ライフサイエンスコーパス: indolent

1 CLL) occurs in 2 major forms: aggressive and indolent.

2 Whereas most PN are clinically indolent, a subset progress to atypical neurofibromatous

3 ajor/partial R: 0%/47%/25%) and according to indolent/advanced M was 92% (major/partial R: 56%/36%) a

4 Twenty-five adult patients with indolent and advanced forms of mastocytosis and 20 healt

5 A distinction between indolent and aggressive disease is a major challenge in

6 genomic alterations associated with resected indolent and aggressive early lung ADCs.Methods: DNA was

7 ide useful criteria to differentiate between indolent and aggressive FMF and confirm the existence of

8 Distinction between indolent and aggressive FMF may have important therapeut

9 ere identified as useful for differentiating indolent and aggressive forms of PCa.

10 across multiple lymphoma subtypes, including indolent and aggressive forms.

11 re 3.71 (0.1-8) and 2.47 (0.5-8.6) years for indolent and aggressive M, respectively.

12 Distinguishing between indolent and aggressive prostate adenocarcinoma remains

13 Differentiating between indolent and aggressive prostate cancers (CaP) is import

14 lines into established gene expression-based indolent and aggressive subtypes.

15 We have isolated two syngeneic cell lines (indolent and aggressive) through in vivo selection by im

16 ies between these DLBCL subtypes and various indolent and extranodal lymphoma types, suggesting a sha

17 1q-binding dnDSA could differentiate between indolent and harmful dnDSA causing antibody-mediated rej

18 le noninvasive method to distinguish between indolent and high risk IPMNs.

19 GC) B cells leading to the development of an indolent and largely incurable disease.

20 liably informative biomarkers to distinguish indolent and lethal prostate cancer is one reason this d

21 irst-line treatment option for patients with indolent and mantle-cell lymphoma.

22 Why some tumors remain indolent and others progress to clinical relevance remai

23 and care, such as use of new terminology for indolent and precancerous disorders.

24 ic profiles of plasma exosomes, both between indolent and progressive CLLs as well as within the indi

25 TDT) and identify correlates associated with indolent and rapid growth.

26 especially driven by increased diagnosis of indolent and well-differentiated papillary subtype and e

27 ar ataxia type 28 disease--in a patient with indolent ataxia and PEO.

28 activity in chronic lymphocytic leukemia and indolent B cell non-Hodgkin's lymphomas.

29 Hairy cell leukemia (HCL) is a rare, indolent B-cell disorder in which single courses of clad

30 Waldenstrom macroglobulinaemia is an indolent B-cell lymphoma with clearly defined criteria f

31 Follicular lymphoma (FL) is an indolent B-cell non-Hodgkin lymphoma able to transform i

32 of dulanermin to rituximab in patients with indolent B-cell non-Hodgkin lymphoma was tolerable but d

33 Eight patients with relapsed CD37+ indolent B-cell non-Hodgkin lymphoma were included for R

34 In phase 1b, patients (age >/=18 years) with indolent B-cell non-Hodgkin lymphoma with stable disease

35 rmin and rituximab in patients with relapsed indolent B-cell non-Hodgkin lymphoma.

36 e disease response (LDR) of 46 patients with indolent B-cell non-Hodgkin lymphomas (NHLs) or chronic

37 dal marginal zone lymphoma (NMZL) is a rare, indolent B-cell tumor that is distinguished from splenic

38 The frequency of cancers with indolent behavior has increased with screening.

39 if a multigene classifier is associated with indolent behavior of invasive breast cancers in women fo

40 ficiency and the clinical course ranges from indolent behavior to that of an aggressive malignancy.

41 ons, two large subgroups, both with a rather indolent behavior, can be distinguished: a low-grade tri

42 e most common subtype and is associated with indolent behavior, local recurrence, and insensitivity t

43 t' IPMNs that warrant surgical removal from 'indolent/benign' IPMNs that can be observed.

44 er has limitations related to the frequently indolent biology of the disease.

