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1 ad chronic myelogenous leukemia, and one had mycosis fungoides.
2 tes the results to skin stage and outcome in mycosis fungoides.
3 10q and MSI in advanced cutaneous stages of mycosis fungoides.
4 arge proportion of patients with early stage mycosis fungoides.
5 ssessment of peripheral blood involvement in mycosis fungoides.
6 feature of the large-cell transformation of mycosis fungoides.
7 usly as a single dose to eight patients with mycosis fungoides.
8 red with the staging system for conventional mycosis fungoides.
9 rived from patients with Sezary syndrome and mycosis fungoides.
10 pression in lesional skin from patients with mycosis fungoides.
11 systemic treatment in patients with stage IB mycosis fungoides.
12 specially in Sezary syndrome and transformed mycosis fungoides.
13 ype may contribute to disease progression in mycosis fungoides.
14 was associated with an older age of onset of mycosis fungoides.
16 s antibody (1) had clinical efficacy against mycosis fungoides; (2) was well tolerated; (3) had a low
17 n 18 patients (25%), including 12 of 57 with mycosis fungoides (21%) and six of 16 with Sezary syndro
19 as found to be more prevalent in tumor stage mycosis fungoides (47%) than early stage disease (20%) a
20 patients [82.3%]), had disease classified as mycosis fungoides (48 patients [61.5%]), and had advance
21 tificates for two such cancers, melanoma and mycosis fungoides (a cutaneous lymphoma), using routinel
22 ease that recapitulates many key features of mycosis fungoides, a common variant of cutaneous T-cell
23 pendent prognostic variable in patients with mycosis fungoides after correcting for age, skin, and ly
24 er of the small intestine, eye melanoma, and mycosis fungoides, among men in a European, multicenter
25 the 54 samples (24%), 12 from patients with mycosis fungoides and 1 from a patient with Sezary syndr
26 have analyzed 51 samples from patients with mycosis fungoides and 15 with Sezary syndrome using meth
29 amples from 59 patients with Sezary syndrome/mycosis fungoides and 66 samples from unique patients wi
31 eous T-cell lymphoma, and mogamulizumab, for mycosis fungoides and adult T-cell leukaemia/lymphoma.
33 has also shown promise in the management of mycosis fungoides and extranodal natural killer/T-cell l
37 that recapitulated the cardinal features of mycosis fungoides and Sezary syndrome and maintained his
38 common in both early and advanced stages of mycosis fungoides and Sezary syndrome and that these gen
47 approximately 30% of patients with advanced mycosis fungoides and Sezary syndrome cutaneous T-cell l
48 aneous T-cell lymphoma (CTCL), including the mycosis fungoides and Sezary syndrome forms of the disea
49 lastic cells (Sezary cells) in patients with mycosis fungoides and Sezary syndrome is essential for d
50 ined lesional skin biopsy specimens from 113 mycosis fungoides and Sezary Syndrome patients for activ
51 lly reverse or suppress the abnormalities of mycosis fungoides and Sezary syndrome to the point at wh
52 ous T-cell lymphoma (CTCL), particularly the mycosis fungoides and Sezary syndrome variants, has been
53 276 patients with cutaneous T cell lymphoma (mycosis fungoides and Sezary syndrome) using 2,4-dinitro
54 oproliferative processes, mainly composed of mycosis fungoides and Sezary syndrome, the aggressive fo
55 inhibit malignant T cells in skin lesions in mycosis fungoides and Sezary syndrome, the most common f
56 Discoveries regarding the pathophysiology of mycosis fungoides and Sezary syndrome, the two most comm
66 S) were required to have stage IA-IIIB CTCL (mycosis fungoides and/or Sezary syndrome) and at least >
68 atients had Sezary syndrome, eight (18%) had mycosis fungoides, and one (2%) had primary cutaneous T-
69 lar lymphoma, diffuse large B-cell lymphoma, mycosis fungoides, and peripheral T-cell lymphoma, respe
70 goid, transient acantholytic dermatosis, and mycosis fungoides, and should be considered in elderly p
72 mas, with particular emphasis on tumor stage mycosis fungoides, as it is in these cases that p53 over
73 PTEN may be important in the pathogenesis of mycosis fungoides, but our data imply that this gene is
75 n vivo chicken embryo model xenografted with mycosis fungoides cells showed that PKCo blockage abroga
76 n vivo chicken embryo model xenografted with mycosis fungoides cells showed that PKCtheta blockage ab
77 on of a number of PKCo target genes found in mycosis fungoides cells significantly correlated with th
78 f a number of PKCtheta target genes found in mycosis fungoides cells significantly correlated with th
79 The ISCL/EORTC recommends revisions to the Mycosis Fungoides Cooperative Group classification and s
85 cutaneous staging system for folliculotropic mycosis fungoides (FMF) has been purported to better est
86 s suggest that patients with folliculotropic mycosis fungoides (FMF) have a worse prognosis than pati
87 aviolet B-related step in the progression of mycosis fungoides from plaque to tumor-stage disease.
88 its total absence in PBLs from patients with mycosis fungoides, inflammatory cutaneous or hematologic
95 (CTCL) comprising 10 cases with early-stage mycosis fungoides (MF) and 10 cases with late-stage MF o
96 SHV/HHV-8 is involved in the pathogenesis of mycosis fungoides (MF) and related disorders, we used a
99 ective retinoid that can induce apoptosis of mycosis fungoides (MF) and Sezary syndrome (SS) cells.
