Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 145 cases of intraabdominal disease, a laparotomy was considered the next diagnostic step, but peritoneoscopy was performed instead. In 37 cases with a suspicion of metatastic carcinoma, peritoneoscopy with guided biopsy demonstrated carcinoma in 29. In 32 cases, with biopsy-proven cirrhosis of the liver with high suspicion of a hepatoma, peritonescopy demonstrated the presence of hepatoma in 12. In 28 cases, protracted unexplained jaundice was present; nonsurgical causes for jaundice were found in 15. In 48 cases an exudative (protein greater than 2.5 per 100 ml) ascites was present. In 19 cases, either tuberculosis or carcinomatous implants of the peritoneum were found, and ovarian carcinoma was found in 9. Peritoneoscopy with guided biopsy obviated the need for laparotomy in 90% of these cases.
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PMID:Peritoneoscopy and guided biopsy in the diagnosis of intraabdominal disease. 18 49

After a suspension of tumor pieces was grafted into newborn and adult (CBA X C57BL/6J)F1 and BALB/c mice, the growth of Lewis lung adenocarcinoma and mammary gland adenocarcinoma was inhibited in newborn mice, whereas sarcoma of the rectum (SR-1-75) grew at the same rate in newborn and adult recipients. Neonatal thymectomy stimulated the growth of hepatoma (H-2-73) in newborns. The degree of tumor growth inhibition was age-dependent: The maximum inhibition was observed in 1- to 6-day-old recipients, but later it gradually decreased. The hepatoma (H-2-73) and ovarian carcinoma (OC-1-75) with inhibited growth in newborns and the tumor (SR-1-75) with uninhibited growth had equally low immunogenicity. The data suggested that newborns possess factors that inhibit tumor growth but these factors disappear with increased age of recipients.
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PMID:Nonimmune and immune surveillance. II. Effect of recipient's age, tumor immunogenicity, and neonatal thymectomy on tumor growth inhibition. 27 51

The activity of deoxycytidine kinase (EC 2.7.1.74), an important pyrimidine salvage enzyme, was elevated 5- to 30-fold in human ovarian carcinoma and OVCAR-5 cells, in human colon carcinoma and HT-29 cells, in rat hepatoma 3924A solid tumors and cells, and in rat sarcoma as compared with the respective control normal cells. There was an inverse relationship between cell doubling time and deoxycytidine kinase activity in 8 cancer cell lines, with rapidly growing HL-60 cells (20 hr) showing the highest, and slower-growing lung H69 cells (60 hr) the smallest, increase in enzyme activity. In time-sequence studies in human HL-60, OVCAR-5, PANC-1, and rat hepatoma 3924A cells, there was a significant rise in deoxycytidine kinase activity after 3-6 hr of seeding, with peak increases (3.5- to 4-fold) at 48-72 hr in the log phase in comparison with values of the respective plateau phase cells (96-144 hr). In extracts of various cancer cells, the high deoxycytidine kinase activity was competitively inhibited by difluorodeoxycytidine (DFDC), with Ki = 7 to 30 microM. The Km for deoxycytidine in various carcinoma cell lines ranged from 0.3 to 0.7 mM and addition of DFDC increased the apparent Km from 0.7 to 4 mM. Deoxycytidine kinase activity in human HL-60 cells was inhibited by the end product, dCTP, with IC50 = 3 microM; dCTP elevated the Km for deoxycytidine from 0.35 to 0.9 mM. dTTP reversed the inhibition by dCTP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased deoxycytidine kinase activity in cancer cells and inhibition by difluorodeoxycytidine. 129 79

Tiazofurin (TR), an inhibitor of IMP dehydrogenase, causes remissions and induced differentiation in human leukemia through lowering the concentrations of GTP and dGTP. A deoxycytidine analog, difluorodeoxycytidine (DFDC), is an anti-tumor agent phosphorylated by deoxycytidine kinase, resulting in decreased concentration of dCTP, leading to inhibition of DNA synthesis. In HL-60 cells DFDC induced differentiation and inhibited proliferation in a dose-dependent manner (IC50 = 4 nM); TR provided synergism with DFDC. DFDC inhibited proliferation in OVCAR-5 human ovarian carcinoma cells (IC50 = 25 nM) and colony formation in PANC-1 human pancreatic carcinoma cells (IC50 = 2 nM) and rat hepatoma 3924A cells (IC50 = 22 nM). TR and DFDC are synergistically cytotoxic in hepatoma cells and additive in PANC-1 cells. The two drugs together should be helpful in treating leukemias and solid tumors in humans.
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PMID:Synergistic action of tiazofurin and difluorodeoxycytidine on differentiation and cytotoxicity. 134 74

