Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of urachal carcinoma with elevated serum carcinoembryonic antigen (CEA) level in a 36-year-old man. En bloc resection was performed. The production of CEA was proved histologically. The level of serum CEA returned to the normal value after operation. Seventeen postoperative months the level of serum CEA was noted to be elevated again, and 2 months later symptoms appeared and tumor recurrence was revealed on computer tomographic scan. Radiotherapy and chemotherapy were done without any noticeable response. He died of tumor progression. In our case, serum CEA gave useful information as a tumor marker. It showed specificity for the tumor and helped evaluation of tumor resection as well as detection of tumor recurrence.
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PMID:[Urachal carcinoma producing carcinoembryonic antigen: a case report]. 255 78

Pooled F(ab')2 fragments of three MAbs against distinct epitopes of carcinoembryonic antigen (CEA) were used for radioimmunotherapy of nude mice bearing a subcutaneous human colon carcinoma xenograft. 9-10 d after transplantation when tumor nodules were in exponential growth, 36 mice were treated by intravenous injection of different amounts of 131I-labeled MAb F(ab')2. All 14 mice injected with a single dose of 2,200 (n = 10) or 2,800 microCi (n = 4) showed complete tumor remission. 8 of the 10 mice treated with 2,200 microCi survived in good health for 1 yr when they were killed and shown to be tumor free. Four of nine other mice treated with four fractionated doses of 400 microCi showed no tumor relapse for more than 9 mo. In contrast, all 15 mice injected with 1,600-3,000 microCi 131I-control IgG F(ab')2 showed tumor growth retardation of only 1-4 wk, and 15 of 16 mice injected with unlabeled anti-CEA MAb F(ab')2 showed unmodified tumor progression as compared with untreated mice. From tissue radioactivity distributions it was calculated that by an injection of 2,200 microCi 131I-MAb F(ab')2 a mean dose of 8,335 rad was selectively delivered to the tumor, while the tissue-absorbed radiation doses for the normal organs were: peripheral blood, 2,093; stomach, 1,668; kidney, 1,289; lung, 1,185; liver, 617; spleen, 501; small intestine, 427; large intestine, 367; bone, 337; and muscle, 198. These treatments were well tolerated since out of 19 mice with complete tumor remission only 4 required bone marrow transplantation and 17 were in good health for 6-12 mo of observation. The results demonstrate the selective destruction of established human colon carcinoma transplants by intravenous injection of either single or fractionated doses of 131I-MAb F(ab')2.
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PMID:Ablation of human colon carcinoma in nude mice by 131I-labeled monoclonal anti-carcinoembryonic antigen antibody F(ab')2 fragments. 270 19

The clinical course of colorectal carcinoma may be monitored by tumor markers such as carcinoembryonic antigen (CEA), carcinoma antigen (CA) 19-9 and CA-50. Alkaline phosphatase isozymes were previously used to study the clinical course of testicular and gynecologic tumors. In this study we investigated 8 patients with advanced colorectal carcinoma. Their sera were analyzed for the tumor markers CEA, CA 19-9, CA-50 and three alkaline phosphatase isozymes: the nonspecific liver isozyme LAP, the intestinal isozyme IAP and the placental isozyme PLAP. Rising levels of CEA, CA 19-9 and CA-50 were seen as expected, and PLAP also showed rising levels during tumor progression. LAP remained elevated. This indicates an association between progression of colorectal carcinoma and a raised serum content of alkaline phosphatase isozymes.
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PMID:Significance of alkaline phosphatase isozymes in the monitoring of patients with colorectal carcinoma. 281 31

