Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

L-Asparagine synthetase appears in serum approximately 7 days after the s.c. implantation of 1 X 10(5) cells of Leukemia 5178Y/AR (resistant to L-asparaginase) and increases in activity as the neoplasm grows and metastasizes. The principal source of the enzyme is the primary tumor. After intravranial inoculation of tumor, the rate of leakage of the enzyme is more pronounced than when the subcutaneous, intramuscular, or intraperitoneal routes are used. 1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (NSC 79037), a nitro-sourea effective in the palliation of L5178Y/AR, temporarily halts the influx of enzyme into the blood stream, as does surgical excision of the s.c. tumor nodules. Treatment of mice with L-asparaginase within 24 hr of inoculation of the tumor markedly augments both tumor growth and the rate of penetration of L-asparagine synthetase into the circulation. Several other L-asparagine synthetase into the circulation. Several other L-asparaginase-resistant tumors also were found to spill L-asparagine synthetase into the serum, but the correlation between this phenomenon and the specific activity of the enzyme in homogenates of the tumor was imperfect.
Cancer Res 1976 Sep
PMID:L-Asparagine synthetase in serum as a marker for neoplasia. 1 81

Circulation in the blood stream of neuroblastoma cells was confirmed by establishment of a cell line from the peripheral blood of a child with disseminated disease. The morphologic, enzymatic, and chromosomal pattern of this cell line was similar to a cell line established from the primary tumor on a previous occasion. The peripheral blood smear did not demonstrate tumor cells but increased numbers of atypical monocytes; lymphoblasts were evident, which may have been unrecognized neuroblasts.
Cancer 1977 Jun
PMID:Isolation and characterization of a neuroblastoma cell line from peripheral blood in a patient with disseminated disease. 1 66

In a retrospective study at the University of Louisville Affiliated Hospitals, 42 patients with carcinoid tumors not arising in the anorectal area were identified in ten years (1962-1972). The ileum was the organ most frequently involved with primary tumor (28%). The nonappendiceal gastrointestinal tumors were multiple in 28%, metastatic in 66%, and associated with a second malignancy in 25%. Of the symptomatic small-bowel tumors, 83% were metastatic at the time of diagnosis. Carcinoid syndrome was observed in only two patients, both of whom had liver metastases and elevated urinary 5-HIAA levels. Resections for cure were done on 25 patients, palliative resections on six, and biopsy on six. Six tumors were from autopsy meterial. Among the 24 patients treated and followed up for five years, the survival rate was only 16%. In those patients having resection for cure, the five-year survival rate was 39%, exculding appendiceal tumors. The advanced stage of disease at time of discovery and the dismal prognosis for invasive carcinoids are contrary to many clinicians' impressions of the nature of carcinoid tumors but entirely consistent with several other recent reports (James Ewing Society meeting, April 1973).
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PMID:Clinical aspects of invasive carcinoid tumors. 5 Jun 23

Secondary cell-mediated cytotoxicity generated in vivo against a syngeneic Gross virus-induced lymphoma [(C58NT)D] in WF rats was detected by the 4-hour 51Cr release assay. At 30 days or more following primary tumor cell inoculation, after the tumors had regressed, lymphoid cells had little or no detectable direct cytotoxic reactivity. At rechallenge with tumor cells, high levels of cytotoxicity were detected in the peritoneal exudate, peripheral blood, mesenteric lymph node, and spleen cells. The secondary cellular immune response after challenge developed earlier, reached higher levels, and lasted longer than the primary immune response. The secondary cytotoxic reactivity was shown to be immunologically specific by the use of various tumor cells both as target and inhibitor cells. Treatment of immune spleen cells with specific antiserum to rat T-cells and complement abolished their cytotoxic reactivity, whereas removal of complement receptor-bearing cells or phagocytic cells did not reduct the cytotoxicity. These data demonstrated that specific-memory T-cells persisted for long periods in the lymphoid organs of immune rats and could rapidly become cytotoxic from rechallenge with the tumor.
J Natl Cancer Inst 1976 Jun
PMID:Secondary cell-mediated cytotoxic response to challenge of rats with syngeneic Gross virus-induced lymphoma. 6 41

