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1 R2-IgG dual seropositive patients (one-third thymoma).
2 bodies may expand the serological profile of thymoma.
3 ity of lung, breast, or ovarian carcinoma or thymoma.
4 ty in patients with octreotide scan-positive thymoma.
5 s integrated upstream from c-myc in a second thymoma.
6 usceptible to the spontaneous development of thymoma.
7 CSF and frequently present with a malignant thymoma.
8 ans has been implicated in lympho-epithelial thymoma.
9 for the treatment of patients with advanced thymoma.
10 1957 and 1997 with a pathologic diagnosis of thymoma.
11 second primary malignancies in patients with thymoma.
12 (60.0%) in the second group had a malignant thymoma.
13 nction by distinct mechanisms in suppressing thymoma.
14 n the management of early stage and advanced thymoma.
15 ation are not impaired in the development of thymoma.
16 ure locally advanced, unresectable malignant thymoma.
17 is suggested for patients with unresectable thymoma.
18 s in the management of patients with limited thymoma.
19 rolled, 25 with thymic carcinoma and 16 with thymoma.
20 diagnostic evaluation of patient with cystic thymoma.
21 ndidiasis, ectodermal dystrophy syndrome) or thymoma.
22 receptors), were prevalent in patients with thymoma.
23 apy is well-tolerated and active in relapsed thymoma.
24 derwent complete resection of a stage IVA B3 thymoma.
25 derstand the somatic genetic architecture of thymoma.
26 ut it has not been reached for patients with thymoma.
27 objective was response rate in patients with thymoma.
28 PFS and overall survival than patients with thymoma.
29 is responsible for the development of T cell thymomas.
30 a thymic carcinoma and four were noninvasive thymomas.
31 from supF-tagged proviruses in two resulting thymomas.
32 the more rapid onset and higher incidence of thymomas.
33 in culture and in primary retrovirus-induced thymomas.
34 ing paraneoplastic phenomena associated with thymomas.
35 T cell maturation while going on to develop thymomas.
36 no extensive sequencing has been reported in thymomas.
37 /sec and 1.29 x 10(-3) mm(2)/sec), high-risk thymoma (1.16 x 10(-3) mm(2)/sec and 1.14 x 10(-3) mm(2)
38 both readings (P = .01 and .20) of low-risk thymoma (1.30 x 10(-3) mm(2)/sec and 1.29 x 10(-3) mm(2)
41 occur in myasthenia gravis, especially with thymoma, a myopathy associated with Waldenstrom's macrog
44 for TCR gene translocations in p53-deficient thymomas, although abundant aneuploidy involving frequen
45 cloned proviral U3 sequences from the first thymoma and generated an infectious chimeric virus, MCF
47 ia; infections, particularly B19 parvovirus; thymoma and other solid tumors; or a variety of other di
48 patients with histopathologically confirmed thymoma and serum available to test for synaptic autoant
49 ibodies to voltage-gated potassium channels; thymoma and small-cell lung cancer are the most common u
54 ifferentiate low-risk thymoma from high-risk thymoma and thymic carcinoma were 1.25 and 1.22 x 10(-3)
57 in culture and in primary retrovirus-induced thymomas and encodes a nuclear, sequence-specific DNA-bi
61 rmalities and systemic tumours (teratoma and thymoma), and they do not develop SIADH-like hyponatraem
63 table adenocarcinoma, melanoma, sarcoma, and thymoma, and also a transgenic model of spontaneous brea
64 pecific CTL to the P815 mastocytoma, the EL4 thymoma, and the Lewis lung carcinoma is dependent on tu
69 erologic parallels to APS-I in patients with thymomas are not explained purely by deficient TSAg tran
71 ithmic usefulness as negative predictors for thymoma (as recognized for neuronal voltage-gated calciu
75 om a proximal Lck promoter construct develop thymomas at an early age, whereas transgenic mice expres
78 that multiple lineages of tumors, including thymoma, breast cancer, colon cancer, and melanoma cell
79 mutation in 82% of type A and 74% of type AB thymomas but rarely in the aggressive subtypes, where re
80 0) and B7.2 (CD86) cDNAs into the EL4 T cell thymoma cell line and examined the transfectants for the
85 n, made by whole cell fusion between a mouse thymoma cell line, and to microcell hybrids made with a
89 se the silencer and enhancer in CD4-negative thymoma cells and double-negative immature thymocytes.