The expression of blood group-related and tumor-associated antigens was examined in pancreatic adenocarcinomas and in the normal pancreas of hamsters to determine if this expression correlated with the host blood group and/or stage of carcinogenicity, respectively. Pancreatic tumors were induced by 4 weekly treatments of hamsters with N-nitrosobis(2-oxopropyl)amine (BOP) and analyzed immunohistochemically during different stages of tumor progression with polyclonal antibodies (PoAbs) and monoclonal antibodies (MoAbs) against A, B, O and Lewis (Le) isoantigens, including X, Y and CA 19-9 monosialoganglioside (gastrointestinal cancer antigen, GICA), as well as with PoAbs detecting human carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP) and the beta-subunit of human chronic gonadotropin (beta-HCG). The red blood cells of both control and tumor-bearing hamsters expressed AB and Le(a+b+)-like blood group types, as detected by polyvalent antisera. However, none of the MoAbs reacted with the hamster red blood cells. In the pancreas, all PoAbs against blood group antigens reacted with hyperplastic ducts and ductules at very early stages of carcinogenesis, as well as with neoplastic lesions, but not with normal pancreatic cells, except for the acinar cells, which were stained with PoAb-B, PoAb-Lea and PoAb-Leb. None of the MoAbs showed any affinity for the normal pancreatic cells; however, they reacted to various degrees with induced hyperplastic and neoplastic tissue. Reactivities of several MoAbs with malignant cells were greater than those with hyperplastic lesions: MoAb-B was highly reactive with all induced lesions, MoAb-A less reactive, and MoAb-H and MoAb-Ley (which has 6 sugar chains) detected only some cancer cells. Neither of the two MoAb-Lex (with 5 carbohydrate chains) reacted with carcinoma cells, although they did bind to a few hyperplastic cells. Neither MoAb-Lea and MoAb CA 19-9, nor PoAbs against CEA, AFP and beta-HCG, reacted with any normal, hyperplastic or malignant cells. These results demonstrate the differential reactivity of these PoAbs and MoAbs in normal and malignant pancreatic tissue and show that blood group antigens, especially the B isoantigens, are specific markers for induced pancreatic duct tumors in hamsters.
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PMID:Blood-group antigen expression during pancreatic cancer induction in hamsters. 331 27

In Columbus, OH, 46 patients with measurable metastatic colorectal cancer were treated with leucovorin (LV) 80 mg/m2/20 h intravenous (IV) infusion followed by 5-fluorouracil (5-FU) 400 mg/m2 IV bolus daily for three days and then once weekly. Many patients had liver (62%) and/or multisite metastases (53%), carcinoembryonic antigen (CEA) greater than 10 (76%), documented tumor progression before entry (51%), and tumor-related symptoms (36%), but also good performance status (84%). Prior therapy consisted of radiotherapy (RT) in 18%, chemotherapy in 22%, both in 4%, and none in 56%. There were 36% objective responses and 31% stabilization, which we believe is a significant change in the natural history of these patients. Median survival was 8 months. Improved survival was seen in patients with single- rather than multiple-site involvement. Decreasing CEA levels were seen in 59% (always in responders or patients with stable disease), and correlated with longer survival time (11.0 v 5.5 months, P = 0.01). Palliation of tumor related symptoms occurred in 75%, with or without antitumor effect. One patient with prior RT died of neutropenic sepsis after only the three-day load, so we now recommend only weekly therapy in previously radiated patients. Otherwise, toxicity was mild, manifest as weakness in 62%, nausea in 53%, or diarrhea in 47%, which was the most common dose-limiting side effect. The occurrence or absence of toxicity did not predict outcome. Because of equivalent efficacy, mild toxicity, and less expense, this regimen should be considered for patients who desire therapy.
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PMID:Leucovorin plus 5-fluorouracil: an effective treatment for metastatic colon cancer. 349 15

Tumor specimens were obtained from seven patients with large bowel carcinomas at operation of the primary neoplasm and by resection of local recurrences or metastases 2 1/2 to 36 months later. All specimens were evaluated with regard to nuclear DNA distribution as measured by flow cytometry and expression of carcinoembryonic antigen (CEA), secretory component, epithelial IgA, and HLA-DR antigens, as determined by immunofluorescence staining of tissue sections. Both the DNA distributions and the immunohistochemical staining patterns were similar in the primary and secondary tumors. These findings are in keeping with a monoclonal or oligoclonal tumor progression in advanced large bowel carcinoma.
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PMID:Preservation of cytometric DNA distribution and epithelial marker expression after tumor progression of human large bowel carcinomas. 386 Dec 31

Tumour progression in 340 patients with resected gastrointestinal primary tumours was monitored using the gradual increase in carcinoembryonic antigen (CEA) in serum. The commencement of the rise in CEA generally preceded clinical detection of the cancer by several months. The degree to which the rise in CEA correlated with the recurrence of cancer was investigated. There was a marked difference in the distribution of the rises in CEA between local tumour growth and distant metastases. CEA increases of more than 1 microgram CEA/l serum in 10 days occurred exclusively in patients with distant metastases. There was a further marked difference in the distribution of the CEA increase between the group with liver metastases and the groups with peritoneal carcinomatosis or other metastases. The site of the primary tumour had no influence on the CEA increase during formation of metastases.
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PMID:[Carcinoembryonic antigen: diagnosis and tumor progression in gastrointestinal tumors]. 407 92