45 Here we reveal how the behaviour of indolent breast cancer cells in the lung is determined b

46 The detection of these indolent cancer cells has led to overdiagnosis, one of t

47 inhibitors stimulate metastatic outgrowth of indolent cancer cells, specifically in the bone.

48 Purpose Follicular lymphoma (FL) is an indolent cancer, with effective but rarely curative trea

49 m cannot fully differentiate aggressive from indolent cancers and results in many benign masses being

50 le stage result in many benign neoplasms and indolent cancers being resected without clear benefit.

51 ly precise identification of the fraction of indolent cancers in a stop-screen trial design, and we d

52 2 (1980-1985) and show that the fraction of indolent cancers is not precisely identifiable.

53 g cancer screening detects a large number of indolent cancers that generally belong to the adenocarci

54 erging strategies to reduce overdiagnosis of indolent cancers through an understanding of tumour hete

55 reening is overdiagnosis of slow growing and indolent cancers.

56 rotein panel can distinguish aggressive from indolent cancers.

57 stronger affinities and longer half-lives in indolent cases, and weaker, short-lived contacts mediati

58 isms by which prostate cancer shifts from an indolent castration-sensitive phenotype to lethal castra

59 We found that indolent cells retained the dormant phenotype, whereas a

60 otes the formation of fibronectin fibrils by indolent cells that drive integrin-dependent pro-surviva

61 Indolent cells were found to secrete a high level of sec

62 lymphoproliferative disorder" because of its indolent clinical behavior and uncertain malignant poten

63 -grade serous carcinomas and have relatively indolent clinical behavior.

64 subclonal mutations and is characterized by indolent clinical course and favorable outcome.

65 hich may contribute to their relatively more indolent clinical course and responsiveness to therapy.

66 n a MCL xenograft model, consistent with the indolent clinical course of the human SOX11-negative man

67 of these patients suggests that RALD has an indolent clinical course whereas JMML is fatal if left u

68 er panNETs are generally characterized by an indolent clinical course, with a rate of relapse or meta

69 ture B-cell neoplasm characterized by rather indolent clinical course.

70 d as: 95 RS, 117 HAC, and 120 histologically indolent CLL (HIC).

71 on in CLL and determined tsRNA signatures in indolent CLL and aggressive CLL vs. normal B cells.

72 Similar results were obtained for indolent CLL.

73 is a large-vessel vasculitis with a chronic, indolent course affecting the aorta and its main branche

74 t lung cancers that manifest as NSNs have an indolent course and can be managed with annual follow-up

75 cal entity where a subset of patients has an indolent course of disease that mimics monoclonal gammop

76 L) is a chronic B-cell leukemia noted for an indolent course that ultimately results in cytopenias an

77 Though most patients have an indolent course with a life expectancy comparable to tha

78 Although the majority of SMZLs show an indolent course with a median survival of approximately

79 neous and systemic involvement, and a fairly indolent course with better response to treatment.

80 ong to the luminal A subtype connected to an indolent course, and basal-like MDA-MB-231 connected to

81 The disease often takes an indolent course, but in approximately one-third of the p

82 Although it often has an indolent course, prostate cancer remains the third-leadi

83 However, in most cases, NLPHL has an indolent course, which raises the question of to what ex

84 mors occurred only in the stomach and had an indolent course.

85 diagnosis, and small thyroid cancers have an indolent course.

86 appears to be a distinct entity with a more indolent course.

87 arely fully recover, and often experience an indolent death.

88 Follicular lymphoma (FL) is an indolent disease but transforms in 2% to 3% of patients

89 Most patients are characterised by an indolent disease course and an anergic phenotype of thei

90 The relatively indolent disease course and excellent response to intrav

91 4-34/IGKV2-30 BCR Ig) display a particularly indolent disease course.

92 -grade glioma does not generally indicate an indolent disease course.

93 metastatic melanoma, which markedly turns an indolent disease into a lethal phase, is prone to preser

94 ents as well for as patients with limited or indolent disease is not defined.

