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PubMed1986

Carcinoembryonic antigen in breast cancer. Clinical review.

Carcinoembryonic antigen is widely used as a tumor marker for gastrointestinal neoplasms. Its role in the management of other tumors is poorly defined. This review considers the place of carcinoembryonic antigen measurement in the management of breast cancer and concludes that sufficient data exist to support its use in clinical practice. Of the many potential uses, the major role for carcinoembryonic antigen measurement in breast cancer is in following patients with advanced disease, especially patients with bone metastases.

Bone Neoplasms↗
PubMed1992

The visualization of gastroenteropancreatic endocrine tumors.

In this review, we evaluate radiological techniques currently used to localize gastroenteropancreatic (GEP) endocrine tumors. We also describe the visualization, using intravenous (IV) administration of two isotope-labeled somatostatin analogues (123I-Tyr3-octreotide and 111In-DTPA-octreotide) of islet-cell tumors in 25 patients and carcinoids in 39 patients. The primary tumor and previously unrecognized distant metastases were visualized in 20 of the 25 patients (80%) and in 37 of the 39 patients (95%). Parallel in vitro detection of somatostatin receptors on those tumors also visualized in vivo showed that ligand binding to the tumor in vivo represents binding to specific somatostatin receptors. The detection of somatostatin receptors on tumors in vivo predicted a good suppressive effect of octreotide on hormonal hypersecretion by these tumors. It is an easy, quick, and harmless procedure that is valuable in the localization of primary endocrine pancreatic tumors and their often radiologically and clinically unrecognized metastases. Future prospective controlled studies comparing this procedure with other radiological investigative techniques should demonstrate its sensitivity and specificity and determine the place of somatostatin receptor imaging in the localization of GEP endocrine tumors.

Angiography↗
PubMed1988

The urokinase type of plasminogen activator in cancer of digestive tracts.

The amounts of urokinase (UK) antigen and tissue plasminogen activator (t-PA) antigen were determined in plasma, urine and tissues of patients with cancer of digestive tracts. Urinary levels of UK, but not those of t-PA increased in patients with cancer, and generally decreased after the removal of cancer by operation. Urinary UK levels kept increasing in patients with recurrence of cancer or with metastasis into liver or peritoneum. Plasma levels of t-PA, but not those of UK decreased in patients with cancer. When the amounts of UK were compared in cancer tissues and their adjacent normal mucosal layer, cancer tissues always had higher levels of UK, but t-PA levels were same between tumor tissues and normal mucosa. The results suggest that the type of plasminogen activator was UK-type in cancer of digestive tracts.

Adenocarcinoma↗
PubMedDate not supplied

Regional treatment of hepatic metastases and hepatocellular carcinoma.

Hepatic metastases represent a common site of dissemination for a number of primary malignancies related in part to the dual blood supply, large blood flow, and receptive environment of the hepatic parenchyma. Although this review focuses on regional therapy, we have included sections on systemic therapy to better interpret the results with intrahepatic therapy. We will also discuss the efficiency of hepatic arterial ligation, embolization, and radiotherapy of hepatic metastases. Primary gastrointestinal neoplasms are particularly prone to produce hepatic metastases. Because colorectal carcinoma metastasizes to the liver in up to 70% of patients with advanced disease, the treatment of hepatic metastases is a relevant topic. We will discuss the systemic and regional therapy of colorectal, gastric, and gallbladder cancers. Breast carcinoma and malignant melanoma frequently metastasize to the liver, and we have described systemic and regional treatments of these diseases. Because sarcomas are often treated by regional therapy, we have included a section on the treatment of hepatic sarcomas. Neuroendocrine tumors (carcinoid and islet cell), although often slow growing, frequently metastasize to the liver and then cause symptomatic problems. Much of the work done with embolization and hepatic ligation in the treatment of hepatic metastases has been performed in neuroendocrine tumors, and these studies, as well as the systemic and regional chemotherapy of hepatic metastases, will be described. The last section concerns the treatment of hepatocellular carcinoma. We have outlined the staging systems used. We then detail the results of systemic and intrahepatic therapy, embolization, and hepatic ligation in the treatment of hepatocellular carcinoma. Because hepatic metastases are a frequent problem, many patients are available for clinical investigation. It is hoped that newer strategies for the treatment of liver metastases will lead to higher response rates and perhaps control of local disease. These therapeutic approaches may also give us leads to the treatment of systemic disease.

Antineoplastic Agents↗
PubMed1986

Suppression of monocyte mediated anti U562 cytotoxicity by soluble factors in the serum of cancer patients and in the supernatant of K562 cell culture.

Anti U562 cytotoxicity of monocytes isolated from blood of patients with alimentary tract cancer was shown to be depressed compared to monocytes of healthy individuals. A serum factor was demonstrated in the patients which depressed the cytotoxicity of healthy donor monocytes. Such suppressive factor was also produced by the K562 cell line and its production was blocked by indomethacin, a prostaglandin synthesis inhibitor, as well as by thymus preparations TFX and Thymex L.

