (junctional dermal, compound, Spitz, Reed, blue nevi, balloon-cell nevus, lentigo maligna) were analyzed by immunohistochemistry with anti-cellular apoptosis susceptibility antibodies. The percentage of cellular apoptosis susceptibility-positive cells as well as the intensity on a four-point scale was evaluated. In normal skin, expression of cellular apoptosis susceptibility was primarily found in the basal cell layer of the epidermis. Benign melanocytic lesions that stained positive for cellular apoptosis susceptibility (13 of 27) showed a homogeneously distributed staining pattern with a mean of 5+/-12% cellular apoptosis susceptibility positive cells. Five out of 7 lentigo maligna melanoma, 11 out of 12 superficial spreading melanoma and all acrolentiginous (n=7) and nodular (n=6) melanoma showed immunoreactivity of medium (++) to high ( ) intensity. Vertical growth phases of primary cutaneous melanoma stained stronger than horizontally growing cell clusters. All metastases (n= 23) stained strongly positive, the staining pattern being inhomogeneous. Cellular apoptosis susceptibility detection in clinical stages according to UICC showed an increase from 43+/-34% cellular apoptosis susceptibility positive cells in stage I, to 53+/-26% in stage II, 68+/-24% in stage III and 72+/-24% in stage IV, respectively. Because the expression of cellular apoptosis susceptibility correlates predominantly with advanced stages of melanoma, staining with anti-cellular apoptosis susceptibility antibodies may be useful for diagnosis of melanoma and possibly as an immunohistochemical prognostic factor in cutaneous melanocytic lesions.
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PMID:Expression of the proliferation and apoptosis-associated CAS protein in benign and malignant cutaneous melanocytic lesions. 1021 71

Basal cell carcinoma is the most frequent of all cancers. Its incidence has risen those last decades because of the increase in sun exposure habits. People with light skin complexion are particularly at risk. Ionizing radiations, arsenicism, various genodermatoses (Gorlin syndrome, xeroderma pigmentosum, nevus sebaceous) are other pre-disposing factors. Basal cell carcinoma usually present as small lesion with a pearly border and telangiectasias. Other clinical types must also be recognized such as the nodular, the infiltrative, the superficial and the pigmented forms. They are usually located on the head and trunk. The prognosis of basal cell carcinoma is usually good since they can be cured by surgical excision and because they usually do not metastasize. However, large, multiple or recurrent basal cell carcinomas can be difficult to treat. In these cases, cryosurgery, radiotherapy or intralesional interferon-alfa may be needed.
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PMID:[Basal cell carcinoma]. 1033 93

The diagnosis of pancreatic cancer usually depends upon symptoms; consequently it is late when there is no chance for cure. At this point, pain, anorexia, early satiety, sleep problems and weight loss are present. Back pain also may be prominent, which predicts unresectability and shortened survival after resection. However, earlier recognition of symptoms of pancreatic cancer might improve early detection of the cancer. For example, 25% of patients have symptoms compatible with upper abdominal disease up to 6 months prior to diagnosis and 15% of patients may seek medical attention more than 6 months prior to diagnosis. These symptoms erroneously may be attributed to problems such as irritable syndrome. Symptoms, however, may be less common. For example a quarter of patients with pancreatic cancer may have no pain at diagnosis, and half, particularly those with pancreatic head tumors, may have little pain compared with patients with body-tail tumors. However, if the tumor is suspected because of predisposing conditions, earlier diagnosis may be possible. These conditions include diseases such as chronic pancreatitis, intraductal papillary mucinous tumor (IPMT), and recent onset of diabetes mellitus, particularly if the diabetes occurs during or beyond the sixth decade. In addition inherited syndromes also are associated with an increased risk of pancreatic cancer including familial pancreatic cancer, hereditary pancreatitis, familial adenomatous polyposis syndrome (FAP) and familial atypical multiple mole melanoma (FAMMM) syndrome (hereditary dysplastic nevus syndrome). Of these conditions, recent onset of diabetes may be the best clue and should be included in a clinical profile of patients prior to the onset of symptoms to identify a high-risk group to apply screening strategies for detection of early disease. Contrary to a clinical aphorism that pancreatic cancer patients are elderly, lean and recently may have developed diabetes, we found that patients who develop pancreatic cancer are overweight prior to onset of symptoms compared to controls (body mass index, 28 vs 25). Forty percent had the diagnosis of diabetes made at the time of diagnosis of pancreatic cancer and more patients with a resectable tumor had diabetes (58%) compared to patients with locally unresectable or metastatic disease (37%). Perhaps, screening overweight persons who have new-onset diabetes may lead to a diagnosis of asymptomatic, early, resectable pancreatic cancer.
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PMID:Pancreatic cancer: clinical presentation, pitfalls and early clues. 1043 7