The anti-proliferative activity of human interferon (HuIFN) was enhanced by dipyridamole, 2,6-bis-(diethanolamino)-4,8-dipiperidinopyrimido-[5,4-d]-py rimidine, when tested against various human tumor cell lines, including KT (breast carcinoma), PLC/PRF/5 (hepatoma), MGC-I, U251-SP and T98 (glioma), HAC-2 and SHIN-3 (ovarian carcinoma), and MM-ICB (melanoma). The enhancement occurred irrespective of the kind of HuIFN used (alpha, beta or gamma) and the original degree of susceptibility of the cells to HuIFN. Even low doses down to 0.01 microM of dipyridamole that had no intrinsic anti-proliferative activity could enhance the effect of HuIFN. The enhancement of HuIFN effects seems not to be caused by induction of HuIFN production, because neither anti-viral activity nor HuIFN antigens were detected in culture medium in cells treated with dipyridamole. Mopidamole, a derivative of dipyridamole lacking one piperidine residue, produced little enhancement of the effects of HuIFN. Among ovarian cancer cell lines tested, the enhancement of the activity of HuIFN by dipyridamole for HAC-2 and SHIN-3 cells was equivalent to or greater than that for 3 chemotherapy agents (adriamycin, vincristine, and a camptothecin derivative). However, neither HOC-21 ovarian cancer cells nor HEC-1 endometrial adenocarcinoma cells were susceptible to any combinations. When MGC-1, U251-SP, and HAC-2 cells were injected into nude mice, the growth of tumors was more markedly inhibited by the subcutaneous administration of HuIFN in combination with oral administration of dipyridamole than by the HuIFN alone. Thus, this combination therapy seems to be worth trying for human cancer, although the enhancement of the effects of HuIFN by dipyridamole varied among the cell lines examined.
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PMID:Dipyridamole enhances an anti-proliferative effect of interferon in various types of human tumor cells. 137 1

A reassessment of the risks of using oral contraceptives regarding cancer of the cervix, endometrium, ovary, breast and biliary system was commissioned in the form of a series of reviews, published in the journal Contraception, June 1991: this is the introduction to the reports. Since 1977, the risks of developing epithelial ovarian cancer and endometrial cancer have been clearly shown to be reduced and that protection persists for years even in ex-pill users. The chance of getting hepatocellular carcinoma is slightly higher in developed countries, still extremely rare; while not noticeably increased in those developing countries that have high liver cancer rates. The likelihood of getting cervical cancer is increased in some studies but not in others, reflecting the difficult problem of controlling of patterns of sexual behavior in this area. Even though broad analyses of breast cancer risks are reassuring, some detailed studies that focus on certain age groups of women do find increased breast cancer. A special multi-center, hospital-based, case-control study in developing countries, sponsored by WHO, concluded that the results of studies on cancer from developing countries are applicable to developing countries as well. So the overall benefits of using oral contraceptives outweigh the risks, both for women in areas where maternal morbidity and mortality are high, because of the effectiveness of the pill in preventing pregnancy; and in industrialized areas, where the benefits of preventing ovarian cancer alone is enough to make pill use safer than other methods, such as the condom. There appears to be no way to predict cancer risks for any subgroup of women who should avoid taking the pill.
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PMID:Oral contraceptives and neoplasia: an introduction. 186 31

We have recently found presence of a high concentration of a novel type of kinin, hydroxyprolyl3-bradykinin (Hyp3-BK) in human tumor ascites in addition to conventional bradykinin (BK). Because of their potential physiological activity, it is of interest to know how these bradykinins can be degraded in ascites. Degradation of two synthetic kinins, BK and Hyp3-BK, added to the ascitic fluid from patients with ovarian carcinoma and hepatoma, were analyzed by reversed phase HPLC. Both kinins were degraded into their desArg9-BK or -Hyp3-BK and desPhe8-Arg-9-BK or -Hyp3-BK products following incubation with the ascitic fluid. The rate of the degradation of BK and Hyp3-BK was the same. The formation of desArg9-BK was completely inhibited by kininase I inhibitor, while the formation of desPhe8-Arg9-BK was not completely inhibited by a kininase II inhibitor. The degradation of both kinins was inhibited completely by EDTA. The results indicate the presence of other metalloprotease(s) which cleaves kinins in the ascitic fluid, in addition to kininase I and kininase II. The carboxypeptidase A and carboxypeptidase B inhibitor, benzyl malic acid, failed to block degradation of both kinins. A rapid cleave of Phe-Arg into Phe and Arg was also found in the ascitic fluid. Thus, the major degradation products of kinins in the ascitic fluid were demonstrated to be either desArg9-BK or Hyp3-BK, desPhe8-Arg9-BK or -Hyp3-BK, phenylalanine and arginine. Lysyl-BK and lysylhydroxyprolyl3-BK were rapidly converted into BK and hydroxyprolyl3-BK by the ascitic fluid.
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PMID:Degradation pathway of kinins in tumor ascites and inhibition by kininase inhibitors: analysis by HPLC. 216 Jan 86

