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1  WT-1 expression was observed in the primary renal tumor.
2 atment and more than 2.0-fold in the primary renal tumor.
3 ilms tumor (WT) is the most common pediatric renal tumor.
4 al Ewing's sarcoma (PNET/EES) is a very rare renal tumor.
5 sion of cyclin D1, a common feature of human renal tumors.
6  protein kinase pathways in brain but not in renal tumors.
7  for diagnosing, characterizing, and staging renal tumors.
8 n an increased detection of incidental small renal tumors.
9 s in 5 families with unilateral and solitary renal tumors.
10  significant uterine fibroids and aggressive renal tumors.
11 n alphavbeta3 expression and angiogenesis in renal tumors.
12 rizes current developments in the imaging of renal tumors.
13 t somatic BHD mutations are rare in sporadic renal tumors.
14 r understanding the origins of nonhereditary renal tumors.
15 ere found to be elevated in the TSC2-related renal tumors.
16 I clinical trials for the treatment of small renal tumors.
17 radiofrequency ablation for the treatment of renal tumors.
18 d is not yet widely utilized in the study of renal tumors.
19 iderable interest in the treatment of select renal tumors.
20 is peptide also inhibits the invasiveness of renal tumors.
21 ocation is cytogenetically balanced in these renal tumors.
22 found to develop variable size and number of renal tumors.
23 14.3, an area known to be lost in hereditary renal tumors.
24  months of estrogen treatment and in primary renal tumors.
25 ns from 5 patients with no family history of renal tumors.
26 enal cell carcinoma and no family history of renal tumors.
27 r cell carcinoma), and 10 patients had other renal tumors.
28 eat promise in the differential diagnosis of renal tumors.
29  solitary kidney or in the face of bilateral renal tumors.
30  costs for patients with small (< or = 4-cm) renal tumors.
31 tablished procedure for the treatment of T1a renal tumors.
32 wth and metastasis of tumor cells, including renal tumors.
33 49 and H1975 lung, as well as A498 and 786-O renal tumors.
34 ution and current status of cryoablation for renal tumors.
35 ing of the genetics and molecular biology of renal tumors.
36 FN-gamma secretion by HC/2G-1 in response to renal tumors.
37 nimally invasive nephron-sparing surgery for renal tumors.
38 olipomas; and 16 (8%), other or unclassified renal tumors.
39  has demonstrated variable growth rate among renal tumors.
40 an the past in the preoperative diagnosis of renal tumors.
41  are important advances in the management of renal tumors.
42 afe and effective for the treatment of solid renal tumors.
43 d imaging-guided biopsy in the management of renal tumors.
44 ced to make possible new methods of managing renal tumors.
45 can be effective treatments for select small renal tumors.
46 age, 68.1 years) underwent RF ablation of 15 renal tumors.
47 rwent RF ablation for 26 liver tumors and 17 renal tumors.
48 tion was detected in 11 of 39 (28%) sporadic renal tumors: 2 of 7 (29%) renal oncocytomas, 1 of 9 (11
49 forming laparoscopic partial nephrectomy for renal tumors 4-7 cm in size has clearly been demonstrate
50  adult patients with pathologically verified renal tumors: 9 patients with clear cell subtype of the
51 y prevailing methods used for nonextirpative renal tumor ablation.
52 f outcomes prior to routine clinical use for renal tumor ablation.
53 ogy of these eight ASPL-TFE3 fusion-positive renal tumors, although overlapping in some aspects that
54                    DNA was extracted from 26 renal tumor and paired lymphocyte samples and amplified
55                 A relationship between these renal tumors and ASPS was initially suggested by the cyt
56 tudy also expands the histologic spectrum of renal tumors and FH mutations associated with HLRCC.
57 -AKT pathway was activated in both human BHD renal tumors and kidney tumors in BHD(d/+) mice.
58       Analyses of ovarian cancers, pediatric renal tumors and multiple breast cancer cell lines showe
59 ged 6 1/2, 7, and 11 years) with adenomatous renal tumors and polycythemia.
