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)

This report summarizes our experience during a four-year period with the repair of 8 thoracic cage and 3 diaphragmatic defects requiring reinforcement with prosthetic material. Defects as large as the entire left hemidiaphragm or the right anterior chest wall including ribs two through six from the midsternum to the midaxillary line were adequately repaired. The technical approach utilized to obtain a secure, nonmobile thoracic cage involved the placement of sutures through drill holes or around ribs, rather than through the periosteum or pericostal soft tissues. Successful diaphragmatic repair was dependent on proper anchoring of the medial border of the prosthesis, placing sutures in the pericardium as necessary. Skin coverage for thoracic cage defects was achieved with widely undermined and advanced local tissue or previously delayed pedicle flaps. All patients had good evidence of chest wall stabilization after operation, and all were removed from mechanical ventilation within three days. One patient died of myocardial infarction twenty days after operation, and a second patient died later of metastatic disease. On the basis of our experience, we conclude that the range of chest wall lesions that can be surgically corrected or palliated is increased by the use of prosthetics implanted with techniques described here.
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PMID:Repair of chest wall defects with prosthetic material. 45 17

Various tumorlike reactions of the oral mucous membranes under the term Epulis are summarized. These histologically different benign or malignant neoplasms of the gingiva are not very frequent. The differential diagnosis on a clinical basis like symptoms and macroscopic appearance is not easy. Sometimes under these harmless appearing lesions highly aggressive and malignant tumors may be hidden; as there are carcinomas, sarcomas, metastases, tumors of the salivary glands or malignant lymphomas. The therapy of choice is the complete removal including the underlaying periosteum. Occasionally the adjacent bone and tooth have also to be resected. Because of the harmless clinical appearance a histological examination is always required. Some clinical and pathohistological impressive examples are presented.
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PMID:[Differential diagnosis of epulis-type changes in the mouth]. 161 53

The role of the lingual periosteum in the spread of tumours is not yet clear. We examined the histological behaviour of 60 cancers of the tongue and floor of the mouth lying close to the mandible. There were no tumour cells in the periosteal lymphatics. This is in accord with clinical experience that tumour invasion of the periosteum is not associated with an increased rate of metastases to the cervical lymph nodes. From our experience, we conclude that (1) a radical resection of the mandible is mandatory for every lesion lying in the gingivo-lingual gutter that invades bone; (2) for tumours close to, but not directly invading the lingual surface of the mandible, marginal resection of the alveolar ridge is appropriate and provides an adequate margin.
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PMID:[Mandibular resection in cancer of the tongue and/or mouth floor]. 191 87

The authors reviewed 76 magnetic resonance (MR) images of 38 patients with osteosarcoma treated with preoperative chemotherapy (intraarterial cisplatin with or without systemic chemotherapy). Histologic maps of the surgical tumor specimens in 33 cases were correlated with either late-chemotherapy or postchemotherapy MR images. There were four MR patterns--dark, mottled or speckled, homogeneous, and cystic--that corresponded to different amounts of tumor matrix, granulation tissue, hemosiderin deposits, fluid-filled cysts, and residual viable tumor. Nested foci of residual viable tumor could not be specifically identified, although tumor progression or skip metastases were accurately depicted in four patients. Other findings included (a) peritumoral edema in the soft tissues and intramedullary space that shrank with chemotherapy, (b) chemotherapy effect in the surrounding soft tissues, (c) a dark rim around the extramedullary component of the tumors corresponding to a collagenous capsule continuous with the periosteum, (d) development of metaphyseal hemorrhages and bone marrow infarcts, and (e) intramedullary vascular channels.
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PMID:Osteosarcoma: MR imaging after preoperative chemotherapy. 229 60

A model system of prostate adenocarcinoma (PA) in Lobund-Wistar rats is described in which the transplanted tumor cells (PA-III) were inoculated sc over the calvaria. A local tumor developed that, when attached to the bone, caused erosion and fragmentation of the bone, with adjacent osteoplastic changes and metastases to the lungs. The attachment of the tumor to the bone was enhanced if the periosteum was scratched during the inoculation of tumor cells. The destructive effect on bone structure was also induced by in vivo transplanted PA-I and PA-IV cells, but not by PA-II cells. In rats that were pretreated with dichloromethylene diphosphonate, the local PA-III tumors developed with metastases to the lungs, but the calvariae were intact.
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PMID:Effects of dichloromethylene diphosphonate on the osteolytic and osteoplastic effects of rat prostate adenocarcinoma cells. 293 88