The authors present a group of six patients with pigmented tumours of the iris and the iridocorneal angle where they performed excision of the tumour by iridectomy (3 patients) or iridiocycletomyy (3 patients). In all six patients with a pigmented tumour of the iris an impaired blood-ocular fluid barrier was found and colouration of the tumour mass by fluorescein. In one patient a heavily pigmented tumour was detected which masked the vascular network. Impaired permeability was found more markedly at the margins. Histological examination confirmed in five instances melanoma of the iris, in one instance a pigmented naevus was involved. During the mean observation period of 32.5 months none of the patients developed a relapse or metastases. Consistent with the extent of the surgical intervention, within 6 months at the latest in all patients the disorder of the blood-ocular fluid barrier improved.
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PMID:[Surgical treatment of pigmented tumors of the iris and iridociliary region]. 1059 77

Patients with high-risk (thick, deeply invasive) primary melanoma were, in the past, managed by wide local excision and elective node dissection or wide local excision alone, with subsequent lymphadenectomy if the regional nodes developed clinically detectable metastases. We recently developed a more logical approach called selective lymph node dissection. To be effective, this requires close collaboration of surgeons, pathologists, and nuclear medicine physicians. The draining lymph node basin is identified preoperatively by lymphoscintigraphy. During surgery, a marker dye (isosulfan blue) and radioactive technetium labeled albumin are injected intradermally around the primary melanoma and the afferent lymphatics are followed up to the first lymph nodes of the ipsilateral regional nodal basin. The surgeon excises the blue-colored and maximally radioactive sentinel nodes and the pathologist critically evaluates these for the presence of a metastatic tumor. If the sentinel nodes are tumor free, no further nodal dissection is undertaken; if a tumor is present, a complete dissection of the nodal basin is performed. We have examined 1,119 sentinel lymph nodes from 669 patients treated by selective lymph node dissection. We identified melanoma cells in sentinel nodes from 126 patients (17.8%). A single node contained tumors in 67% of patients, 2 nodes were positive in 25%, and the remaining 12% of patients had three tumor-containing nodes. Melanoma cells were dispersed singly or in variably sized groups, usually in the peripheral nodal sinus. In around 40% of patients, immunohistochemistry is required to identify minute numbers of tumor cells. With experience, pathologists identify tumors in hematoxylin and eosin (H&E) preparations in an increasing proportion of lymph nodes. Tumor cells are more frequent in the sentinel nodes of patients with primary tumors of deeper Clark level and greater Breslow thickness. Tumor cells must be discriminated from capsular nevus cells, interdigitating dendritic leukocytes, macrophages, and intranodal neural tissues.
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PMID:The pathologist's role in sentinel lymph node evaluation. 1065 39

Light microscopic studies have shown that nevus cell nests and melanoma nests are surrounded by basement membrane (BM) material containing type IV collagen and laminin. This study confirms this by electron microscopy and relates it to proteins which interact with the basement membrane. Nevi except for dysplastic and Spitz nevi, malignant melanomas, and melanoma metastases were studied by immunohistopathology, routine electron microscopy (EM), and immunoelectron microscopy. The lesions were incubated with monoclonal antibody (moAb) against type IV collagen, laminin, and the integrin alpha6 and studied by light microscopy. In addition, melanomas were studied by immuno-EM after incubation with a moAb against matrix metalloproteinase-2 (MMP-2). Nevus cell nests and melanoma nests are surrounded by BM material containing type IV collagen and laminin by immuno-EM. The BM material various in thickness and is amorphous. Type IV collagen, laminin, and MMP-2 are synthesized by melanoma cells as well as adjacent fibroblasts. Destruction or loss of the BM is not mandatory for melanoma invasion or even metastasis. Possibly the BM material is a protective wall for melanoma cells. Interactions between melanocytes and the extracellular matrix of which the BM is a part, can be traced back to the migration of melanocytes from the neural crest.
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PMID:Melanocytes in nevi and melanomas synthesize basement membrane and basement membrane-like material. An immunohistochemical and electron microscopic study including immunoelectron microscopy. 1102 22