60 pression of HIF-alpha subunits in 45 primary renal tumors and related this to tumor subtype, the pres
61 iochemical profiles characteristic of benign renal tumors and renal cancers of different grades.
62 ic biomarkers and therapeutic strategies for renal tumors and renal ischemia.
63                              Sensitivity for renal tumors and specificity for renal cysts were establ
64  benign skin tumors, and to a lesser extent, renal tumors and spontaneous pneumothorax.
65 s were > 4 cm in diameter, except in lung or renal tumors), and one was treated with alcohol ablation
66 ancers, including ovarian cancers, pediatric renal tumors, and breast cancers.
67 ught new insights into the classification of renal tumors, and may provide new markers that identify
68  promise for the treatment of selected small renal tumors, and MR imaging can be used to monitor the
69 re accurate preoperative clinical staging of renal tumors, and the necessity of completing all the co
70                                        Small renal tumors appear to be similar to larger ones in natu
71                                              Renal tumors are a family of neoplasms ranging from the
72 ivities were directed against a broad set of renal tumor-associated antigens, including telomerase re
73 coming a standard of care for selected small renal tumors at high volume centers.
74 ts the expression of integrin alphavbeta3 in renal tumors but represents angiogenesis only when tumor
75 or the minimally invasive treatment of small renal tumors but will remain experimental until the reso
76                   Screening for asymptomatic renal tumors by abdominal imaging is not cost-effective
77 g of a ketogenic diet promotes the growth of renal tumors by recruiting ERK1/2 and mTOR which are ass
78 e non-PSA-producing prostate cell line PC-3, renal tumor cell line R11, and cervical adenocarcinoma c
79          Coculture experiments revealed that renal tumor cell lines induced a time-dependent decrease
80 RNA (siRNA) knockdown of Nox4 in 786-0 human renal tumor cells expressing empty vector (PRC) or wild-
81  HIF2-alpha expression and activity in 786-0 renal tumor cells, even in the absence of functional VHL
82 B pathway as a therapeutic strategy to treat renal tumors characterized by biallelic VHL inactivation
83 s technique may prove useful for ablation of renal tumors completely in one session, but long-term fo
84 ome with classic "second hits" detectable in renal tumors, conventional genetic analysis has not reve
85 ce imaging have many indications for imaging renal tumors, CT, with new uses and improved diagnostic
86                                  The present renal tumor demonstrated morphologic and immunohistochem
87 ic follow-up of radiofrequency ablated small renal tumors demonstrates little or no residual contrast
88         Several lines of evidence, including renal tumors derived from TSC2+/- animals, suggest that
89 mens and in melanoma, leukemia, ovarian, and renal tumor-derived cell lines, suggesting that increase
90   We describe gene expression profiles in 41 renal tumors determined by using DNA microarrays contain
91 xpected number of metachronous contralateral renal tumors developing after an initial diagnosis of RC
92 crossed to p62(-/-) mice were protected from renal tumor development.
93 ress-induced apoptosis and markedly promotes renal tumor development.
94                                   Twenty-six renal tumors (diameter range, 1.0-4.6 cm; mean, 2.6 cm)
95 c findings in two TSC patients with multiple renal tumors, each of whom had the germline mutation TSC
96 J-BV bladder tumors (EGF+) or human SN12-PM6 renal tumors (EGF-).
97 nimally invasive nephron-sparing surgery for renal tumors encompasses extirpative laparoscopic partia
98 e subtraction enables accurate assessment of renal tumor enhancement, particularly in the setting of
99 of c-fos, was detected in 67% of the primary renal tumors examined, by Southern blot analyses.
100          Therefore, it was hypothesized that renal tumors express hKIM-1 and release this protein int
101 hown to be localized preferentially in early renal tumor foci after 3.5-4.0 months of estrogen treatm
102 eclin1 almost completely blocked macroscopic renal tumor formation in Tsc2(+/-) mice.