Adult↗
PubMed1984

Effect of taurocholic acid feeding on methyl-nitro-N-nitroso-guanidine induced gastric tumors.

Bile reflux is generally accepted as a causative factor of gastric cancer after partial gastrectomy. The present study was designed to evaluate the promotion, by the per oral administration of taurocholic acid, of methyl-N-nitro-N'-nitrosoguanidine (MNNG)-induced gastric carcinogenesis. MNNG (83 mg/l) was given in the drinking water to half the male Wistar rats during 12 weeks while the other half served as controls. After this treatment half of the MNNG-treated animals and half of the controls were placed under a diet containing 0.2% of taurocholic acid while the other animals received the standard diet. At the 40th week after initiation of MNNG, surviving animals were killed. Their stomachs and their duodenums were observed for macro and microscopic examination. Macroscopically there were 7 animals bearing gastric tumors in the MNNG group and 15 in the MNNG + bile group (P less than 0.05). Microscopically there were 7 animals with severe antral dysplasia in the MNNG group, 7 rats with fundic dysplasia and 18 with severe antral dysplasia in the MNNG + bile group. Both groups developed an identical number of duodenal tumors which were invasive adenocarcinomas or angiosarcomas. In this experiment taurocholic acid significantly promoted gastric carcinogenesis. It is postulated that surgical techniques inducing duodenal reflux in the stomach may produced a 'high risk' group of patients in which a long and careful follow-up is required.

Adenocarcinoma↗
PubMed1983

Primary hepatocellular cancer--present results and future prospects.

Hepatocellular cancer is an enormously difficult clinical problem. This review provides an overview of selected basic and applied aspects of the care of hepatoma patients. Important pathophysiologic and prognostic features are now recognized. Initially, chemotherapy programs focused on the use of those agents commonly employed for gastrointestinal neoplasms (fluoropyrimidines, anthracyclines and alkylators). When employed as a conventional intravenous bolus, only Adriamycin is a reproducibly effective agent. However, because of the unique dual vascular supply of the liver and tumor, the use of intraarterial (IA) infusion chemotherapy has become more popular. In this regard, of promise are the application of IA FUDR and Adriamycin, the use of totally implanted infusion systems, and hepatic artery embolization. Furthermore, combinations of whole liver irradiation with chemotherapy seem efficacious. New directions for the therapy of hepatoma patients will focus on superior drug-radiation combinations, exploration of isotopic immunoglobulin, and hormonal therapy. There is currently no standard therapy for hepatoma patients, but prospects for the future have never been so bright.

Administration, Oral↗
PubMed1990

Radiation therapy for AIDS-related Kaposi's Sarcoma.

Between March 1982 and October 1987, 375 fields in 187 patients with AIDS-related Kaposi's Sarcoma were treated in the Department of Radiation Oncology at the University of California in San Francisco (UCSF). Field sizes ranging from 2 x 2 cm to total skin received doses of 8 Gy in a single fraction to 15-40 Gy in 5-10 fractions. Seventy-four percent of the patients have died. Response to treatment was achieved in over 90% of treated fields, with a median time to progression of 21 months and an actuarial freedom from relapse at 6 months of 69% (97 patients alive). There was no difference in outcome regardless of the fractionation regimen used. Severe reactions were noted in 17% of treated fields, but this incidence was significantly lower when a single fraction of 8 Gy was used (p less than 0.001). Radiation therapy plays an important palliative role in this devastating disease. This review supports the use of a single 8 Gy fraction for all Kaposi's Sarcoma lesions of the skin. Further data regarding single fraction therapy for lesions of other sites are needed.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Surgical treatment of stage IV melanoma.

Surgical therapy plays an important role in the management of selected patients with metastatic melanoma. Patients are frequently symptomatic from metastatic lesions, have few effective therapeutic options, and are faced with dismal outcomes. Surgical resection may provide successful palliation of symptomatic lesions with low morbidity and operative mortality. In carefully selected patients, resections performed with curative intent may result in improved survival if a pattern of disease recurrence suggestive of favorable tumor biology is present, and if complete resection of tumor is achieved. Because the majority of post-surgical metastatic patients eventually relapse and succumb to distant disease, adjuvant immunotherapeutic strategies are currently being evaluated.

Adrenal Gland Neoplasms↗
PubMed2004

The phenotype of gut endocrine tumours.

Endocrine tumours of gut and pancreas tract are rare entities originating from cells of the diffuse endocrine system. The endocrine phenotype is assessed by the expression of general and specific endocrine markers. General endocrine markers associate to organelles like large dense core vesicles (e.g. chromogranin A) and small synaptic-like vesicles (e.g. synaptophysin), or to the cytosol, like neuron specific enolase and protein gene product 9.5 (PGP9.5). The specific markers correspond to the hormones produced by tumour cells. Two major categories of endocrine tumours are identified as (i) well-differentiated and (ii) poorly differentiated neoplasms. Well-differentiated tumours/carcinomas (also known as carcinoids) express all general markers of endocrine differentiation and various hormones. Poorly differentiated endocrine carcinomas lack large dense core vesicles markers (chromogranin A), while widely express synaptophysin and cytosol endocrine markers. The clinical behaviour of endocrine tumours spans from benign to low-grade malignant for well-differentiated tumours/carcinomas to high grade malignant for poorly differentiated carcinomas. The Multiple Endocrine Neoplasia type 1 syndrome (MEN1) gene is involved in the genesis of a proportion of both well- and poorly differentiated sporadic tumours. p53 gene abnormality appears as restricted to poorly differentiated endocrine carcinomas.

