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

Cancer of the gastrointestinal tract represents a major international health problem. At the present time surgical resection for limited stages of disease represents the only treatment which can consistently provide long-term disease-free survival. Unfortunately, the majority of patients present with either microscopic metastatic disease in distant sites or advanced tumour growth which exceeds the limits of surgical resection. Relatively little progress has been made in the development of effective forms of non-surgical therapy. Gastric cancer, however, has been demonstrated to have greater sensitivity to forms of chemotherapy and radiation therapy than was previously appreciated. During the past decade, more effective forms of palliative therapy have been developed for patients with advanced disease, and approximately 15% of the cases with locally unresectable gastric cancer can now achieve long-term disease-free survival with combined forms of treatment. Unfortunately, similar progress has not been made in the management of pancreatic cancer or advanced colon cancer. The recent experience of the Gastrointestinal Tumor Study Group with the use of combined radiotherapy and chemotherapy for rectal cancer has demonstrated that improved disease-free survival can be achieved for patients with Dukes B and C disease. Overall, the current limited efficacy and considerable toxicity of conventional therapies strongly support the development of new approaches to the management of gastrointestinal cancer; this includes the exploitation of the recent progress that has been made in our understanding of cell proliferation and cell cycle control, and the importance of oncogenes and growth factors for regulation of these processes. Ultimately, our understanding of the molecular genetics of gastrointestinal cancer might allow for development of more effective means for both prevention and treatment at the molecular level.
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PMID:Therapy of gastrointestinal cancer. 391 66

Evaluation of diagnosis and treatment modalities in pancreas cancer is hampered by the lack of a suitable staging system. The current staging protocol of the American Joint Committee is arranged as follows: intrapancreatic disease (stage I), localized invasion (stage II), positive regional lymph nodes (stage III), and distant metastases (stage IV). Primary size is not taken into account and may represent an important determinant of survival, as it does in other malignancies. Primary size as a criterion of operability may assume increasing importance, given the demonstrated accuracy of sonography and computed tomography. Chart review was undertaken of the 119 consecutive patients with pancreas cancer presenting at Grady Hospital between 1976 and 1981. Ninety-one per cent were histologically confirmed. The presence or absence of metastases continues to be the most important factor predicting survival (P less than 0.001). It was demonstrated, however, that patients with primary lesions less than 5 cm lived significantly longer than those with primaries greater than or equal to 5 cm (P less than 0.02). Using the currently recommended American Joint Committee protocol, there was no difference in survival curves among stages, I, II, and III. The median survival times were 7.5 months, 5 months, and 5 months, respectively. Between combined stages I, II, and III and stage IV (median survival, 1.0 month), there was a significant difference (P less than 0.001) in survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Can survival in pancreatic adenocarcinoma be predicted by primary size or stage? 396 22

Intra-abdominal spread of tumor is a common cause of treatment failure in patients with pancreatic cancer. We have reviewed 62 patients with pancreatic cancer undergoing repeat laparotomy in order to learn what factors are associated with the high risk of intra-abdominal metastases. Patients who underwent two or more operative biopsy procedures were at a markedly increased risk of developing intra-abdominal tumor seeding. These metastases were not detectable by preoperative computed tomography scan or ultrasound. This information affirms that multiple biopsies of pancreatic tumors increase the risk of local disease failure, and regimens based on nonoperative staging are likely to incorrectly minimize the extent of tumor involvement.
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PMID:Rapid intra-abdominal spread of pancreatic cancer. Influence of multiple operative biopsy procedures. 398 84

Out of 248 pancreatic cancer patients, 82 with hematogenous metastases were clinicopathologically analyzed. The incidence of hematogenous metastases on laparotomy were 31% in the liver, 1.2% in the lung, and 0.4% in the adrenal gland and navel. The incidence of liver metastasis, which was present in 23% and 46% of the patients with carcinoma of the head of the pancreas and of the body and tail of the pancreas, respectively, was higher than that of carcinomas of the other digestive organs. In the autopsy findings of the cases submitted to tumor resection, early metastases to the liver, lung, cerebellum and ovary were recognized to have occurred postoperatively. A higher rate of liver metastasis with lymph node involvement in the early stage of the disease was peculiar to pancreatic cancer.
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PMID:[Hematogenous metastasis in pancreatic cancer]. 402 Nov 4

