Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pretherapeutical multi-step-check method of the diagnosis of malignancy is suggested as a basis of an individual therapy of tumours. It must comprise clinical tumour diagnosis (staging)--the tumour localizations, size and spreading of metastases--histopathological and histochemical grading of malignancy, and histological classification. Results of these diagnostic methods of 186 squamous-cell carcinomas of the head and neck were related to the survival rate. Histochemical LDH and G6PDH reactions and histopathological grading (G 1-group and G 3-group) are important criteria for prognosis.
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PMID:[Multifactorial malignancy analysis--modern knowledge in the practical diagnosis of head and neck tumors]. 649 60

Multi-step check method of the diagnosis of malignancy is applied as a synthesis of results of staging, histological classification, histopathological and histochemical grading, to 210 squamous cell carcinomas of the mesopharynx. Among the examined carcinomas, extended tumours were predominant (61%) (T3; T4). No definite relationship between size and prognosis of the tumours was seen. 81% of the carcinomas had regional lymph node metastases. Their rate of cure (41%) was lower than that of the carcinomas without metastases. Histological grading showed that prognosis of the G 1-carcinomas was superior to that of the G 3-carcinomas. Definite histological grading also enabled clear gradation of malignancy of G 2-carcinomas and carcinomas of the lymphatic tissue after histochemical grading. 5-year survival rate of all the therapy results were found after radical resection (50%) and after combined surgical irradiation therapy (63%). The survival rate of the patients with exclusive irradiation therapy was lower (29%).
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PMID:[Mesopharynx cancers--multifactorial malignancy analysis and therapeutic results]. 652 86

Among 263 patients who suffered from endometrial carcinoma and died of their disease or unrelated causes autopsies showed metastases or recurrences in 165 cases. The conditions for metastatic spread were analysed from the morphological parameters of the tumour. The incidence and localization of above all the lymph node metastases are closely correlated to the grading and the depth of invasion (I 0 to I 3/3) of the primary tumour. The incidence of pelvic lymph node metastases is 8.7% at an invasion depth I 1/3,33% at an invasion depth of I 3/3 of the myometrium. Tumours with the invasion depth I 1/3 show metastases in the para-aortic lymph nodes in 17.3% and at the invasion depth I 3/3 in 50% of the cases. At an invasion depth of I 3/3 17% had exclusively para-aortic lymph node metastases. Pelvic lymph node metastases were found in tumours of the grading G 1 in 5.7% of the cases, in grading G3 in 26% of the cases. The tumour grading and primary extent of the endometrial carcinoma area are closely correlated. At a grading G1 90% of the cases were in stage I/II and only 10% in stage III/or IV. At a grading G3 23.8% of the cases were stage I/II and 76.2% of the cases stage III/IV. Based on the presented analysis it is recommended to supplement the conventional treatment at an invasion depth I 2/3 of I 3/3 with radiotherapy of the para-aortic lymph nodes since 27.3 to 50% of these cases show para-aortic metastases. In 17% of the endometrial carcinomas with an invasion depth I 3/3 exclusively para-aortic lymph node metastases were found which do not respond to conventional treatment.
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PMID:[Conditions of metastatic spread of endometrial cancer: analysis of autopsy findings and clinical data]. 692 9

The overexpression of epidermal growth factor receptor (EGFR) in human epithelial cancers has been associated with aggressive disease, poor patient prognosis, and a high incidence of metastases. In the present study, block copolymer micelles are conjugated with epidermal growth factor (EGF), which acts as both a targeting ligand for the drug carrier and an apoptotic factor against EGFR-overexpressing cancers. Drug-free EGF-conjugated micelles are shown to result in cell-cycle arrest at the G 1 phase and subsequent induction of cell-type-specific apoptosis in EGFR-overexpressing breast cancer cells as demonstrated by flow cytometric analysis. EGF delivered as EGF-conjugated micelles was found to be 13-fold more potent than free EGF; the IC 50 was decreased from 0.98 +/- 0.1 nM for free EGF to 0.076 +/- 0.01 nM for EGF micelles. The apoptotic micelles, however, are non-antiproliferative to cells expressing a low level of EGFR, suggesting that the apoptotic micelles have minimal or no toxicity against normal healthy tissues. Ellipticine, a chemotherapeutic agent, was loaded into the EGF-micelles after it had been shown, using the combination index-isobologram equation, to act synergistically with EGF. A 10-fold increase in EGF content in the ellipticine-loaded micelles lowered the IC 50 of ellipticine in EGFR-overexpressing breast cancer cells by more than 18-fold. The EGF-micelles have the potential to be further pursued as a versatile nanotechnology platform for targeted delivery of a wide range of chemotherapeutic agents as a combination therapy for the treatment of EGFR-overexpressing cancers.
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PMID:Apoptotic epidermal growth factor (EGF)-conjugated block copolymer micelles as a nanotechnology platform for targeted combination therapy. 1786 44

