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)

In recent decades, surgical treatment of familial adenomatous polyposis, chronic ulcerative colitis, and muscle-invasive bladder cancer has undergone a revolution. Specifically, ileoanal reservoir and neobladder have become the new "gold standard" of definitive surgical therapy for these disorders. This article discusses issues in surgical construction, indications, contraindications, perioperative care concepts, and nursing and health professional implications related to these two procedures. These interventions include screening candidates for ileoanal reservoir or neobladder to rule out Crohn's disease or metastatic cancer and educating candidates for continent diversions about the proposed procedure(s) and associated events, potential complications, postoperative exercise, sexual health and function issues, and the benefits of support group participation so they can gain a realistic understanding of ultimate functional outcomes. Questions for future research are addressed.
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PMID:Continent diversions: the new gold standards of ileoanal reservoir and neobladder. 1536 31

Enhancement of the therapeutic effect of conventional drugs is currently an active treatment strategy for breast cancer, as shown in the clinical application of trastuzumab with chemotherapeutic agents, which prolonged survival even for metastatic disease. Cyclo-oxygenase 2(COX-2)inhibitors, which are chemoprevention agents for familial polyposis coli, are now contributing to this strategy in combination with chemotherapeutic and endocrine drugs. As an endocrine application, overexpression of COX-2 contributes to increased expression of aromatase in the breast tumor. In addition, it is also known to promote rich micro-vessels within the tumor through up-regulation of prostaglandin E2(PGE2), which can induce vascular endothelial growth factor(VEGF)and basic fibroblast growth factor(bFGF)in cancer cells, and can directly modulate endothelial cell proliferation. Since both rich vasculature and accelerated estrogen synthesis are thought to contribute to unfavorable conditions for the response to endocrine therapy, inhibiting COX-2 with COX-2 inhibitors is a promising strategy to potentiate endocrine therapy.
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PMID:Novel sensitizing agents: potential contribution of COX-2 inhibitor for endocrine therapy of breast cancer. 1555 Aug 58

Authors report a case of mesenteric fibromatosis, not associated to familial adenomatous polyposis or Gardner's syndrome. It is generally considered benign lesion without metastases, though local recurrences are very frequent. No symptoms are usually referred until compression of the surrounding organs, due to the mass growing, takes place. Surgical therapy is considered treatment of choice.
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PMID:[Mesenteric fibromatosis: a case report]. 1596 Mar 69

Hepatic arterial infusion chemotherapy has been often selected as a therapeutic option for advanced hepatocellular carcinoma with multiple intrahepatic metastases and/or portal vein thrombosis. We successfully treated and obtained CR in the 2 cases of far advanced hepatocellular carcinoma with intraarterial infusion chemotherapy (FAP). Case 1 was a 71-year-old male who had advanced hepatocellular carcinoma with intrahepatic metastasis (IM3) which was recurrent after two surgeries. He received hepatic arterial infusion chemotherapy (FAP: 5-fluorouracil 500 mg/day: continuous infusion, day 1-5, adriamycin 10 mg/day, day 1, CDDP 10 mg/day, day 1). After 10 courses, abdominal CT revealed that the viable lesions had completely disappeared (CR). This patient is still alive with no recurrence after 21 months from the beginning of this treatment. Case 2 was a 74-year-old male who had advanced hepatocellular carcinoma with portal vein thrombi (Vp4) and intrahepatic metastasis (IM3). He received FAP arterial infusion chemotherapy with the same protocol as case 1. After 8 courses of this therapy, CT revealed that these lesions had disappeared (CR). This patient is still alive with no recurrence after 9 months from the beginning of this treatment. For 15 patients with advanced hepatocellular carcinoma using a same protocol, the response rate of this therapy was 33.3% (CR & PR). These findings suggested that combined arterial infusion chemotherapy of FAP may be feasible and a promising modality for the advanced HCC with intrahepatic metastases and/or portal vein thrombosis.
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PMID:[Successful treatment of combined intraarterial (5-fluorouracil and adriamycin and cisplatin) infusion chemotherapy for advanced hepatocellular carcinoma with multiple intrahepatic metastases and/or portal vein thrombosis--two case reports]. 1631 58