Aside from imaging techniques several (radio-)immunological analyses are used for tumor diagnosis. Oncofetal antigens, for instance the carcinoembryonic antigen (CEA) and alpha-fetoprotein (AFP), have become the most important substances for many malignancies. However, nearly all of the so-called tumor markers are not suitable for early diagnosis or screening either because of low sensitivity or low tumor specificity. On the other hand follow-up measurements give a very sensitive index of the success of treatment and may indicate tumor progression when other signs are still not present. In some carcinomas and under some clinical circumstances tumor specific markers are available and mandatory for detection and/or staging: AFP in hepatoma, acid phosphatase in metastasizing carcinoma of the prostate and serum thyreoglobulin in differentiated thyroid cancer.
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PMID:[Radioimmunoassays in oncology]. 618 74

CA 125 and CA 19-9 are antigenic determinants associated with human epithelial ovarian carcinomas. Murine monoclonal antibodies have been raised against these determinants, and immunoradiometric assays have been developed to monitor antigen levels in the serum of cancer patients. This study was undertaken to determine whether concomitant measurement of CA 125, CA 19-9, and carcinoembryonic antigen would provide a more precise correlation with tumor progression or regression than could be obtained with any single assay. Among 105 patients with surgically demonstrable epithelial ovarian carcinoma, serum CA 125 levels were elevated (greater than 35 U/ml) in 83%, CA 19-9, levels (greater than 37 U/ml) in 17%, and carcinoembryonic antigen levels (greater than or equal to 2.5 ng/ml) in 37%. Within individual samples, no correlation was found among values for the three markers, but patients with elevated CA 19-9 levels also had increased levels of CA 125. At least one of the three markers was elevated in 90% of the subjects. When 41 patients were monitored serially over 2 to 60 months, alterations in CA 125 levels correlated with disease progression or regression in 94% of instances, whereas alterations in CA 19-9 levels correlated in 33% and alterations in carcinoembryonic antigen levels in 25% of instances. Concomitant measurement of CA 125, CA 19-9, and carcinoembryonic antigen did not prove superior to measurement of CA 125 alone in the monitoring of patients with epithelial ovarian carcinoma.
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PMID:Monitoring human ovarian carcinoma with a combination of CA 125, CA 19-9, and carcinoembryonic antigen. 620 31

Twenty-three patients with unresectable hepatocellular carcinoma were given doxorubicin 60 mg/m2 I.V. day 1 and streptozotocin 0.5 g/m2 I.V. days 1-5 every 3 weeks. This regimen was chosen because of the activity of doxorubicin and nitrosoureas in hepatocellular carcinoma and the ability to administer both drugs in full doses. Twelve patients were fully ambulatory, 14 had normal serum bilirubin, 11 had pathologic proof of cirrhosis, and 11 had no known extrahepatic tumor dissemination. Partial responses lasting 10 and 14 months occurred in two patients (9%), one had stable disease for 15 months, 12 had documented tumor progression within 4 months, and eight died within 6 weeks of the start of chemotherapy. Median survival of all patients was only 3 months (range 0.3-27), but eight (35%) lived more than 1 year. Of these eight, two responded to doxorubicin and streptozotocin, another two to subsequent chemotherapy, and four had no tumor response whatever. More than 90% of the intended doses of doxorubicin and streptozotocin was administered, with severe leukopenia in three patients, moderate thrombocytopenia in one, and moderate proteinuria in nine. There were no drug-related deaths. Various physical, radiologic, and biochemical parameters were employed in detecting tumor response and progression. Initially abnormal physical examination of the liver, hepatic radionuclide and computed tomographic (CT) scans, and serum alpha-fetoprotein levels improved in both responding patients. Tumor progression was detected by physical examination (7/12), radionuclide (10/12) and CT liver scan (3/7), rising alpha-fetoprotein (5/12), and rising carcinoembryonic antigen (3/8). Physical examination and radionuclide liver scan together documented all tumor response and progression. The combination of doxorubicin and streptozotocin has only modest activity in hepatocellular carcinoma and appears no more active than doxorubicin alone.
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PMID:Combination chemotherapy of hepatocellular carcinoma with doxorubicin and streptozotocin. 631 Sep 86


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