95 Ig-unmutated CLL, where typically have more indolent disease with median survivals close to 25 years

96 emarkably heterogeneous course, ranging from indolent disease with no need for immediate therapy to r

97 During the period of indolent disease, 2HG concentration varied by less than

98 Conclusion WT-GIST is an indolent disease, and most patients survive with disease

99 Most cases are of effusion-limited, indolent disease, with an excellent prognosis after impl

100 atment tolerability for patients living with indolent disease.

101 cessary prostate biopsy and overdiagnosis of indolent disease.

102 in T2 vs T1 bladder cancer and aggressive vs indolent disease.

103 ons on the natural history of this otherwise indolent disease.

104 ed in a prostate cancer cell line resembling indolent disease.

105 de of Sfrp2 expression reduces the burden of indolent disease.

106 observation or less invasive approaches for indolent disease.

107 n of aggressive disease and overtreatment of indolent disease.

108 agnosed with prostate cancer will experience indolent disease; hence, discovering genetic variants th

109 d NK-cell lymphocytosis, which are similarly indolent diseases characterized by cytopenias and autoim

110 hich breast cancers progress from relatively indolent ductal carcinoma in situ (DCIS) to invasive duc

111 n of MNK1 inhibitors to delay progression of indolent ductal carcinoma in situ to invasive ductal car

112 fter excision and the MALT lymphoma remained indolent during the course of her pregnancy without radi

113 ive (My-La, HUT78, HH, MAC2A, and MAC2B) and indolent (FE-PD and MAC1) CTCL cell lines.

114 ne FL model confirm their pathogenic role in indolent FL.

115 yzing genomic data from two large cohorts of indolent FLs, we identify a pattern of mutually exclusiv

116 However, the role of such lesions in indolent follicular lymphoma (FL) is unclear and individ

117 essive Burkitt lymphoma was more likely than indolent follicular lymphoma to express matriptase alone

118 Most prostate cancer cases remain indolent for long periods of time, but metastatic progre

119 lymphoma (MCL), but it is absent in the more indolent form of MCL.

120 ering forms showed a lower FMD compared with indolent forms (P < .001).

121 Biomarkers that could discriminate indolent from aggressive and drug resistance disease are

122 candidate diagnostic markers to distinguish indolent from aggressive disease.

123 is and, consequently, for differentiation of indolent from aggressive phenotypes.

124 his scenario in follicular lymphoma (FL), an indolent GC-derived malignancy.

125 tic maturation in CLL was associated with an indolent gene expression pattern and increasingly favora

126 Here we used the indolent growth dynamics of chronic lymphocytic leukaemi

127 ts with metastatic renal-cell carcinoma show indolent growth of metastases.

128 opment, the release of bioactive amines, and indolent growth of the tumors.

129 In multivariable analysis, indolent growth was associated with larger tumor diamete

130 Indolent growth was more common in nonviral than viral c

131 Over one-third (38%) of HCCs had indolent growth, 36.8% intermediate growth, and 25.2% ra

132 iting rapid growth and over one-third having indolent growth.

133 In summary, frequent RB pathway lesions in indolent, high-risk FLs indicate an untapped therapeutic

134 tiated PanNETs with small size are typically indolent; however, a limited subset metastasize to the l

135 Thus, indolent human glioma cells deficient for TF remain viab

136 Haematological exploration found an indolent IgG-kappa multiple myeloma.

137 Sustained, indolent immune injury of the vasculature of a heart tra

138 rst, locoregional tumor behavior may be more indolent in older patients for some disease sites but mo

139 The clinical course of NLPHL is indolent in the majority of cases.

140 Prostate cancers remain indolent in the majority of individuals but behave aggre

141 ought to be due to chronic inflammation from indolent infections, leading to malignant transformation

142 imaging may be confounded by the presence of indolent infectious nodules in imaging studies.

143 ostate stem cells, blocks the progression of indolent intraepithelial prostatic lesions into aggressi

144 opical corticosteroids in the therapy of any indolent keratitis.

145 We propose the term indolent lesion of epithelial origin, or IDLE, for those

146 t potential are common, and screening brings indolent lesions and their precursors to clinical attent

147 re DCIS were included as a representation of indolent lesions with limited invasive capacity.