Both adult (I) and embryonic (II) forms of uridine kinase have been identified in the transplantable EL-4 leukemia of C57BL/6 mice and in the P815Y mastocytoma of DBA/2 mice. Only Species I is found in primary tumor cells of lymphoid orgin (virus-induced feline lymphosarcoma, human acute and chronic lymphocytic leukemia) and in normal calf thymocytes and porcine peripheral blood lymphocytes; Species I was induced 4-fold upon stimulation of the normal blood lymphocytes with phytohemagglutinin. The level of uridine kinase activity in the feline lymphosarcoma of thymus-dependent lymphocyte orgin and childhood lymphocytic leukemia of possible thymus-dependent lymphocyte or null-cell origin was similar to the induced level in phytohemagglutinin-stimulated normal lymphocytes, i.e., thymus-dependent lymphocytes. In contrast lymphocytes of a patient with chronic lymphocytic leukemia of thymus-independent lymphocyte origin had a level of uridine kinase activity comparable to that of the unstimulated normal lymphocytes or thymocytes. The uridine kinase activity in the EL-4 tumor cells was repressed by acute treatment of the mice with 5-azacytidine.
Cancer Res 1977 Apr
PMID:Uridine kinase activities in normal and neoplastic lymphoid cells. 6 93

Hepatomas secreting large amounts of alpha-fetoprotein were induced in Fischer rats by the continuous feeding of 0.06% 3'-methyl-4-dimethylaminoazobenzene. Serum alpha-fetoprotein concentrations in the 59 hepatoma-bearing rats ranged from 92--3260 microgram/ml (mean, 972 microgram/ml; median, 830 microgram/ml) at the time of primary tumor transplantation.
Cancer Lett 1977 Jul
PMID:Induction of hepatomas secreting large amounts of alpha-fetoprotein. 7 Feb 69

Carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP), and carcinoplacental alkaline phosphatase (CPALP) were detected simultaneously in the sera and body fluids of two male patients with gastric carcinoma matestatic to the liver. At autopsy, widely disseminated gastric cancer of Borrmann III type with liver metastases was revealed in both bases. Histologically, they were moderately differentiated tubular and papillary adenocarcinomas with marked cellular atypia and necrosis. In Case 1, the properties of CPALP were identical to Nagao type CPALP, and in Case 2 the Variant type CPALP. Using immunofluorescence, CEA and CPALP were demonstrated in both primary and metastatic cells. However, only in Case 2 was AFP observed in some of the primary tumor cells.
Cancer 1977 Mar
PMID:Carcinoembryonic antigen, alpha-fetoprotein and carcinoplacental alkaline phosphatase in gastric carcinoma metastatic to the liver. 7 44

Leukocyte migration tests under agarose (Clausen technique) were performed in 28 patients tentatively diagnosed as having any malignancy with the use of a 3 M KCl-extract panel prepared from bronchogenic, gastric, colonic, renal, and mammary carcinoma, corresponding normal tissues, carcinoembryonic antigen (CEA), and human encephalitogenic protein (HEP). 17 out of 22 proven carcinoma patients showed sensitization by reaction with optimal concentrated KCl-extract of cancer from the same organ type as their own tumor. In some cases positive reactions could be observed also with normal tissue antigen (NTA) of tumor organ type (7/22) or with an additional carcinoma extract of organ type differing from patients own primary tumor (8/22). Gastrointestinal carcinomas, especially, showed sensitization to CEA (7/12) contrary to nongastrointestinal carcinomas (1/10). With HEP no positive reactivity could be found (0/10). With the use of tumor antigen panel (5 antigens) only few positive reactions (MI less than 0.80 or greater than 1.20) could be observed in 6 patients with nonmalignant diseases (1/30 tests) and 8 healthy blood donors (1/40 tests). A widespread individual screening program using tissue antigens for patients suspected of malignancies could give a pattern of reactivities and improve the recognition of cell-mediated sensitization against tumor tissues.
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PMID:Checking of carcinoma patients with the leukocyte migration technique (LMT) under agarose. 8 Jul 56