Biomarkers, Tumor↗
PubMed2006

Follow-up after surgical treatment for cancer of the gastrointestinal tract.

BACKGROUND: Presently, no evidence-based guidelines for the follow-up of patients after surgery for gastrointestinal cancer are available. As a consequence, follow-up strategies may differ between hospitals depending on preference of physicians. We investigated which follow-up procedures are currently employed after surgery for gastrointestinal cancer in the Netherlands. METHOD: A questionnaire was sent to all surgical departments in the Netherlands. The questionnaire focused on frequency of follow-up visits and diagnostic procedures after surgical treatment for oesophageal, gastric, pancreatic and colorectal cancer and psychosocial issues during follow-up. RESULTS: The response rate was 90% (83/92). In the majority of hospitals, surgeons treated patients with colorectal (100%) and gastric (96%) cancer in their own centre, whereas patients with pancreatic (64%) and oesophageal (61%) cancer were more often referred to a tertiary centre. For all patients treated for gastrointestinal cancer, three to four follow-up visits were made in the first year, followed by at least two annual visits thereafter. After colorectal surgery, blood tests (78%), colonoscopy (75%) and abdominal ultrasound (57%) were frequently performed. In other gastrointestinal malignancies, procedures were in most cases only performed if symptoms occurred. In almost three-quarters of patients, psychosocial problems were observed, which were dealt with by surgeons in two-thirds of patients. The majority of patients treated for gastrointestinal cancer were pre- and postoperatively discussed in a multidisciplinary setting. Oncologists, gastroenterologists and dieticians were the most frequently consulted specialists after surgery for gastrointestinal cancer. CONCLUSION: Patients frequently visit the outpatient clinic after surgery for gastrointestinal cancer in the Netherlands. Whereas follow-up after colorectal cancer surgery focuses on finding recurrent disease and metachronous lesions in the colorectum, this is less clear after oesophageal, gastric and pancreatic cancer surgery. Further studies are needed to establish what is the most effective follow-up protocol after different types of gastrointestinal cancer surgery.

Blood Cell Count↗
PubMed2006

Epigenetic mechanisms and gastrointestinal development.

This review considers the hypothesis that nutrition during infancy affects developmental epigenetics in the gut, causing metabolic imprinting of gastrointestinal (GI) structure and function. Fundamentals of epigenetic gene regulation are reviewed, with an emphasis on the epigenetic mechanism of DNA methylation. Recent data indicate that transient nutritional and other stimuli during critical periods of prenatal and early postnatal development can affect the establishment or developmental maturation of gene-specific DNA methylation, thereby inducing permanent changes in gene expression. Although epigenetic processes are clearly involved in postnatal mammalian GI development, we currently know very little about these mechanisms. Data indicating that epigenetic gene regulation plays an important role in GI development and pathology are reviewed, and suggestions for future research in this area are offered.

Animals↗
PubMed2004

Histone-deacetylase inhibitors induce the cathelicidin LL-37 in gastrointestinal cells.

UNLABELLED: Histone-deacetylase (HDAC) -inhibitors enhance acetylation of core proteins and this is linked to formation of transcriptionally active chromatin in various cells. In this study, the effect of HDAC inhibitors (butyrate, trichostatin A (TSA)) on the expression of the cathelicidin LL-37 in colon, gastric and hepatocellular cells was investigated. METHODS: LL-37 expression was assessed in colon, gastric and hepatocellular cancer cells after treatment with HDAC-inhibitors. In parallel, histone H4 and HMGN2, a non-histone protein, acetylation was evaluated. In addition, the intracellular signalling pathway MEK-ERK was explored. RESULTS: In contrast to normal colon epithelial cells, gastrointestinal cancer cells lacked LL-37 expression. LL-37 was induced following treatment with HDAC-inhibitors in all investigated cell lines. This induction was time-dependent in butyrate-treated cells while TSA exerted a transient effect. Induction of LL-37 by butyrate was paralleled by acetylation of the histone H4 and the non-histone HMGN2. Again, TSA resulted in transient acetylation. Furthermore, inhibition of MEK-ERK blocked HDAC inhibitor-induced LL-37 expression in colonic and gastric cells. CONCLUSIONS: We have previously shown that butyrate induces LL-37 in colon epithelial cells. In the present study, we demonstrate that cathelicidin expression is modulated by HDAC-inhibitors in various gastrointestinal cells including gastric and hepatocellular cells. This is paralleled by changes in the acetylation of distinct core proteins suggesting a common regulatory mechanism of cathelicidin LL-37 regulation in these cells.

Animals↗