103 ho underwent RF ablation and cryoablation of renal tumors from June 19, 2003, to February 28, 2004, w
104 d MMP-9 were significantly higher in primary renal tumors from patients with either synchronous or me
105 ollected from an additional 42 patients with renal tumors, from 30 normal control subjects, and also
106 nefits of performing partial nephrectomy for renal tumors greater than 4 cm.
107  role of c-Met signaling axis on CNI-induced renal tumor growth and tested the anti-tumor efficacy of
108 k response on AKT Ser473 phosphorylation and renal tumor growth by other phosphoinositide 3-kinase (P
109  Age at diagnosis correlated negatively with renal tumor growth rate (P = .03).
110  In vivo, HNK markedly inhibited CNI-induced renal tumor growth; and it decreased the expression of p
111                                              Renal tumors had significantly lower ADCs (median, 189.3
112 aging-guided RF ITA for treatment of primary renal tumors has a high success rate.
113 se 4-hydroxyestradiol induces DNA damage and renal tumors in hamsters, and this metabolite is formed
114                          Delivery of FGF9 to renal tumors in mice yielded microvessels that were cove
115 ppressor gene predispose patients to develop renal tumors in the hamartoma syndrome, Birt-Hogg-Dube (
116 e observed, respectively, for carcinomas and renal tumors in the poorest income quintile.
117 graft tumors, and development of spontaneous renal tumors in Tsc2(+/-) mice.
118  CNI treatment increased the growth of human renal tumors in vivo, and the expression of CXCR3-B was
119  CNI treatment increased the growth of human renal tumors in vivo, and the Ras-Raf pathway is signifi
120   CsA also promoted the progression of human renal tumors in vivo, wherein VEGF is overexpressed.
121                  Most sporadically occurring renal tumors include a functional loss of the tumor supp
122 es equivalent oncological results for larger renal tumors including those of 4-7 cm and even for grea
123 vailable treatment for patients with a small renal tumor is a form of nephron-sparing tumor excision
124 ing a live donor evaluation in which a small renal tumor is detected, a careful analysis of risk and
125                      The management of small renal tumors is changing from radical nephrectomy to nep
126 nt decisions for small incidentally detected renal tumors is cost-effective and can prevent unnecessa
127  50 renal cysts was less than 5%; for the 50 renal tumors, it was 97% or higher.
128 ected group of patients with small exophytic renal tumors laparoscopic partial nephrectomy became an
129 omy has become the standard of treatment for renal tumors less than 4 cm in size.
130                                          For renal tumors less than 4-7 cm (T1 lesions), partial neph
131 s preincubated with the autologous apoptotic renal tumor line in the presence of IFN-alpha.
132 nd beta chains of the HC/2G-1 TCR recognized renal tumor lines, demonstrating that tumor recognition
133                      We have also shown that renal tumor lines, including SK-RC-45, induce apoptosis
134                                        Small renal tumors (&lt;or=3.5 cm) were similar to larger tumors
135 ing kidney donors, the surgical treatment of renal tumors may result in loss of function of the remai
136                                   Of the 198 renal tumors (median size, 3.4 cm; range, 1.1-20.0 cm) i
137 d with other p120 isoforms, is predictive of renal tumor micrometastasis and systemic progression, fo
138                                  In the A498 renal tumor model, 7c exhibited superior efficacy over 3
139 othesis by using an estrogen-induced hamster renal tumor model, a well established animal model of ho
140 ibe herein eight morphologically distinctive renal tumors occurring in young people that bear the ide
141 kidney tumorigenesis, we studied 39 sporadic renal tumors of different cell types: 7 renal oncocytoma
142                              Growth rates in renal tumors of different sizes, subtypes, and grades re
143 the treatment and outcomes for children with renal tumors on a global level.
144 has become a widely accepted option for most renal tumors, open surgery remains the standard in manag
145     Complex partial nephrectomy for multiple renal tumors, or multiplex partial nephrectomy, requires
146 s were followed up according to our standard renal tumor protocol.