Extrahepatic biliary obstruction can be caused by cancer metastatic from the colon to the lymph nodes adjacent to the bile duct. This report details our experience with eight such cases treated at the Massachusetts General Hospital in the last seven years. The interval between resection of the primary tumor and appearance of jaundice averaged 13 months. The location of the obstruction, preferably defined preoperatively by cholangiography, was low on the common duct in three cases and high in the porta hepatis in five. Relief of biliary obstruction was accomplished by biliary-enteric bypass (four cases), internal biliary stenting by permanent indwelling tube (two cases), or by portal irradiation (two cases). In addition to palliating the symptoms of obstructive jaundice, the period of comfortable survival appears to have been extended: the bypassed patients lived 13-38 months. Erosion of tumor into the duodenum, with resulting gastrointestinal hemorrhage, was an additional problem in three patients. Our overall experience illustrates the value of distinguishing this subgroup of patients from the larger number whose jaundice results from extensive liver metastases, and of treating aggressively those with extrahepatic biliary obstruction.
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PMID:Extrahepatic biliary obstruction by metastatic colon carcinoma. 8 27

From 1973--1975, 31 patients with biopsied primary osteogenic sarcoma were treated with preoperative chemotherapy followed by surgical ablation of the primary tumor. Surgery was delayed in order to obtain a custom-fitted prosthetic bone implant in an attempt to avoid amputation. Preoperative chemotherapy included high dose methotrexate (HDMTX) with citrovorum factor rescue (CFR) and adriamycin (T-5 protocol) and was administered for 3 months preoperatively and continued with the inclusion of cyclophosphamide for approximately 5 months postoperatively. At a follow-up period of 30--52 months, 23 of 31 patients (75%) are surviving (21 of 23 with no evidence of disease). Histologic examination of primary tumor removed at surgery revealed varying degrees of tumor destruction (from very little effect to no evidence of viable tumor) attributable to the effect of chemotherapy. The 21 patients that are disease-free survivors had a more complete effect of preoperative chemotherapy on the primary tumor. Some patients achieving favorable effects upon the primary tumor did so only after the dose of HDMTX was escalated to greater than the starting dose of 8 g/m2. Preoperative chemotherapy for all patients with osteogenic sarcoma would seem to offer the following advantages: 1) Evaluation of the effect of HDMTX with CFR on the primary tumor with escalation of the dose of HDMTX until a clinical response is observed, thus defining the dose of HDMTX effective in that patient, to be continued postoperatively as adjuvant therapy; 2) The early use of systemic therapy to eradicate distant microfoci of disease that will eventually kill the patient if not adequately treated by effective chemotherapy; 3) Allow more time for postoperative healing without the need to start adjuvant chemotherapy immediately; and 4) Provide the surgeon time to plan resection surgery. To date, 20 additional patients with biopsy proven osteogenic sarcoma have been treated with more aggressive preoperative chemotherapy (T-7) for approximately 2 1/2 months prior to definitive surgery (resection or amputation). Doses of HDMTX were escalated where necessary and good clinical responses were obtained in 19 of 20 patients. In the majority of patients, no evidence of viable tumor was found on histologic examination of the surgically removed primary tumor. All 20 patients are surviving free of active disease at this brief follow-up period of 4--20 months.
Cancer 1979 Jun
PMID:Primary osteogenic sarcoma: the rationale for preoperative chemotherapy and delayed surgery. 8 51


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