Activation of the Wnt signaling pathway initiates the transformation of colorectal epithelial cells, although the transition to metastatic cancer requires angiogenesis. We have investigated the expression of the von Hippel-Lindau (VHL) tumor suppressor in the intestines from humans and mice. Here, we show that VHL expression is regulated by TCF4 and is restricted to the proliferative compartment at the bottom of intestinal crypts. Accordingly, VHL is completely absent from the proliferative intestinal pockets of Tcf4(-/-) perinatal mice. We observed complementary staining of the hypoxia-inducible factor (HIF) 1alpha to VHL in normal intestinal epithelium as well as in all stages of colorectal cancer (CRC). To the best of our knowledge, this is the first report demonstrating the presence of nuclear HIF1alpha in normoxic healthy adult tissue. Although we observed upregulated levels of VHL in very early CRC lesions from sporadic and familial adenomatous polyposis patients - presumably due to activated Wnt signaling - a clear reduction of VHL expression is observed in later stages of CRC progression, coinciding with stabilization of HIF1alpha. As loss of VHL in later stages of CRC progression results in stabilization of HIF, these data provide evidence that selection for VHL downregulation provides a proangiogenic impulse for CRC progression.
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PMID:Interplay between VHL/HIF1alpha and Wnt/beta-catenin pathways during colorectal tumorigenesis. 1640 33

Mesenteric fibromatosis, sclerosing mesenteritis, inflammatory pseudotumor, and extrapleural solitary fibrous tumor constitute a loosely associated group of benign fibrous tumors and tumorlike lesions of the mesentery. These lesions are linked histologically by the presence of fibroblasts or fibrosis and anatomically by their location within the mesentery. Although rare, and distinctly different in pathogenesis and biologic behavior, these fibrous lesions have pathologic and radiologic features that overlap with one another and with more common neoplastic and nonneoplastic lesions of the mesentery. Mesenteric fibromatosis is a locally aggressive, benign proliferative process that may occur sporadically or in association with familial adenomatous polyposis. It most frequently manifests as a focal mesenteric mass and may simulate lymphoma, metastatic disease, or a soft-tissue sarcoma. Sclerosing mesenteritis is a rare idiopathic disorder that most commonly produces a stellate mass within the mesentery and should be differentiated from metastatic disease, specifically metastatic carcinoid, because it frequently responds to conservative or medical management. Inflammatory pseudotumor (inflammatory myofibroblastic tumor) is a benign, chronic inflammatory disorder of unknown cause that manifests as a solid mesenteric mass, indistinguishable from malignancy. Extrapleural solitary fibrous tumor is a tumor of submesothelial origin that is identical to the solitary fibrous tumor of the pleura. When located in the mesentery or peritoneal cavity, extrapleural solitary fibrous tumor has an imaging pattern that must be differentiated from metastatic disease, soft-tissue sarcomas, and other benign and malignant neoplasms of the mesentery and peritoneum. Knowledge of this group of benign fibrous tumors and tumorlike lesions of the mesentery is important in the preoperative evaluation of a mesenteric mass.
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PMID:From the archives of the AFIP: benign fibrous tumors and tumorlike lesions of the mesentery: radiologic-pathologic correlation. 1641 55

Adrenal masses are commonly discovered incidentally in patients with familial adenomatous polyposis, and adrenal malignancies have been rarely reported. Individuals with familial adenomatous polyposis frequently undergo abdominal CT-scan examinations for surveillance or symptoms. Adrenal lesions often are detected unexpectedly and are thus becoming a common clinical problem in this population. Adrenal lesions encompass a heterogeneous spectrum of pathologic entities, including primary adrenocortical and medullary tumors, benign or malignant lesions, hormonally active or inactive lesions, metastases, and infections. When an adrenal mass is detected, the clinician needs to address two crucial questions: 1) is the mass malignant? and 2) is it hormonally active? This article presents three new cases of incidental adrenal lesions in familial adenomatous polyposis, reviews the medical literature for this setting, and provides an overview of the diagnostic clinical approach and management of the adrenal findings in familial adenomatous polyposis patients.
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PMID:An evidence-based, multidisciplinary approach to the clinical considerations, management, and surveillance of adrenal lesions in familial adenomatous polyposis: report of three cases. 1704 48