147 inheritance of multiple benign skin lesions, renal tumors, pulmonary blebs, and pneumothoraces.
148 enal cell carcinomas (CC-RCCs) but not other renal tumors, raising a question about the importance of
149 1 literature on pediatric Wilms tumor, other renal tumors, rhabdomyosarcoma of the pelvis, paratestic
150 ogous dendritic cells transfected with total renal tumor RNA have been shown to be potent stimulators
151 studies, as well as primary estrogen-induced renal tumor RNA, for reference.
152 activities against allogeneic tumors because renal tumor RNA-transfected DCs stimulated polyclonal CT
153                                              Renal tumor RNA-transfected dendritic cells were adminis
154 vement of delivery of care in the setting of renal tumor(s) in a solitary kidney.
155 enetically and histologically different from renal tumors seen in other hereditary renal syndromes an
156    Thus, patients newly diagnosed with small renal tumors should be referred to centers with expertis
157  grade clear cell carcinomas and sarcomatoid renal tumors) show aberrant expression of cadherin-6, in
158 R imaging-guided percutaneous cryotherapy of renal tumors shows promise for the treatment of selected
159 weight 3.2-kb transcript was observed in the renal tumor, similar to that seen in the newborn mouse k
160 ndard of care for small renal masses, if the renal tumor size and complexity are amenable to such a s
161                                      Complex renal tumors, such as hilar and endophytic lesions, have
162 the entire spectrum of histological types of renal tumors, suggesting its major role in kidney cancer
163                             The mechanism of renal tumor suppression by VHL protein is only partly el
164 mechanism by which pVHL protein functions in renal tumor suppression remains unclear.
165  candidate regulatory factor in VHL-mediated renal tumor suppression.
166 ish called NBP which is an ortholog of human renal tumor suppressor Kank.
167 echanism by which VHL protein functions as a renal tumor suppressor remains largely unknown.
168 domain protein Jade-1 (PHF17) is a candidate renal tumor suppressor stabilized by pVHL.
169 ed ccRCC, HIF1alpha has been implicated as a renal tumor suppressor, whereas HIF2alpha is considered
170                   Therefore, Jade-1 may be a renal tumor suppressor.
171 ive about the management of small, localized renal tumors that are being discovered with increasing f
172  in some cases, caused partial regression of renal tumors that were implanted in the dorsal flank of
173 ression of CXCR3-B may prevent the growth of renal tumors through the inhibition of antiapoptotic HO-
174 orescence in situ hybridization in all seven renal tumors thus analyzed, which contrasts sharply with
175 in mononuclear leukocytes infiltrating human renal tumor tissue.
176  tissues examined as compared to the matched renal tumor tissues (67%, 1.2-fold to>10-fold, n=18).
177 on]; range, 53-92 years), each with a single renal tumor, underwent one percutaneous cryoablation tre
178 n-expressing cell line isolated from a mouse renal tumor, was characterized for synthesis, processing
179 ally fused to partner proteins in subsets of renal tumors, we found that wild-type, unfused TFE3 stim
180 lopment or progression of nonproximal tubule renal tumors, we performed a detailed microsatellite all
181                                   Twenty-six renal tumors were found in the 25 patients.
182                              At surgery, 152 renal tumors were identified (77 clear cell, 22 papillar
183  in the exon 11 hotspot, significantly fewer renal tumors were observed in patients with the C-deleti
184 rs, when given as single agents, but induced renal tumors, when given together.
185 molecular markers to better characterize all renal tumors will better enable individualized therapy.
186                                              Renal tumors with c-met genotype show a distinctive papi
187 hereditary renal syndromes and most sporadic renal tumors with papillary architecture.
188                         Twenty-five sporadic renal tumors with prominent papillary architecture and w
189                              Cryoablation of renal tumors with ultrasound monitoring may be performed
190 ith blood flow, and (d) subcutaneous and (e) renal tumors without blood flow, which was achieved by s

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