Serum levels of CA 125 and markers reputed as specific for cancers in relevant locations (squamous cell carcinoma, SCC, carcinoembryonic antigen, CEA, CA 19.9, alpha-fetoprotein, AFP) were determined in 107 patients with gastrointestinal (GI) carcinomas. The aim of this study was to assess their individual and combined sensitivities, and the power of CA 125 in excluding primary ovarian epithelial cancer from GI primary. Serum CA 125 levels (in U/ml) ranged from nondetectable to 400 in patients with esophageal, to 570 in those with gastric, and to 300 in patients with colorectal carcinoma. The levels for liver secondaries, pancreatic, and hepatocellular carcinoma were 480, 2,720 and 1,100 U/ml, respectively. Serum SCC antigen was elevated in all patients with esophageal cancer, CEA or CA 19.9 in 52% of patients with gastric cancer and in 63% with liver secondaries, and CEA in 95% of patients with colorectal cancer; whereas serum CA 125 above 65 U/ml was found in 25% of this subgroup, but only in those with already an elevated concentration of specific marker(s). Serum CEA or CA 19.9 was elevated in 71%, CA 125 in 59% of patients with pancreatic cancer; the latter mostly in those with already elevated CEA or CA 19.9. Serum AFP was elevated in 84% and CA 125 in 40% of patients with hepatoma; the latter mostly in those with already an elevated AFP. CA 125 values exceeding 1,000 U/ml were found in 1 patient with pancreatic cancer (2,720 U/ml) and in 2 with hepatoma (1,050 and 1,100 U/ml). These findings illustrate the nonspecificity of the CA 125 antigen, its small if any advantage compared to the specific markers, and they diminish its role as a marker for primary ovarian cancer from GI primary unless it exceeds 2,800 U/ml.
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PMID:Serum levels of CA 125 in patients with gastrointestinal cancers. 248 Jun 31

The murine monoclonal antibody (Mab) against human common epithelial ovarian carcinoma, CF511, was generated by immunising mice with human fetal tissue extract from early first trimester, followed by booster injection of an ovarian cancer cell line. Mab CF511 recognised the 600 kDa sialylated glycoprotein as different from previously known tumour associated-marker antigens. Distribution of the Mab CF511-recognised antigen (CF511 antigen) in various tissues and sera was investigated. In immunohistochemical analysis, Mab CF511 reacted strongly with tumour cells of ovarian serous, clear cell, endometrioid and undifferentiated carcinoma and partially with those of mucinous carcinoma. Mab CF511 also reacted with breast carcinoma as well as lung carcinoma. In normal tissues, Mab CF511 cross-reacted with only five tissues, namely lung, breast, thyroid gland, fallopian tube and uterus. Serum levels of CF511 antigen were tested by ELISA inhibition using Mab CF511. This assay showed the circulating CF511 antigen levels to be elevated in 25 of 36 sera from patients with various clinical stages of common epithelial ovarian carcinoma compared to three of 47 and three of 111 sera from patients with other benign gynaecological diseases, including ovarian cysts, uterine fibroids with or without endometriosis and normal healthy subjects, respectively. For the relation between antigen levels and clinical stages of common epithelial ovarian carcinoma, greater than 34.0% ELISA inhibition was detected in 100% of patients with advanced stages (FIGO III and IV) compared with in 35.3% with early stages (FIGO I and II) patients. While patients with breast carcinoma (100%) and lung carcinoma (100%) also had elevated circulating CF511 antigen levels, patients with hepatoma, colorectal carcinoma and gastric carcinoma had no detectable elevation of antigen. Although the test showed a high degree of specificity, the detection of an elevated CF511 antigen level would not be so helpful in distinguishing patients with ovarian carcinoma from those with either breast carcinoma or lung carcinoma. These data suggest that CF511 antigen is a useful new ovarian tumour marker for diagnosis and management of the disease.
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PMID:Serum levels and biochemical characteristics of human ovarian carcinoma-associated antigen defined by murine monoclonal antibody, CF511. 260 5

Forty-six patients who had been evaluated because of skeletal metastases of unknown origin, were reviewed. Twenty-six of the patients were referred to an orthopedic surgeon before confirmation of the metastases by biopsy; 20 others were referred to an oncology clinic after a diagnosis of bone metastases had been established. A simple diagnostic sequence consisting of a medical history, physical examination, routine laboratory studies, chest roentgenogram, technetium 99m phosphonate bone scintigram, and intravenous pyelogram identified the site of the primary tumor in 14 patients; 7 of the primaries were lung carcinomas, 4 were hypernephromas, 2 were breast carcinomas, and 1 was a prostate carcinoma. In two other patients, the histologic findings from the biopsy study were diagnostic; one had a thyroid carcinoma and one, a prostate carcinoma. Further extensive diagnostic workups revealed the site of origin in only four additional patients; two had hypernephromas which were discovered by computed axial tomography of the abdomen; one had an ovarian carcinoma and one had a hepatoma, both of which were found at laparotomy. On the basis of this study, a simple diagnostic strategy is recommended for patients with histopathologically confirmed skeletal metastases of unknown origin: medical history, physical examination, routine laboratory studies, chest radiograph, and technetium 99m phosphonate bone scintigram, followed by computed axial tomographic examination of the abdomen and pelvis. In female patients, it may be judicious to use mammography. If this regimen fails to reveal the primary site, it is unlikely that it will be identified with further extensive diagnostic procedures.
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PMID:The search for the primary tumor in patients with skeletal metastases of unknown origin. 301 75


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