Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We wished to identify the efficacy of enucleation (excavation) in the treatment of renal cell carcinoma. Surgical specimens from 26 patients with polar or peripheral lesions, 50 per cent of which were found incidentally by computerized tomography scan, were considered amenable to this form of treatment and were studied by ex situ enucleation after standard radical nephrectomy. Eleven patients were determined to have unsuccessful enucleation after histopathological study demonstrated capsular invasion, vascular invasion, residual tumor in the bed or multicentric tumors. Preoperative computerized tomography assessment did not accurately predict success of enucleation. The presence of a fibrous pseudocapsule of compressed renal parenchyma, which might facilitate a dissection plane and successful enucleation, did not correlate with tumor size. Microscopic examination of pseudocapsular integrity frequently revealed areas of thinning, disruption and penetration by neoplasm. When parenchymal preservation is necessary in the treatment of renal cell carcinoma, as wide a margin of adjacent renal parenchyma as possible should be excised with the tumor. In this study enucleation alone was associated with a significant risk of incomplete excision and, therefore, potential for treatment failure. We do not recommend enucleation in the presence of a normal contralateral kidney.
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PMID:Ex situ study of the effectiveness of enucleation in patients with renal cell carcinoma. 337 98

We report a case of sarcomatoid renal cell carcinoma and simultaneous transitional cell carcinoma of the renal pelvis in a 77 year old man admitted for uroseptic fever persisting for two months. Seven years earlier he underwent cystectomy with ureterosigmoidostomy for transitional cell carcinoma of the bladder. CT scan described a severe hydronephrosis with dilated pelvis, several pseudocystic formations with renal parenchima thinning and absence of contrast excretion. Radical nephrectomy was performed consequent to a clinical diagnosis of uroseptic fever in secondary hydronephrosis due to stenosis of ureterosigmoidostomy. Tumors were suspected on cut section and confirmed by histological examination.
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PMID:[Sarcomatoid carcinoma of the kidney associated with urothelial carcinoma: report of a case with unusual clinical presentation]. 1087 65

A 65-year-old man presented with sudden onset of gross hematuria and urinary retention. Computed tomographic scan (CT) showed a cystic multilocular enhancing lesion (9 cm in diameter) at the left renal hilum causing thinning and lateral displacement of the left renal parenchyma. Left hydronephrosis and a renal calculi were observed. We performed radical nephrectomy suspecting a cystic renal cell carcinoma. Microscopic examination and immunohistochemical studies confirmed the diagnosis of the carcinoid tumor. The tumor cells were fully positive for neuron-specific enolase and keratin, and partially positive for chromogranin-A. One of the resected lymph nodes was positive for metastasis. Additional gastrointestinal tract examinations for carcinoid tumor were negative. However, he was concurrently diagnosed with poorly differentiated prostate cancer and hormonal therapy was started. He is free of recurrent carcinoid tumor nine months postoperatively. This case is the 31st report of renal carcinoid tumors in Japan.
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PMID:[Renal carcinoid tumor presenting as bladder tamponade: a case report and review of the Japanese cases]. 1611 10

To investigate further the antiangiogenic potential of sunitinib for renal cell carcinoma (RCC) treatment, its effects on tumor vasculature were monitored by dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) using an orthotopic KCI-18 model of human RCC xenografts in nude mice. Tumor-bearing mice were treated with various doses of sunitinib, and vascular changes were assessed by DCE-MRI and histologic studies. Sunitinib induced dose-dependent vascular changes, which were observed both in kidney tumors and in normal kidneys by DCE-MRI. A dosage of 10 mg/kg per day caused mild changes in Gd uptake and clearance kinetics in kidney tumors. A dosage of 40 mg/kg per day induced increased vascular tumor permeability with Gd retention, probably resulting from the destruction of tumor vasculature, and also caused vascular alterations of normal vessels. However, sunitinib at 20 mg/kg per day caused increased tumor perfusion and decreased vascular permeability associated with thinning and regularization of tumor vessels while mildly affecting normal vessels as confirmed by histologic diagnosis. Alterations in tumor vasculature resulted in a significant inhibition of KCI-18 RCC tumor growth at sunitinib dosages of 20 and 40 mg/kg per day. Sunitinib also exerted a direct cytotoxic effect in KCI-18 cells in vitro. KCI-18 cells and tumors expressed vascular endothelial growth factor receptor 2 and platelet-derived growth factor receptor beta molecular targets of sunitinib that were modulated by the drug treatment. These data suggest that a sunitinib dosage of 20 mg/kg per day, which inhibits RCC tumor growth and regularizes tumor vessels with milder effects on normal vessels, could be used to improve blood flow for combination with chemotherapy. These studies emphasize the clinical potential of DCE-MRI in selecting the dose and schedule of antiangiogenic compounds.
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PMID:Dynamic contrast-enhanced magnetic resonance imaging of vascular changes induced by sunitinib in papillary renal cell carcinoma xenograft tumors. 1972 85