An orthotopic xenograft of the human pancreatic tumor was established by inoculating human pancreatic tumor AsPC-1 cells into the duodenal lobe of the pancreas of the athymic nude mouse. Microscopically, the xenograft was formed by a heterogeneous population of tumor cells, displaying moderately to poorly differentiated adenocarcinomas with the latter capable of invading the adjacent pancreatic islets or non-endocrine elements. At 4 weeks post-transplantation, the tumor was detectable as a focal implant at the site of inoculation and thereafter grew progressively leading to extensive visceral invasion and metastasis. In contrast to the subcutaneous xenograft, all the mice (9/9) bearing orthotopically transplanted tumor developed secondary foci in the gut and at the peritoneum, with 7, 6, and 4 animals showing additional kidney, mesenteric lymphnodal, and diaphragm metastases, respectively. Distant metastases in the lungs were found in 3 mice and malignant ascites developed in two. Human pancreas cancer associated antigen was detected in the tumor, serum, and ascitic fluid of the mice at 63 +/- 24 micrograms/gm, 15 +/- 6 micrograms/ml, and 5 micrograms/ml, respectively. The finding of these regional and distant metastases was quite different from that in the animal bearing subcutaneously xenografted tumor where no metastases to internal organs was observed. The results suggest the potential use of this experimental system in tumor biology and antigen expression of human pancreatic cancer in vivo.
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PMID:Characterization of the tumorigenic and metastatic properties of a human pancreatic tumor cell line (AsPC-1) implanted orthotopically into nude mice. 402 65

A 10% increased risk of developing a second cancer was observed among approximately 36,000 persons reported to the Danish Cancer Registry with a cancer of the respiratory system during 1943-80. This estimate is markedly influenced by a striking tendency by physicians not to report or the Cancer Registry not to accept a report of a second lung cancer following a primary lung cancer (14 observed vs. 99 expected). A significant 30% excess of all second cancer was seen after laryngeal cancer (368 vs. 282), whereas the 22% excess following cancer of the nasal cavities and paranasal sinuses did not quite reach the level of statistical significance (95% CI = 0.9-1.6). For cancers of the lung and larynx, second cancers arose mainly in the buccal cavity, bladder, kidney (after lung cancer only) and lung (after laryngeal cancer only). These second cancers may be due to common carcinogenic factors, most likely tobacco. Elevated risks of second cancers of the breast, cervix uteri, and other female genital organs were found consistently. Radiotherapy may have contributed to the increased risk of breast cancer, but the excess risk of cancer of the female genital organs other than the cervix was unexpected. Although not significant, the risk of esophageal cancer following cancer of the larynx was below expectation (1 vs. 4.1), which was surprising because alcohol consumption and smoking are thought to be common risk factors for these 2 sites. Significant excesses of pancreatic cancer were observed following cancers of the lung, larynx, and nasal cavities, which might be due to more careful medical surveillance of these patients or to common risk factors such as cigarette smoking. Finally, the risk of a patient developing liver cancer after lung cancer was significantly elevated (22 vs. 11.6). This increase is unlikely to be due to misdiagnosed metastases from the lung, inasmuch as the risk was generally elevated throughout the observation period.
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PMID:Second cancer following cancer of the respiratory system in Denmark, 1943-80. 408 5

