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)

A rapid, simple, and nonradioactive method for diagnosing point mutations of c-K-ras oncogenes in gastroenterologic cancers is described. This method involved the selective amplification of DNA fragments from cancer tissues of surgical specimens with specific oligonucleotide primers, followed by digestion with restriction enzymes that recognized artificially created or naturally occurring restriction sites. To detect codon 12 mutations, an artificial Msp I site was created by introducing a single nucleotide mismatch into the 5' mutagenesis primer. Using a similar approach, an Hae III site was created to detect codon 13 mutations. Bal I and MBo II sites were used to detect codon 61 mutations. A total of 61 gastroenterologic cancer cases were studied. Of 35 cases of colorectal cancer, 7 showed mutations: 6 at codon 12 and 1 at codon 13. In 1 of 2 cases of cholangiocellular carcinoma, point mutation at codon 12 was found. One case of duodenal cancer showed point mutation at codon 12. No mutations were found in the cases of hepatocellular carcinoma (4), gastric cancer (12), esophageal cancer (3), or pancreatic cancer (2).
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PMID:Mutation analysis of K-ras oncogenes in gastroenterologic cancers by the amplified created restriction sites method. 824 18

The aim of this study was to survey the expression of an embryonic cytokine gene, MK, in the normal organs and neoplastic tissues of adults. Northern analysis showed that MK mRNA was exclusively expressed in the kidney among murine organs including thymus, lung, heart, spleen, liver, and kidney. In situ hybridization analysis revealed that MK expression was localized in the proximal tubules and metaplastic Bowman's epithelium, but not in other nephron segments such as glomeruli, loop of Henle, distal tubules, and collecting ducts. To investigate whether MK expression is a marker of tubular cell lineage, several cell lines originating from renal tubules were tested. No expression of MK was detected in PtK1 and LLC-PK1 cells derived from marsupial and porcine proximal tubules or in MDBK and MDCK cells from bovine and canine distal/collecting tubules. Unexpectedly, the MK gene was expressed in a human renal cell carcinoma line, VMRC-RCW, and the expression was up-regulated in the presence of retinoic acid. To elucidate the involvement of MK in the development of tumors, we further examined its expression in a variety of human neoplastic cell lines: YMB-1-C (breast cancer), EBC-1 (lung squamous cell carcinoma), RERF-LC-OK (lung adenocarcinoma), SBC-3 (lung small cell carcinoma), HSC-2 (mouth squamous cell carcinoma), NUGC-2 (gastric cancer), COLO201 (colon cancer), HepG2 (hepatoma), MIA PaCa-2 (pancreatic cancer), MCAS (ovarian cancer), HeLa (cervical cancer), BeWo (chorionic carcinoma), ITO-II (testicular tumor), T24 (urinary bladder tumor), and G-401 (Wilms' tumor). Strong signals were detected in COLO201, HepG2, ITO-II, T24, G-401, and weaker but distinct signals were detected in YMB-1-C, HSC-2, and MCAS cells. The MK gene was, therefore, widely expressed in neoplastic cells originating from genital organs, intestinal tract, liver, mammary gland, and urinary tract, and the expression was not restricted to adenocarcinomas, but was also observed in other types of tumor cells. These findings suggest that a retinoic acid responsive gene, MK, may play a role in the pathophysiology of renal proximal tubules and tumorigenesis in many types of neoplasms.
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PMID:A retinoid responsive cytokine gene, MK, is preferentially expressed in the proximal tubules of the kidney and human tumor cell lines. 843 39

Pancreatic phospholipase A2 (PLA2) is secreted into the pancreatic juice by pancreatic acinar cells as a proenzyme (proPLA2), which is activated by trypsin. Radioimmunoassays with monoclonal antibodies to PLA2 and proPLA2 were used to examine the serum PLA2 and proPLA2 levels simultaneously in patients with various pancreatic diseases. In healthy subjects, proPLA2 proved to be the major form of the enzyme. The serum PLA2 level were found to be significantly increased in patients with acute pancreatitis, the active phase of chronic relapsing pancreatitis, and the early stage of pancreatic cancer. In the terminal stage of pancreatic cancer the serum PLA2 level became low. In patients with chronic pancreatitis, significant correlations were observed between the levels of factors evaluated by the secretin test and the serum total PLA2 and proPLA2 level, but not the PLA2 level. The serum PLA2 and proPLA2 concentrations, and the proportion of proPLA2 in the total, were within normal ranges in patients with liver cirrhosis, hepatocellular carcinoma, and chronic renal failure. These results suggest that simultaneous measurements of serum PLA2 and proPLA2 are clinically useful for diagnosis and monitoring of the active phase of pancreatitis.
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PMID:Simultaneous determinations of pancreatic phospholipase A2 and prophospholipase A2 in various pancreatic diseases. 844 83