90 mitogen-activated protein kinase p38 in EL4 thymoma cells and in freshly isolated murine lymphocytes
91 e Schlafen family members in fibroblasts and thymoma cells either retards or ablates cell growth.
92 in phorbol ester-sensitive EL4 (S-EL4) mouse thymoma cells have been identified as the p120 c-Cbl pro
95 treated mice bearing tumors derived from EG7 thymoma cells that express the well-characterized chicke
96 e released enzymatically from the surface of thymoma cells transfected with cDNAs encoding TCR-alpha
98 Incubation of murine thymocytes or S49 mouse thymoma cells with dibutyryl-cAMP, 8-bromo-cAMP, cholera
99 omain and that, unlike the result with mouse thymoma cells, both PIG-L and GlcNAc-PI-de-N-acetylase a
107 l large granular lymphocytic (LGL) leukemia, thymoma, chronic lymphocytic leukemia, and non-Hodgkin's
108 ese questions based on an index patient with thymoma, chronic visceral leishmaniasis, myasthenia grav
113 tion was dispensable for tumorigenesis since thymomas developed with or without the RAG-1 or RAG-2 ge
117 , a strain in which 100% of the mice develop thymoma due to thymocyte-specific inactivation of p53 by
118 eover, expression of a high level of CD80 on thymoma EL4 cells conveys immunity in mice with a target
120 he overlap of myasthenia, neuromyotonia, and thymoma, emphasizing the importance of appropriate tumor
123 liferative expansion of T cells in vitro and thymoma formation in vivo were prevented by the absence
124 both readings used to differentiate low-risk thymoma from high-risk thymoma and thymic carcinoma were
125 c mice overexpressing the c-myc oncogene and thymomas from mice deficient for the ataxia telangiectas
127 s, B7W-transfected J558 plasmocytoma and EL4 thymoma grow significantly more slowly than those transf
128 tumor-draining lymph nodes (TDLN) during EL4 thymoma growth, this event was insufficient to promote t
130 To date, only seven patients (33.3%) with thymoma have died, compared with 16 patients (69.6%) wit
134 hese proviruses are thought to contribute to thymoma induction by enhancer-mediated deregulation of c
135 identified and classified 193 patients with thymoma into 4 groups: (1) lacking neurological autoimmu
141 cell focus-inducing (MCF) viruses to induce thymomas is determined, in part, by transcriptional enha
143 TSAgs showed the expected underexpression in thymomas, levels were increased for four of the five TSA
144 est x-ray or computed tomography to rule out thymoma, lymphocyte immunophenotype studies, anti-nuclea
145 ated mutations in this patient suggests that thymomas may evolve through mechanisms distinctive from
148 RNA was translated in the presence of murine thymoma microsomes which, in contrast to the canine panc
150 either the pathologic diagnosis (presence of thymoma) nor the age at surgery proved to be negative pr
151 pendent PDAC cells, inactivated c-akt murine thymoma oncogene homolog 1 signaling via mammalian targe
152 required for KRAS activation of c-akt murine thymoma oncogene homolog 1-mammalian target of rapamycin
153 rator-activated receptor gamma, v-AKT murine thymoma oncogene homolog 2, zinc metalloprotease and lip
159 d further, we screened 247 patients with MG, thymoma, or both for clinical features and organ-specifi
162 relevant acquired T cell immunodeficiency in thymoma patients that is distinct from Good's syndrome.
163 ively, in 49 of 121 (40%) and 10 of 121 (8%) thymoma patients, but clinical features seldom occurred
165 bearing established TGF-beta-OVA-expressing thymomas, produce high amounts of IFN-gamma and sensitiz
166 entification of gene(s) which participate in thymoma progression, as well as a model system for scree
171 nt of murine Notch-1 as capable of rendering thymomas resistant to glucocorticoid-induced apoptosis.