FP3 is an engineered protein which contains the extracellular domain 2 of VEGF receptor 1 (Flt-1) and extracellular domain 3 and 4 of VEGF receptor 2 (Flk-1, KDR) fused to the Fc portion of human immunoglobulin G 1. Previous studies demonstrated its antiangiogenic effects in vitro and in vivo, and its antitumor activity in vivo. In this study, patient-derived tumor tissue (PDTT) xenograft models of primary colon carcinoma and lymphatic and hepatic metastases were established for assessment of the antitumor activity of FP3 in combination with capecitabine. Xenografts were treated with FP3, capecitabine, alone or in combination. After tumor growth was confirmed, volume and microvessel density in tumors were evaluated. Levels of VEGF, and PCNA in the tumor were examined by immunohistonchamical staining, level of thymidine phosphorylase (TP) was examined by ELISA, and levels of related cell signaling pathways proteins expression were examined by western blotting. FP3 in combination with capecitabine showed significant antitumor activity in three xenograft models (primary colon carcinoma, lymphatic metastasis, and hepatic metastasis). The microvessel density in tumor tissues treated with FP3 in combination with capecitabine was lower than that of the control. Antitumor activity of FP3 in combination with capecitabine was significantly higher than that of each agent alone in three xenograft models (primary colon carcinoma, lymphatic metastasis, and hepatic metastasis). This study indicated that addition of FP3 to capecitabine significantly improved tumor growth inhibition in the PDTT xenograft models of primary colon carcinoma and lymphatic and hepatic metastases.
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PMID:Antitumor effects of FP3 in combination with capecitabine on PDTT xenograft models of primary colon carcinoma and related lymphatic and hepatic metastases. 2261 73

Previously, we have identified the RUNX1 gene as hypomethylated and overexpressed in post-chemotherapy (CT) primary cultures derived from epithelial ovarian cancer (EOC) patients, when compared with primary cultures derived from matched primary (prior to CT) tumors. Here we show that RUNX1 displays a trend of hypomethylation, although not significant, in omental metastases compared with primary EOC tumors. Surprisingly, RUNX1 displayed significantly higher expression not only in metastatic tissue, but also in high-grade primary tumors and even in low malignant potential tumors. The RUNX1 expression levels were almost identical in primary tumors and omental metastases, suggesting that RUNX1 hypomethylation might have a limited impact on its overexpression in advanced (metastatic) stage of the disease. Knockdown of the RUNX1 expression in EOC cells led to sharp decrease of cell proliferation and induced G 1 cell cycle arrest. Moreover, RUNX1 suppression significantly inhibited EOC cell migration and invasion. Gene expression profiling and consecutive network and pathway analyses confirmed these findings, as numerous genes and pathways known previously to be implicated in ovarian tumorigenesis, including EOC tumor invasion and metastasis, were found to be downregulated upon RUNX1 suppression, while a number of pro-apoptotic genes and some EOC tumor suppressor genes were induced. Taken together, our data are indicative for a strong oncogenic potential of the RUNX1 gene in EOC progression and suggest that RUNX1 might be a novel EOC therapeutic target. Further studies are needed to more completely elucidate the functional implications of RUNX1 and other members of the RUNX gene family in ovarian tumorigenesis.
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PMID:The RUNX1 transcription factor is expressed in serous epithelial ovarian carcinoma and contributes to cell proliferation, migration and invasion. 2344 98