It is generally considered that mineral loss in the bone must amount to 30 per cent or more before any changes become visible to the naked eye in conventional radiography of the skeleton. Early changes in the mandibular bone during radiation therapy are therefore difficult to detect. Abnormalities of the bone caused by irradiation are vascular and cellular in nature. Morphometry detects the changes earlier than conventional radiography. Nineteen patients with a malignant process in the oral cavity or the naso- or hypopharynx but with no evidence of metastases in the mandibular periosteum or bone marrow were given radiation therapy. They were investigated using morphometry together with orthopantomography. The investigation demonstrated a decrease in the number of trabeculae and an increase in the amount of marrow space and compact bone during irradiation. Thus it is possible to detect early radiographic changes by morphometry, but this method is more laborious than scintigraphy. The abnormalities of the mandibular bone were reversible, which signifies the recovery of bone after irradiation with therapeutic doses.
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PMID:Morphometry of orthopantomographic mandibular bone changes during radiation therapy. 407 49

Nearly all primary prostatic carcinomas have been found to express the androgen receptor (AR) protein, which is the intracellular mediator of androgen action. To gain a better insight into the mechanisms of androgen independence of advanced prostatic carcinoma, it is important to know whether the AR is also present in metastases of androgen-independent tumors. We have assessed the status of the AR and the prostate-specific antigen in 22 metastases of 18 patients with progressive prostate cancer. In 18 cases, the metastases were localized in bone, in 3 cases in the epidural space, and in 1 case in the periosteum. All but one patient had received some kind of endocrine treatment for prostatic carcinoma. Paraffin-embedded tissue sections were stained for the AR following a streptavidinbiotin-peroxidase protocol with the polyclonal antibody PG-21, which is directed against amino acids 1 through 21 of the rat and the human AR. The percentage of AR-positive cells was evaluated on the basis of an arbitrary 4-point scale. All 22 tumor metastases displayed AR positivity. One AR-positive metastatic lesion did not stain for prostate-specific antigen, but in all other metastases, this protein was detected by means of immunohistochemistry. The present study provides evidence that, unlike androgen-independent prostatic carcinoma cell lines, distant prostatic carcinoma metastases do express the AR. These findings indicate that the AR may be involved in the progression of prostate cancer.
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PMID:Distant metastases from prostatic carcinoma express androgen receptor protein. 754 9

Malignant small cell tumor of the thoracopulmonary region (MSCT) was first described in 1979 and has been referred to as the Askin tumor. This malignant neoplasm is a member of the peripheral primitive neuroectodermal tumor (PPNET) family and typically involves the periosteum, soft tissue, and extrapulmonary tissue of the thoracic wall. MSCT may also involve the lung parenchyma by local extension or may arise de novo in peripheral lung tissue. Local recurrence, abdominal involvement by tumor extravasation across the diaphragm, and skeletal metastatic disease are relatively common. However, metastasis to the head and neck region and in particular to the oral cavity is extremely rare. We present a recurrent intrapulmonary MSCT with metastasis to the oral cavity in an adolescent Hispanic boy, and review the literature regarding this member of the PPNET family. Differentiation from neuroblastoma may be made based on immunoreactivity for beta 2 microglobulin and HBA71 and lack of immunoreactivity for chromogranin in PPNET and MSCT. Ultrastructural features commonly seen in MSCT and PPNET are round to ovoid tumor cells with occasional cytoplasmic processes with relatively few pleomorphic dense core granules. These tumors lack the gangliocytic and Schwann cell differentiation that is characteristic of neuroblastoma. MSCT and PPNET have a common reciprocal cytogenetic translocation [t(11;22)q(24;q12)], which is shared with Ewing's sarcoma. Prognosis in MSCT is quite dismal, with a 2-year survival of 38% and a 6-year survival of only 14%.
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PMID:Recurrent intrapulmonary malignant small cell tumor of the thoracopulmonary region with metastasis to the oral cavity: review of literature and case report. 757 Oct 88

