Search PubMed⌕ Search

PubMed · 16299791

Palliative therapy.

Abstract

There are a wide variety of palliative treatments for esophageal cancer. The aim of most treatments is to maintain oral food intake, which should stabilize or even improve quality of life. Stent placement is currently the most widely used treatment modality for palliation of dysphagia from esophageal cancer. Stent placement offers a rapid relief of dysphagia, however, the rate of complications (late hemorrhage) and recurrent dysphagia (stent migration, tumor overgrowth) is relatively high. The scientific evidence to advocate the use of anti-reflux stents for the prevention of gastro-esophageal reflux is currently too low. Photodynamic therapy is mostly used in North America; however, due to the high costs of the treatment, the long-lasting side effects and the necessity of repeated treatments, it is not an ideal treatment for palliation of malignant dysphagia. Nd:YAG laser is a relatively effective and safe treatment modality, although laser treatment is also expensive, technically difficult and requiring repeated treatment sessions at 4-6 weeks intervals. Single dose brachytherapy compares favorably to stent placement in long-term effectiveness and safety. Effective treatment strategies are probably 12 Gy given in one fraction or 16 Gy given in two fractions. Palliative chemotherapy offers response rates in recent trials (including partial and complete responses) ranging from 35% to 50%. Whether palliative chemotherapy also results in a survival benefit is not established yet. For clinical trials on palliation of esophageal cancer, the measurement of quality of life is an important outcome measure. The cancer-specific EORTC QLQ-C30 and the esophageal cancer-specific EORTC-OES-18 are validated measures for establishing quality of life status. For the future, a multimodality approach with stent placement or brachytherapy in combination with chemotherapy may be indicated.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Marjolein Y V Homs, Ernst J Kuipers, Peter D Siersema. 2005-12-01. Palliative therapy.. https://doi.org/10.1002/jso.20366

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Complete loss of PTEN expression as a possible early prognostic marker for prostate cancer metastasis.

The EGF/IGF growth factors are potent mitogens that regulate cell proliferation and cell survival and are involved in prostate cancer development. Using laser microdissection technology and real-time PCR, together with immunohistochemistry, we have explored the growth factor and integrin dependent PI3-kinase/PTEN/Akt signalling pathway in prostate cell lines and tumour samples by analysing EGF-R, IGF1-R, ILK, beta3 integrin, PTEN and p-Akt protein expression. We provide evidence that loss of PTEN expression rather than upregulated EGF/IGF1 receptor expression was responsible for increased p-Akt in neoplastic prostate cells. We therefore compared PTEN expression in patient biopsies at first time diagnosis recruited prospectively (Study I, 112 patients) and patients with confirmed metastasis recruited retrospectively from the Luxembourg cancer registry (Study II, 42 patients). In Study I, loss of PTEN expression at first time diagnosis was found in 26 of 112 patients (23%). In Study II, 25 of the 42 patients (59%) with lymph node metastasis had complete loss of PTEN expression in both the neoplastic glands of the prostate and the invasive prostate cancer cells in the lymph node, and of these 13 (52%) exhibited already loss of PTEN expression at first diagnosis. These findings demonstrate that loss of PTEN expression is an important factor in progression towards metastatic disease and could potentially serve as an early prognostic marker for prostate cancer metastasis.

Adenocarcinoma↗

Tissue factor expression is a clinical indicator of lymphatic metastasis and poor prognosis in gastric cancer with intestinal phenotype.

BACKGROUND AND OBJECTIVES: Tissue factor (TF), which normally safeguards vascular integrity by inducing hemostasis upon injury, has received widespread attention in the pathogenesis of cancer progression and metastasis. Aberrantly expressed TF in cancer cells has been reported to be associated with advanced stages of malignancy in various cancers. METHODS: The expression of TF and microvessel density (MVD) were immunohistochemically evaluated in 207 gastric cancers, and their relationship with clinicopathological features was examined. RESULTS: TF was preferentially expressed (41.8%) in intestinal-type cancer at a significantly higher rate than that in diffuse-type cancer (12.1%, P<0.0001). The expression of TF was associated with advanced stage of disease and showed a positive correlation with a higher rate of lymphatic and venous invasion and lymphatic metastasis in intestinal-type, but not in diffuse-type carcinoma. Moreover, TF expression was associated with high MVD in the tumor and a worse outcome only in intestinal-type carcinoma. CONCLUSIONS: TF may be critically involved in tumor progression in intestinal-type, but not in diffuse-type, gastric carcinoma. The difference in clinical features between these two histological types might be partially dependent on TF expression profile.

Adenocarcinoma↗

Expression profiling identifies microRNA signature in pancreatic cancer.

microRNAs are functional, 22 nt, noncoding RNAs that negatively regulate gene expression. Disturbance of microRNA expression may play a role in the initiation and progression of certain diseases. A microRNA expression signature has been identified that is associated with pancreatic cancer. This has been accomplished with the application of real-time PCR profiling of over 200 microRNA precursors on specimens of human pancreatic adenocarcinoma, paired benign tissue, normal pancreas, chronic pancreatitis and nine pancreatic cancer cell lines. Hierarchical clustering was able to distinguish tumor from normal pancreas, pancreatitis and cell lines. The PAM algorithm correctly classified 28 of 28 tumors, 6 of 6 normal pancreas and 11 of 15 adjacent benign tissues. One hundred microRNA precursors were aberrantly expressed in pancreatic cancer or desmoplasia (p < 0.01), including microRNAs previously reported as differentially expressed in other human cancers (miR-155, miR-21, miR-221 and miR-222) as well as those not previously reported in cancer (miR-376a and miR-301). Most of the top aberrantly expressed miRNAs displayed increased expression in the tumor. Expression of the active, mature microRNA was validated using a real-time PCR assay to quantify the mature microRNA and Northern blotting. Reverse transcription in situ PCR showed that three of the top differentially expressed miRNAs (miR-221, -376a and -301) were localized to tumor cells and not to stroma or normal acini or ducts. Aberrant microRNA expression may offer new clues to pancreatic tumorigenesis and may provide diagnostic biomarkers for pancreatic adenocarcinoma.

Adenocarcinoma↗