The risk of developing a second primary cancer was evaluated in approximately 64,000 persons diagnosed with cancer of the digestive system in Connecticut during 1935-82. Significant excesses of all second cancers combined were observed following cancer of the esophagus (58 observed vs. 33 expected), small intestine (41 vs. 24), and colon (2,268 vs. 1,714). A slight excess of multiple primaries was observed following cancer of the liver and biliary tract (47 vs. 40). The observed number of second cancers was nearly equal to the expected number for persons initially diagnosed with cancers of the stomach (251 vs. 258), rectum (952 vs. 941), and pancreas (40 vs. 40). Persons with initial cancers of the small intestine, colon, and rectum also had excess second cancers arising primarily in the colon, which suggested the influence of common etiologic factors or possibly misclassified metastases in some. Shared dietary, socioeconomic, or hormonal factors may explain the excess of uterine and ovarian cancers among patients with colon cancer and the excess of breast cancer among patients with colon and rectal cancers. Oral and respiratory cancers occurred more frequently than expected in persons with an initial esophageal cancer, which is likely due to common risk factors of cigarette smoking or alcohol intake, or both. The elevations in cancer of the prostate among males with cancers of the esophagus, small intestine, colon, rectum, liver/biliary, and pancreas are probably artifacts associated with increased medical surveillance of cancer patients. The prostate cancer excesses were limited to the first year after diagnosis of the initial cancer or decreased over time for all but cancer of the colon and small intestines. Increased medical surveillance may also contribute to the excess renal and bladder cancers seen within 5 years of diagnosis of stomach cancer. Excesses were also seen for second pancreatic cancer among small intestine and liver/biliary cancer patients and second kidney and brain cancers among those with colon cancer. The deficits of stomach and rectal cancer among persons initially diagnosed with the same tumors, respectively, were anticipated because surgical removal of the organ is the primary form of treatment. Patients with rectal cancer also had deficits of stomach and pancreatic cancers. Future research should clarify the role of diet, alcohol, metabolic and endocrine factors, and host susceptibility on the risk of second neoplasms following cancer of the digestive system.
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PMID:Second cancer following cancer of the digestive system in Connecticut, 1935-82. 408 13

Metastases to the breast from extramammary carcinomas are rare. Carcinoma of the male breast is generally regarded as primary in origin and uncommon, accounting for less than 0.42% of all malignancies in men. Tow men who presented with breast malignancies in the course of their prostatic carcinoma are described. One was metastasis to the breast from prostatic cancer, the other from pancreatic cancer. The prostatic origin of these carcinomas, was confirmed by histological findings and immunocytochemical demonstration of prostatic acid phosphatase with the avidin-biotin-complex method.
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PMID:[Breast metastases from extramammary malignancies in men]. 409 74

Human pancreatic ductal adenocarcinoma line Capan-1 was studied in tissue culture and the nude mouse. In tissue culture, the neoplastic cells grew as large epithelial-like mucin-producing cells. Subcutaneous and intraperitoneal transplantation of neoplastic cells into nude mice resulted in tumor formation characterized by marked invasiveness and distant metastases. Histologically, the tumor appeared as a well-differentiated mucin-producing adenocarcinoma morphologically resembling the tumor of origin. Chromosomal analysis showed a human karyotype with a chromosome number between 51-61. Lactate dehydrogenase and beta 2-microglobulin used as tumor markers were present in both tissue culture and the serum of tumor-bearing mice. The neoplasm, which was characterized by an increased level of cAMP, had lost completely the ability to respond to secretin stimulation. The tumor grown in the nude mouse was resistant to treatment with 5-fluorouracil, behavior identical to that of the original tumor. Diphtheria toxin resulted in complete tumor destruction. Because Capan-1 tumor grown in the nude mouse shows morphologic, biologic, and biochemical characteristics similar to the tumor of origin, it may be an invaluable tool in furthering understanding of the biology of human pancreatic cancer.
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PMID:Human pancreatic adenocarcinoma line Capan-1 in tissue culture and the nude mouse: morphologic, biologic, and biochemical characteristics. 627 35

Seventeen patients with histologically proven pancreatic cancers were studied in order to clarify the relationship of histologic types to plasma carcinoembryonic antigen (CEA) values. Two cases with marked elevation of plasma CEA values having 6100 ng/ml and 2500 ng/ml, respectively, disclosed histologically acinar cell carcinoma and mixed acinar and ductal cell carcinoma, respectively. Despite of massive hepatic metastases, the other 15 cases with ductal cell carcinoma, including 3 cases with cystadenocarcinoma, adenoacanthoma, and undifferentiated pancreatic cancer, respectively, showed normal or very modest elevation of plasma CEA values. No correlation was obtained between plasma CEA values and several biochemical tests. Two patients with marked elevation of plasma CEA value revealed strong staining in the cancerous areas of the pancreas by using a peroxidase-antiperoxidase staining technique. These findings suggest that acinar cell carcinoma of the pancreas may contribute to increase the circulating plasma CEA value.
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PMID:Plasma carcinoembryonic antigen and acinar cell carcinoma of the pancreas. 631 61


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