Endoscopic ultrasonography (EUS) was compared to ultrasonography (US) and CT scan (CT) in order to evaluate its role in the diagnosis and the locoregional spread assessment of pancreatic cancer. Sixty-four patients suspected of pancreatic cancer were studied prospectively, and the results of imaging techniques were compared to histology and surgical exploration. There were 49 cases of pancreatic adenocarcinoma, 11 of pancreatitis, 2 of common bile duct carcinoma, 1 lymphoma and 1 hepatocellular carcinoma with peripancreatic metastatic lymph nodes. EUS was significantly more accurate (91%) than CT (66%) and US (64%) for diagnosis of pancreatic cancer. EUS was able to image all 7 cancers less than 25 mm in diameter, US and CT only one. There were 4 false positives with EUS which were all cases of pseudotumorous pancreatitis. For detecting lymph node involvement, EUS was significantly more sensitive (62%) and accurate (74%) than US (8% and 37%) and CT (19% and 42%), respectively. Invaded lymph nodes adjacent to large tumors and micrometastatic involvement were responsible for this lack of sensitivity. EUS was significantly more sensitive (100%) than CT (71%) and US (17%) for detecting venous involvement. The specificity of EUS was lower (67%) because of duodenal bulb stenosis and large tumors. In conclusion, this prospective and comparative study confirms that EUS is an accurate tool for diagnosis and locoregional spread assessment of pancreatic cancer when performed in a reference center. EUS is of particular interest for small tumours. However, EUS does not enable differentiation of pseudotumorous pancreatitis from adenocarcinoma.
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PMID:Endoscopic ultrasonography in the diagnosis and staging of pancreatic adenocarcinoma. Results of a prospective study with comparison to ultrasonography and CT scan. 849 Nov 38

The advanced tumours of the digestive tract are generally less responsive to conventional chemotherapies. Moreover, preliminary results with IL-2 immunotherapy also seem to show a low efficacy. On the basis of our previous studies suggesting s synergistic action between IL-2 and some neurohormones, such as the pineal indole MLT, a clinical trial was performed to investigate the clinical efficacy and tolerability of an immunotherapy with IL-2 plus MLT in patients with advanced neoplasms of the digestive tract. The study included 35 patients (colorectal cancer: 14; gastric cancer: 8; hepatocarcinoma: 6; pancreas adenocarcinoma: 7). Distant organ metastases were present in 31/35 patients. MLT was given orally at a daily dose of 50 mg at 8.00 p.m., starting 7 days before IL-2, which was given subcutaneously at a dose of 3 million IU/day at 8.00 p.m. for 6 days/week for 4 weeks, corresponding to one cycle of immunotherapy. In nonprogressed patients, a second cycle was given after a 21-day rest period. A complete response was achieved in two patients (gastric cancer: 1; hepatocarcinoma: 1). Six other patients obtained a partial response: (gastric cancer: 2; hepatocarcinoma: 2; colon cancer: 1; pancreas cancer: 1). Therefore, the overall response rate was 8/35 (23%). Stable disease was obtained in 11/35 (31%) patients, whereas the remaining 16 patients (46%) progressed. The response rate was significantly higher in untreated patients than in those previously treated with chemotherapy. Toxicity was low in all patients, who received the treatment as a home therapy. This study shows that the immunotherapy with low-dose IL-2 plus the pineal hormone MLT is a new well tolerated and effective therapy of advanced tumours of the digestive tract, mainly in gastric cancer and hepatocarcinoma.
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PMID:Immunotherapy with subcutaneous low-dose interleukin-2 and the pineal indole melatonin as a new effective therapy in advanced cancers of the digestive tract. 851 25

Because they show high levels in hepatocellular carcinoma, alpha-fetoprotein and des-gamma-carboxyprothrombin are clinically useful tumor markers for differentiating hepatocellular carcinoma from other hepatic diseases. The two are useful complementary markers of hepatocellular carcinoma because they do not correlate with each other. A typical marker of pancreatic cancer is carbohydrate antigen (CA) 19-9. Over a period of more than 10 years, many markers resembling CA19-9 have been identified, but none are markedly superior to CA19-9, and the sensitivity of these markers in pancreatic cancer is only 65%-80%. Tumor markers are not useful for the early diagnosis of either hepatocellular carcinoma or pancreatic cancer. They are, however, considered to be useful for monitoring after treatment.
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PMID:[Tumor markers: neoplasmas in digestive organs]. 869 18

Growing evidence indicates that lysosomal Cathepsins D (CD), B (CB) and L (CL) may promote carcinogenesis and tumor progression. Therefore, we evaluated their potential value as biochemical parameters of malignant progression in patients with benign diseases which may undergo malignant transformation, such as liver cirrhosis (LC) and chronic pancreatitis (CHP) as well as in hepatocellular carcinoma (HCC) and pancreatic cancer (DPC). CD, CB and CL serum levels were determined by immunoenzymatic assays in LC, CHP, HCC or DPC patients and correlated with a number of biochemical and clinical parameters of these diseases. CD serum levels were increased in LC, CHP and HCC, but not in the DPC group as compared to normal subjects (NS) (P < 0.01). Interestingly, higher levels of this enzyme were observed in LC patients compared to HCC patients ( P < 0.01). CB serum concentrations were increased in all patient groups (P < 0.01). However no difference was evidenced between benign and malignant diseases. CL serum levels were significantly increased only in DPC as compared to NS (P < 0.01) or CHP patients (P < 0.02) and in HCC as compared to NS (P < 0.01). The evaluation of CD, CB and CL serum pattern in LC, CHP, HCC and DPC patients may be useful as additional biochemical parameters in the differential diagnosis and therapeutic monitoring of these diseases. Prospective clinical investigations to assess the potential value of these enzymes as biochemical markers of malignant progression of LC or CHP are warranted by the present data.
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PMID:Cathepsin D, B and L circulating levels as prognostic markers of malignant progression. 869 62