Amplification and overexpression of the c-myc gene have been associated with neoplastic transformation in a plethora of malignant tumours. We applied interphase fluorescence in situ hybridization (FISH) with a locus-specific probe for the c-myc gene (8q24) in combination with a corresponding chromosome 8 alpha-satellite probe to evaluate genetic alterations in 8 primary melanomas and 33 advanced melanomas and compared it to 12 melanocytic nevi, 7 safety margins and 2 cases of normal skin. Additionally, in metaphase spreads of 7 melanoma cell lines a whole chromosome 8 paint probe was used. We investigated the functionality of the c-myc gene by detecting c-myc RNA expression with RT-PCR and c-myc protein by immunohistochemistry. 4/8 primary melanomas and 11/33 melanoma metastases showed additional c-myc signals relative to the centromere of chromosome 8 copy number. None of the nevi, safety margins or normal skin samples demonstrated this gain. In 2/7 melanoma cell lines (C32 and WM 266-4) isochromosome 8q formation with a relative gain of c-myc copies and a loss of 8p was observed. The highest c-myc gene expression compared to GAPDH was found in melanoma metastases (17.5%). Nevi (6.6%) and primary melanomas (5.0%) expressed the c-myc gene on a lower level. 72.7% of the patients with c-myc extra copies had visceral melanoma metastases (UICC IV), patients without c-myc gain in 35.0% only. The collective with additional c-myc copies also expressed the gene on a significantly higher level. These results indicate that a c-myc gain in relation to the centromere 8 copy number might be associated with advanced cutaneous melanoma.
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PMID:Extra c-myc oncogene copies in high risk cutaneous malignant melanoma and melanoma metastases. 1113 16

Gestational trophoblastic tumours result from an abnormal proliferation of different types of trophoblasts. The morphological pattern, together with the immunohistochemical aspect, the cytogenetic data and the clinical profile, helps identify each pathological entity. Hydatiform moles represent malformed placentas caused by genetic aberrations of the villous trophoblast. A complete hydatiform mole displays an hydropic degeneration of all the chorionic villi with a more or less marked proliferation of trophoblasts. A partial hydatiform mole is made up of molar vesicles interspersed with normal chorionic villi. In an invasive hydatiform mole or chorioma destruens, molar vesicles penetrate the myometrium giving rise to a mass distorting the uterine wall. A choriocarcinoma is a malignant proliferation of atypical villous trophoblasts without villi formation. Necrosis, haemorrhage, vascular invasion and distant metastases strongly compromise its outcome. A trophoblastic implantation site tumor, clearly less frequent, results from a proliferation of extravillous trophoblasts, particular for their secretion of human placental lactogen hormone (hPL). This tumour, exceptionally malignant, should be differentiated from the exaggerated placental site and its variants. Except for the placental site trophoblastic tumour, and whatever the outcome (benign or malignant), all gestational trophoblastic tumours secrete the beta-subunit of the chorionic gonadotropic hormone (beta-hCG) more or less abundantly. The serum or urinary level of this unit is proportional to the tumour volume and represents a fundamental basis for the follow-up of these tumours. Multidisciplinary care of high-risk cases allows us to cure the disease, and helps the patient recover her reproductive uterine function.
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PMID:[Pathology of gestational trophoblastic tumors]. 1119 98

Malignant melanomas normally arise at the dermoepidermal junction. Development of these tumours in deeper layers of the dermis without having contact with the junction is rare. A small congenital melanocytic nevus localized in the region of the waist band was excised because of mechanical irritation; it had not shown any changes over years. A thorough examination of the whole body did not give any clue to a malignant melanoma. Histologically a compound nevus with the typical architecture of a congenital melanocytic nevus was found. In the deeper dermis there was an isolated nodule of extremely atypical melanocytes with minimal pigmentation of melanin. S100 antigen could be demonstrated throughout the whole tumour whereas HMB45 was only found at the dermoepidermal junction. There was no marking of the tumour cells with a pancytokeratin antibody. A histological relationship between the new tumour and a mixed tumour of the left testicle, which had been excised 3 years ago, could be excluded. We did not find any metastases neither by image-aided methods nor by sentinel lymph node biopsy.
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PMID:[Occult dermal primary melanoma in congenital nevus-cell nevus]. 1124 93

Metastatic disease involving the gastrointestinal tract is a rare pathology and melanoma is the extra-intestinal neoplasm more frequently concerned. Two cases of gastric metastases, revealed by symptoms of upper gastrointestinal bleeding, are reported. In the first case the disease-free interval, after excision of the primary lesion located in the right lower limb, was 13 years; in the second case the primary lesion remained unknown, although it probably originated from a giant congenital nevus of the left foot. Both patients had been affected before by inguinal nodes metastases, treated by radical groin lymphadenectomy; the concomitant multiple metastases to other sites (adrenal glands, retro-peritoneum, liver, lung, small bowel, brain, ovaries) limited surgery to a likely prospect of palliation, conditioning an unfavourable prognosis. Resection of gastrointestinal metastases is justified for the relief of intestinal hemorrhage (as in these reported cases), perforation and obstruction, even if treatment of single non-complicated lesions can have a curative intent. The conclusion is drawn that more aggressive diagnostic and staging procedures are indicated for the early detection of gastrointestinal metastases whenever non-specific abdominal symptoms and a history of melanoma are present.
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PMID:[Gastric metastasis from melanoma. Report of 2 surgically treated cases]. 1126 52


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