In an attempt to develop better therapeutic approaches for metastatic renal cell carcinoma (RCC), the combination of the antiangiogenic drug sunitinib with gemcitabine was studied. Using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), we have previously determined that a sunitinib dosage of 20 mg/kg per day increased kidney tumor perfusion and decreased vascular permeability in a preclinical murine RCC model. This sunitinib dosage causing regularization of tumor vessels was selected to improve delivery of gemcitabine to the tumor. DCE-MRI was used to monitor regularization of vasculature with sunitinib in kidney tumors to schedule gemcitabine. We established an effective and nontoxic schedule of sunitinib combined with gemcitabine consisting of pretreatment with sunitinib for 3 days followed by four treatments of gemcitabine at 20 mg/kg given 3 days apart while continuing daily sunitinib treatment. This treatment caused significant tumor growth inhibition resulting in small residual tumor nodules exhibiting giant tumor cells with degenerative changes, which were observed both in kidney tumors and in spontaneous lung metastases, suggesting a systemic antitumor response. The combined therapy caused a significant increase in mouse survival. DCE-MRI monitoring of vascular changes induced by sunitinib, gemcitabine, and both combined showed increased tumor perfusion and decreased vascular permeability in kidney tumors. These findings, confirmed histologically by thinning of tumor blood vessels, suggest that both sunitinib and gemcitabine exert antiangiogenic effects in addition to cytotoxic antitumor activity. These studies show that DCE-MRI can be used to select the dose and schedule of antiangiogenic drugs to schedule chemotherapy and improve its efficacy.
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PMID:Dynamic contrast-enhanced magnetic resonance imaging of sunitinib-induced vascular changes to schedule chemotherapy in renal cell carcinoma xenograft tumors. 2088 92

Dear Editor, Cutaneous leiomyomas (CL) are rare, benign smooth muscle tumors of the skin (1). There are 3 subtypes with different origins and histopathologic features: piloleiomyoma, genital leiomyoma, and angioleiomyoma (2). Pilar leiomyoma is the most common subtype originating from arrector pili muscles of pilosebaceous unit. It presents as painful solitary or multiple papulonodules (2,3). A 30-year-old woman presented to our outpatient clinic with numerous painless, itchy papules on her gluteal region that had been present for 10 years. Dermatologic examination revealed red-brown, smooth, grouped papulonodules on bilateral gluteal regions (Figure 1). These lesions had appeared after intramuscular injections and had increased in number. Family history was unremarkable. A punch biopsy was performed with pre-diagnoses of keloid and tumoral infiltration. Histopathologic examination showed neoplastic infiltration with large bundles of spindle-like smooth muscle cells with acidophilic cytoplasm under epidermis (Figure 2). Neoplastic cells were stained by smooth muscle markers actin and caldesmon (Figure 3). Based on the clinical and histopathological findings the diagnosis of pilar leiomyoma was established. Pelvic and renal ultrasonographic examinations were normal. The patient's lesions were asymptomatic except for mild itching and she is currently in follow-up without any treatment. Pilar leiomyomas mostly manifest around the ages of 10 to 30 and are located on the trunk and extensor surfaces of the extremities. Lesions are firm, red-brown or skin-colored papulonodules with diameters varying from several mm to 2 cm (2). Differential diagnosis includes dermatofibroma, neurofibroma, smooth muscle hamartoma, neuroma, adnexal tumors, and painful papulonodular lesions such as glomus tumor (1,2). Our case clinically resembled keloid with red-brown, stiff nodules with epidermal thinning. In the literature, a patient with cutaneous pilar leiomyoma was diagnosed with eruptive keloid and treated with cryotherapy and intralesional steroid injections before histopathologic verification of pilar leiomyoma. He had multiple painless, red-purple papulonodules on the chest and arms (3). The case of a 53-year-old man with a history of multiple firm and painful lesions on the back showing segmental distribution and diagnosed with keloid-like leiomyoma was also reported (4). CL should be considered in the differential diagnosis of keloid-like lesions with atypical location and that are resistant to treatment. Cutaneous leiomyomas have different clinical presentations and many differential diagnoses, but CL can be diagnosed by histopathological examination. In all CLs, histopathologic examination shows bundles of spindle-shaped smooth muscle cells with eosinophilic cytoplasm, a cigarette-like nucleus, and a perinuclear halo. Smooth muscle markers actin and desmin are routinely positive. Histopathologic examination in our case also revealed bundles of spindle-like smooth muscle cells with large acidophilic cytoplasm; smooth muscle markers actin and caldesmon were positive. While solitary lesions are frequently sporadic cases, multiple lesions may be related to hereditary conditions such as Reed's syndrome (multiple cutaneous and uterine leiomyomatosis), hereditary leiomyomatosis, and renal cell cancer (2). These two hereditary conditions have been reported to be associated with a heterozygous germline mutation in fumarate hydratase gene (4). Our patient was considered a sporadic case due to lack of family history and uterine leiomyoma and normal renal ultrasonography. Treatment of CL depends on the number of lesions and presence of symptoms (1). Surgical excision is the gold standard in the treatment of solitary and self-limiting lesions (2). However, recurrence can be more commonly observed in patients with multiple lesions (1). Drugs targeting smooth muscle contraction such as nifedipine, nitroglycerin, and phenoxybenzamine are recommended for pain management. Methods such as cryotherapy and carbon dioxide laser ablation have been tested but their efficacy was found to be limited (1,2). In our patient, lesions were asymptomatic and few in number; we thus suggested follow-up without any treatment. CL are rare benign smooth muscle tumors of the skin. They are difficult to diagnose by clinical evaluation, but the diagnosis can be established by histopathologic examination. In patients with atypical keloid-like papulonodular lesions like our patient, pilar leiomyoma should be considered and histopathologic examination should be performed for the diagnosis.
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PMID:Cutaneous Leiomyoma Mimicking a Keloid. 3287 39