We report 25 cases of a peculiar sclerosing epithelioid variant of fibrosarcoma (SEF) simulating an infiltrating carcinoma. The tumors occurred primarily in the deep musculature and were frequently associated with the adjacent fascia or periosteum. The patients' ages were 14 to 87 years (median, 45). Fourteen were male and 11 female. The tumors were located in the lower extremities and limb girdles (12 cases), trunk (9), upper limb girdles (2), and neck (2). They measured 2 to 14.5 cm in greatest dimension (median size, 7 cm) and were gray to white and firm. Histologically, the lesions were characterized by a proliferation of rather uniform, small, slightly angulated, round to ovoid epithelioid cells with sparse, often clear cytoplasm arranged in distinct nests and cords. In all cases there was prominent hyaline sclerosis, sometimes reminiscent of osteoid or cartilage and foci of conventional fibrosarcoma. Occasional myxoid zones with cyst formation and foci of hyaline cartilage, calcification, and metaplastic bone were also seen. Mitotic figures were generally scarce. Vimentin was detected in 13 of 14 cases, epithelial membrane antigen in seven, S100 protein in four, and neuron-specific enolase in two. Cytokeratins were detected with AE1/AE3 and CAM 5.2 in two cases. Leukocyte common antigen, CD68 antigen, HMB45, desmin, and alpha-smooth muscle actin were negative in all cases. In 13 of 14 cases, 75% or more of the cells stained for proliferating cell nuclear antigen (PCNA). Ki67 immunostaining with MIB 1 showed low proliferative activity in all cases, averaging 5% of tumor cells or less. In all cases, p53 was detected by immunohistochemical methods; bcl-2, an antiapoptosis marker, was detected in more than 90% of the cells in 11 of 12 cases. Ultrastructurally, both the epithelioid and spindled tumor cells had features of fibroblasts. Follow-up in 16 cases ranging from 13 months to 17 years 3 months (median, 11 years 4 months) revealed persistent disease or local recurrences in 53% of patients and metastases in 43%. The metastases were to the lungs (4 cases), skeleton (3), chest wall/pleura (3), pericardium (1), and brain (1). Four patients died of disease, four were alive with disease, two were known to be alive but disease status unknown, and six had no evidence of further disease at last follow-up. The data suggest that SEF is a relatively low-grade fibrosarcoma; yet it is fully malignant despite the presence of histologically benign-appearing foci. The proliferation markers PCNA and Ki67 did not correlate with prognosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sclerosing epithelioid fibrosarcoma. A variant of fibrosarcoma simulating carcinoma. 766 Dec 86

The presence of bone metastases predicts the presence of pain and is the most common cause of cancer-related pain. Although bone metastases do not involve vital organs, they may determine deleterious effects in patients with prolonged survival. Bone fractures, hypercalcaemia, neurologic deficits and reduced activity associated with bone metastases result in an overall compromise in the patient's quality of life. A metastasis is a consequence of a cascade of events including a progressive growth at the primary site, vascularization phase, invasion, detachment, embolization, survival in the circulation, arrest at the site of a metastasis, extravasion, evasion of host defense and progressive growth. Once cancer cells establish in the bone, the normal process of bone turnover is disturbed. The different mechanisms responsible for osteoclast activation correspond to typical radiologic features showing lytic, sclerotic or mixed metastases, according to the primary tumor. The release of chemical mediators, the increased pressure within the bone, microfractures, the stretching of periosteum, reactive muscle spasm, nerve root infiltration and compression of nerves by the collapse of vertebrae are the possible mechanisms of malignant bone pain. Pain is often disproportionate to the size or degree of bone involvement. A comprehensive assessment including a trusting relationship with the patient, taking a careful history of the pain complaint, the characteristics of the pain, the evaluation of the psychological status of the patient, neurological examination, the reviewing of diagnostic studies and laboratory findings, and individualization of the therapeutic approach, should precede any treatment. Radiotherapy is the cornerstone of the treatment. Low doses given in a single session are safe and effective, and reduce distress and inconvenience associated with repeated session. Radioisotopes are more imprecise in delivering specific doses of radiation, but have less toxicity and easy administration as well as effectiveness in subclinical sites of metastases, although storage, dispensing and administration should be under strict control. Chemotherapy and endocrine therapy are difficult to measure in terms of pain relief. Prophylactic fixation surgery can lead to improved survival and quality of life of patients with bone metastases. Surgical treatment should be undertaken when fracture occurs. Careful selection of patients for surgical spinal decompression is required. The potential benefits of surgical interventions have to be tempered with patient survival. The use of analgesics according to the WHO ladder is recommended. There is no clear evidence that non-steroidal anti-inflammatory drugs (NSAIDs) have a specific efficacy in malignant bone pain. The difficulty with incident pain is not a lack of response to systemic opioids, but rather that the doses required to control the incidental pain produce unacceptable side-effects at rest. Alternative measures are often required. The inhibition of bone resorption and hypercalcaemia can be reduced by the use of bisphosphonates. This class of drugs potentiate the effects of analgesics in improving metastatic bone pain. Invasive techniques are rarely indicated, but may provide analgesia in the treatment of pain resistant to the other modalities. Neural blockade should never be used as the sole modality for malignant bone pain, but should be considered as a helpful in specific pain situations. Careful appraisal and the application of a correct approach should enable the patient with bone metastases to obtain an acceptable pain relief despite the advanced nature of their malignant disease.
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PMID:Malignant bone pain: pathophysiology and treatment. 906 7


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