173 patients achieved partial response (both had thymoma; response rate, 8%; 95% CI, 2.2% to 25%), 25 had
174 eristic of APS-I patients, and we assayed 26 thymoma samples for transcripts for AIRE and 16 peripher
175 (AIRE) gene, and myasthenia gravis (MG) with thymoma, show intriguing but unexplained parallels.
176 a case of a 60 year-old woman with a cystic thymoma studied with advanced tomographic imaging stydie
177 of the clonality of preleukemic thymuses and thymomas suggested that the change in pseudotyping chara
178 ngiectasia (AT) patients and in mouse Atm-/- thymoma, suggesting the involvement of V(D)J recombinati
180 ailable for patients with advanced/recurrent thymoma (T) or thymic carcinoma (TC) who have progressed
182 oved in four patients (mediastinal teratoma, thymoma, thymic carcinoma and thyroid cancer) and not tr
183 ntraperitoneal challenge with E.G7, the EL-4 thymoma transfected with OVA, results in activation and
184 been documented, including one patient with thymoma treated with the pan-HDAC inhibitor belinostat.
185 lymphocytes (CTL), which lysed melanoma and thymoma tumor cells and inhibited the growth of three un
186 B16/F10.9 murine melanoma, E.G7-OVA, or EL4 thymoma tumors elicited a CTL response to as yet unknown
188 rease in the phosphorylation of v-AKT murine thymoma viral oncogene (AKT) and enhanced the tumorigene
190 xpression of activated forms of v-akt murine thymoma viral oncogene homolog (AKT) and Ras in mouse li
192 gnal-regulated kinase (ERK) and v-akt murine thymoma viral oncogene homolog (AKT) in a subset of huma
196 tase and tensin homolog (PTEN), v-akt murine thymoma viral oncogene homolog (AKT), and mammalian targ
198 on of PIK3CA by miR-10a reduced V-akt murine thymoma viral oncogene homolog 1 (AKT) phosphorylation a
201 protein signalling 4 (RGS4) and V-AKT murine thymoma viral oncogene homolog 1 (AKT1) the data are pro
202 R), the serine/threonine kinase V-Akt murine thymoma viral oncogene homolog 1 (AKT1), and the proteas
205 ed hyperphosphorylation of AKT (v-akt murine thymoma viral oncogene homolog 1), a phenotype reverted
206 primary liver cancer driven by v-akt murine thymoma viral oncogene homolog and neuroblastoma RAS vir
207 ated a compensatory increase in v-akt murine thymoma viral oncogene homolog signaling and decreased e
208 of miR-155 sensitizes cells to v-akt murine thymoma viral oncogene homolog-1 inhibitors in vitro, su
209 nases such as protein kinase A, v-Akt murine thymoma viral oncogene homolog-1, glycogen synthase kina
211 f the phosphoinositide-3-kinase/v-akt murine thymoma viral oncogene homolog/mammalian target of rapam
212 ic and growth properties of the v-akt murine thymoma viral oncogene homolog/mammalian target of rapam
213 onsistent with this suggestion, v-akt murine thymoma viral oncogene homolog/protein kinase B (AKT/PKB
215 hibits the HGF-induced MET-AKT (v-Akt murine thymoma viral oncogene) signaling pathway and decreases
216 rophic signaling (activation of v-akt murine thymoma viral oncogene/protein kinase B [AKT], inhibitio
217 oupled receptors (GPCRs) activate PI3K/v-AKT thymoma viral oncoprotein (AKT) to regulate many cellula
218 kinase 3beta (Gsk3beta) via inactivation of thymoma viral proto-oncogene (Akt) and 3-phosphoinositid
219 vant , phosphatidyl inositol 3 kinase (PI3K)-thymoma viral proto-oncogene (AKT) inhibitors to kill tu
220 n of the insulin receptor substrate 2 (IRS2)-thymoma viral proto-oncogene (Akt) signaling pathway in
221 llular signal-regulated kinase (ERK) and the thymoma viral proto-oncogene (Akt), followed by activati
222 gram during fasting and is then inhibited by thymoma viral proto-oncogene 1 (Akt) after feeding.
230 rable with those previously described for B3 thymomas, with CN gain of chromosome 1q, 5, 7 and X and
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