The aim of the present investigation was to study the origin of the elevated levels of the pancreatic secretory trypsin inhibitor (PSTI) seen in the bloodstream during an acute-phase reaction. PSTI and cationic trypsinogen levels in pancreatic juice and plasma from five patients were measured over 8 days following subtotal pancreatoduodenectomy (Whipple's procedure). Cells from a human hepatocellular carcinoma cell line (Hep G2) and from a human pancreatic cancer cell line (CAPAN-1) were cocultured with endotoxin-stimulated mononuclear white blood cells using a double-chamber technique. Hep G2, CAPAN-1, and mononuclear white blood cells were also cultured as single populations. The median plasma level of PSTI increased from 16.6 micrograms/L at the time of surgery to 155 micrograms/L at the fourth postoperative day. No increase in PSTI levels in pancreatic juice or trypsinogen levels in pancreatic juice and plasma was observed. Culture medium from stimulated hepatocellular carcinoma cells contained significantly elevated levels of PSTI compared with the levels of PSTI from unstimulated cells. Culture medium from pancreatic cancer cells alone contained high levels of PSTI but no difference was observed compared with PSTI levels in medium from stimulated pancreatic cancer cells. The mononuclear white blood cells did not produce PSTI. The results support the view of an extrapancreatic origin of plasma PSTI during the acute-phase reaction and indicate that the liver is the probable source.
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PMID:Extrapancreatic origin of the pancreatic secretory trypsin inhibitor as an acute-phase reactant. 883 Mar 39

Preliminary data would suggest that the pineal hormone, melatonin (MLT), may enhance tamoxifen (TMX) anti-tumour efficacy. Both MLT and TMX have been used as single agents in the palliative treatment of metastatic neoplasms, other than the classical hormone-dependent tumours, without, however, any clear efficacy. On this basis, a phase II study with TMX plus MLT has been performed in untreatable metastatic solid tumour patients. The study included 25 metastatic solid tumour patients other than breast cancer and prostate cancer (six unknown primary tumour; four melanoma; four uterine cervix carcinoma; five pancreatic cancer; three hepatocarcinoma; two ovarian cancer; one non-small-cell lung cancer), for whom no other effective standard therapy was available, because of poor clinical conditions, no response to previous chemotherapies and/or chemotherapy-resistant tumours. Both drugs were given orally every day until disease progression (TMX, 20 mg day-1 at noon; MLT, 20 mg day-1 in the evening). Three patients had a partial response (PR) (12%; 95% confidence limits 2-24%) (one cervix carcinoma; one melanoma; one unknown primary tumour). A stable disease (SD) was achieved in 13 other patients, whereas the remaining nine patients progressed. Performance status (PS) improved in 9/25 patients, whose median score increased from 50% to 70%. Finally, a survival longer than 1 year was observed in 7/25 (28%) patients. This phase II study would suggest that the neuroendocrine combination with TMX plus MLT may have some benefit in untreatable metastatic solid tumour patients, either in controlling cancer cell proliferation or improving the PS.
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PMID:A phase II study of tamoxifen plus melatonin in metastatic solid tumour patients. 891 46

The tumor suppressor genes p53, retinoblastoma (RB), p16, and p15 encode proteins that regulate the cell cycle cooperatively by controlling the transition from G1 to S phase and may play an important role in cell growth and differentiation. To screen for abnormalities in these genes in cancer, we performed genetic analysis in six human pancreatic cancer and five hepatoma cell lines, by single-strand conformation polymorphism (SSCP) analysis, direct sequencing, and the reverse transcriptase-polymerase chain reaction (RT-PCR). All six pancreatic cancer cell lines had p53 mutations, with the concomitant loss of the other normal allele, encoding wild-type p53. Frequent homozygous deletions were found in p16 and p15, but the RB gene was expressed. Four of the five hepatoma cell lines had p53 mutations with loss of the normal allele and aberrant RB. There were no deletions of p16 and p15 in any of the hepatoma cell lines. These findings suggest that alterations in the p53, p16, and p15 genes are common in human pancreatic cancer cell lines, while p53 or RB mutations are common in hepatoma cell lines. Alterations of these tumor suppressor genes may thus be important features in organ-specific carcinogenesis.
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PMID:Alterations in the tumor suppressor genes p53, RB, p16/MTS1, and p15/MTS2 in human pancreatic cancer and hepatoma cell lines. 905 94


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