101 umor, node, metastases (TNM) system used for mycosis fungoides (MF) and Sezary syndrome (SS) is not a
102 CD30 expression of malignant lymphocytes in mycosis fungoides (MF) and Sezary syndrome (SS) is quite
103 p of neoplasms originating in the skin, with mycosis fungoides (MF) and Sezary syndrome (SS) represen
104 ogy and diagnostic techniques as pertains to mycosis fungoides (MF) and Sezary syndrome (SS) since th
105 ic treatment options exist for patients with mycosis fungoides (MF) and Sezary syndrome (SS), but no
106 MTAP in cutaneous T-cell lymphoma subgroups, mycosis fungoides (MF) and Sezary syndrome (SS), is unkn
112 xyadenosine (2-CdA) therapy in patients with mycosis fungoides (MF) and the Sezary syndrome (SS).
131 uced type I IFN gene expression in untreated mycosis fungoides (MF) skin lesions compared with that i
132 hrough stage IIA) cutaneous T-cell lymphoma, mycosis fungoides (MF) type, resulted in clinical respon
134 ND1/BCL1 expression in 18 of 30 SS, 10 of 23 mycosis fungoides (MF), and three of 10 primary cutaneou
135 patients with the cutaneous T-cell lymphoma, mycosis fungoides (MF), are seronegative for human T-cel
136 catter T (T(HS)) cells were CD4(+) in CD4(+) mycosis fungoides (MF), CD8(+) in CD8(+) MF, and contain
138 common subtype of cutaneous T-cell lymphoma, mycosis fungoides (MF), is characterized by proliferatio
141 (CTCL) may present with eczematous lesions, mycosis fungoides (MF), or as exfoliative erythroderma w
142 patients with a diagnosis of CTCL, including mycosis fungoides (MF), Sezary syndrome (SS), or CTCL no
145 nt lymphocytes from Sezary syndrome (SS) and mycosis fungoides (MF), the most common subtypes of cuta
146 f inflammatory cytokines in 12 patients with mycosis fungoides (MF), the most common variant of CTCL.
153 od lymphocyte cultures from 19 patients with mycosis fungoides (MF)/Sezary syndrome (SS) stimulated w
155 ients with treatment refractory CD4(+) CTCL (mycosis fungoides [MF], n = 38; Sezary syndrome [SS], n
157 oma, n = 11; other B-cell lymphomas, n = 10; mycosis fungoides, n = 13; peripheral T-cell lymphoma, n
158 osity was found in over 10% of patients with mycosis fungoides on 9p, 10q, 1p, and 17p and was presen
159 e enrolled adult patients with CD30-positive mycosis fungoides or primary cutaneous anaplastic large-
160 s had anaplastic large-cell lymphoma, 15 had mycosis fungoides or Sezary syndrome (14 with large-cell
161 id) in persistent, progressive, or recurrent mycosis fungoides or Sezary syndrome (MF/SS) cutaneous t
162 ve therefore studied 76 patients with either mycosis fungoides or Sezary syndrome for abnormalities o
163 uppression, such that patients with advanced mycosis fungoides or Sezary syndrome have been compared
164 Among the 8 pivotal trials supporting new mycosis fungoides or Sezary syndrome systemic therapies
165 solid tumours were screened, 35 of whom with mycosis fungoides or Sezary syndrome were enrolled and r
167 ions in patients with relapsed or refractory mycosis fungoides or Sezary syndrome, suggesting it has
168 utaneous T-cell lymphoma (CTCL), or subtypes mycosis fungoides or Sezary syndrome, who had received n
171 DLBCL: OR(allelic) = 1.12, P(trend) = 0.006; mycosis fungoides: OR(allelic) = 1.44, P(trend) = 0.015)
172 haracteristically slow, we hypothesized that mycosis fungoides originates from an accumulation of lym
175 quence of hMLH1 promoter hypermethylation in mycosis fungoides patients and may prevent transcription
176 in 21/35 (60%) SS patients and in 3/8 (38%) mycosis fungoides patients, all of whom had clonal blood
182 utaneously accessible relapsed or refractory mycosis fungoides, Sezary syndrome, or solid tumours.
183 , 2017, and March 31, 2020, 66 patients with mycosis fungoides, Sezary syndrome, other CTCL, or solid
187 BMC is not due to an intrinsic defect in the mycosis fungoides/Sezary syndrome patients' immune acces
188 ns and outcomes of a subset of patients with mycosis fungoides/Sezary syndrome who were treated with
189 d cases of cutaneous T cell lymphoma (CTCL) (mycosis fungoides/Sezary syndrome) undergo large cell tr
190 ould address an unmet need for patients with mycosis fungoides/Sezary syndrome, a set of incurable di
191 f 31 cutaneous T-cell lymphoma (CTCL) cases (mycosis fungoides/Sezary syndrome, SS) as well as in 5 o
193 oportion of cutaneous T-cell lymphoma (CTCL)/mycosis fungoides skin samples and in one melanoma.
194 ients with Sezary syndrome (SS), transformed mycosis fungoides (T-MF), and cutaneous anaplastic large
195 sect key pathological features implicated in mycosis fungoides, the most common cutaneous T-cell lymp
196 evels of TOX were significantly increased in mycosis fungoides, the most common type of cutaneous T-c
197 We also included tissue from two cases of mycosis fungoides, three normal skin biopsies, and three
198 iptomics analysis of skin from patients with mycosis fungoides-type CTCL and an integrated comparativ
201 erythroderma or Sezary syndrome and 11 with mycosis fungoides, were studied for the occurrence of st
202 oss on 1p and 9p were found in all stages of mycosis fungoides, whereas losses on 17p and 10q were li
203 In total, 260 patients with stage IA to IIA mycosis fungoides who had not used topical mechlorethami
204 MSI and disease progression in patients with mycosis fungoides, with 6 of 15 (40%) patients with MSI