The patient was a 44-year-old male in whom low anterior resection of the rectum, partial pneumonectomy, and liver biopsy were performed because of suspicion of synchronous liver and pulmonary metastases of rectal cancer which caused familial adenomatous polyposis. Because anticancer drug sensitivity testing by the HDRA method performed on tissue collected from the cancer immediately postoperatively revealed sensitivity to 5-FU and CPT-11, and measurement of nucleic acid metabolizing enzymes showed a high level of DPD, a 5-FU metabolizing enzyme, combination therapy with TS-1 and CPT-11 was started. TS-1, 120 mg/body, was administered on 14 consecutive days followed by a 7-day rest period, and CPT-11, 120 mg/body, was administered on day 1 and day 8. One cycle was defined as 3 weeks,and cycles were repeated. Grade 2 diarrhea occurred, but the CPT-11 dose was reduced to 100 mg/body, and treatment was continued. CR was achieved when the 4th course had been completed. Thoracic and abdominal CT was performed after 4 courses, but no recurrent foci were detected in the residual lung tissue, and all of the metastatic liver foci had resolved. To date 6 courses have been completed, and no relapses have been detected by thoracic CT. We report a case in which it was possible to predict efficacy as a result of treatment based on anticancer drug sensitivity testing and measurements of nucleic acid metabolizing enzymes.
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PMID:[CR of rectal cancer and synchronous liver and lung metastases obtained with TS-1 plus CPT-11 combination therapy--case report]. 1722 Jun 84

Aggressive fibromatoses, also known as desmoid tumours, are rare fibrous tissue proliferations with a tendency for slow, local infiltrative growth. There is an association with Gardner's syndrome and familial adenomatous polyposis. Histologically they are fairly bland with no abnormal mitoses or necrosis. They do not metastasize, but can cause significant morbidity through their locally destructive effects. Magnetic resonance imaging is the method of choice for diagnosis, pre-treatment planning and post-treatment follow-up. Surgical excision with a wide margin is the treatment of choice. However, there is a tendency for local recurrence and repeated excision may result in a poor functional or cosmetic outcome. Radiotherapy is used to reduce local recurrence rates after excision and is also used to treat inoperable tumours. Long-lasting remissions can be obtained. Treatment is now planned using modern three-dimensional conformal techniques, similar to those used in soft tissue sarcoma management. There is no definite dose-response relationship, but doses of 50-60 Gy in 1.8-2 Gy fractions are recommended. Systemic therapy has been used for lesions not controlled by surgery or radiotherapy, or less commonly, as a primary treatment. Tamoxifen and non-steroidal anti-inflammatory agents are used most often as they are relatively non-toxic, but there is limited experience with cytotoxic chemotherapy and biological agents. There are no randomised trials to help guide the management of this locally aggressive 'benign' tumour and treatment decisions are best made by the local soft tissue sarcoma multidisciplinary team.
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PMID:Fibromatosis: benign by name but not necessarily by nature. 1741 39

Somatic mutations of the PIK3CA gene have recently been detected in various human cancers, including sporadic colorectal cancer. However, mutations of the PIK3CA gene in hereditary colorectal cancers have not been clarified. To elucidate the mutation status in familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC), which are the most common hereditary colorectal cancers, we investigated PIK3CA mutations in 163 colorectal tumors, including adenomas, intramucosal carcinomas and invasive carcinomas. For comparison, we also analyzed mutations of the same gene in 160 sporadic colorectal tumors at various histopathological stages. Analysis at exons 1, 7, 9 and 20 of the PIK3CA gene revealed somatic mutations in 21% (8 of 39) of FAP invasive carcinomas, 21% (7 of 34) of HNPCC invasive carcinomas, 15% (8 of 52) of sporadic invasive carcinomas, and 14% (7 of 50) of sporadic colorectal metastases in the liver. Mutations in FAP and HNPCC carcinomas predominantly occurred in the kinase domain (exon 20), while the majority of mutations in sporadic cases occurred in the helical domain (exon 9). Adenomas and intramucosal carcinomas from all patients exhibited no mutations (0 of 148). Our data suggest that PIK3CA mutations contribute to the invasion step from intramucosal carcinoma to invasive carcinoma in colorectal carcinogenesis in FAP and HNPCC patients at a similar extent to that seen in sporadic patients.
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PMID:Mutations of the PIK3CA gene in hereditary colorectal cancers. 1754 93


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