148 ationale for this change in approach is that indolent lesions with low malignant potential are common

149 that allows for a mixture of progressive and indolent lesions.

150 An indolent liver metastasis from a class 1B UM is infiltra

151 or a chimeric cDNA leads to the formation of indolent liver tumors in mice that closely resemble huma

152 man prostate cancer confined to the gland is indolent (low-risk), but tumors outside the capsule are

153 isk tumors while minimizing overtreatment of indolent, low-risk tumors.

154 lapse was higher in patients with concurrent indolent lymphoma (7.4% v 2.1% at 5 years; P < .01).

155 with DLBCL than for those who relapsed with indolent lymphoma (median 29.9 months v unreached; P < .

156 The treatment of transformed indolent lymphoma (TRIL) often includes salvage chemothe

157 ollicular lymphoma (FL) is the most frequent indolent lymphoma and is characterized by the accumulati

158 is the more effective radiation schedule for indolent lymphoma and should be regarded as the standard

159 Patients with DLBCL with a concurrent indolent lymphoma and those with the GCB subtype had a h

160 ars), compared with patients with concurrent indolent lymphoma at diagnosis (5.2%; P = .46).

161 l lymphoma (DLBCL) present with a concurrent indolent lymphoma at diagnosis.

162 DLBCL patients with concurrent other indolent lymphoma had similar outcomes compared with pat

163 f hematopoietic stem cell transplantation in indolent lymphoma has been defined by the adoption of th

164 essive lymphoma is found in a LN biopsy with indolent lymphoma in a BM biopsy.

165 sease and/or the screening and monitoring of indolent lymphoma in individual patients.

166 FL as a biologically and clinically distinct indolent lymphoma of children and adults characterized b

167 However, the rate of indolent lymphoma relapse was higher in patients with co

168 4.0%; P = .71) subtypes, whereas the rate of indolent lymphoma relapse was higher in patients with th

169 Cumulative incidences of late DLBCL and indolent lymphoma relapses were analyzed as competing ev

170 total of 175 patients with relapsed CD20(+) indolent lymphoma requiring therapy and with previous re

171 ns between slope and risk were strongest for indolent lymphoma subtypes.

172 e in this association between aggressive and indolent lymphoma subtypes.

173 FL is an indolent lymphoma with largely favourable outcomes, alth

174 In two patients MC had evolved into an indolent lymphoma with monoclonal B-cell lymphocytosis.

175 iffuse large-B-cell lymphoma, no evidence of indolent lymphoma, and were previously untreated.

176 e large B-cell lymphoma transformed from any indolent lymphoma, primary mediastinal B-cell lymphoma,

177 ence of the transformation of the underlying indolent lymphoma.

178 y of obinutuzumab with rituximab in relapsed indolent lymphoma.

179 after induction and safety in patients with indolent lymphoma.

180 istics, and outcome of DLBCL with concurrent indolent lymphoma.

181 worse prognosis than those who relapsed with indolent lymphoma.

182 te relapse, owing to increased relapses with indolent lymphoma.

183 eas patients with concurrent DLBCL and other indolent lymphomas (n = 62; 4.7%) had more stage III-IV

184 Chronic leukemias and indolent lymphomas can be well controlled for years in m

185 Patients with concurrent DLBCL and other indolent lymphomas had similar EFS (HR = 1.19) and OS (H

186 ith diffuse large B-cell lymphoma, four with indolent lymphomas) had evidence of clinical activity, a

187 ffuse large B-cell lymphoma (DLBCL), two had indolent lymphomas, and four had chronic lymphocytic leu

188 sing activity as a monotherapy in refractory indolent lymphomas.

189 py induces a high LDR rate in HCV-associated indolent lymphomas.

190 ty in 68 adult patients with M (36 [53%] had indolent M and 32 [47%] had advanced M) treated by 2-CdA

191 me toxicity in various M subtypes, mostly in indolent M, refractory to multiple symptomatic therapies

192 /SLL) and follicular lymphoma (FL) represent indolent malignancies characterized by multiple episodes

193 t and are limited in clinical application to indolent malignancies of low- to intermediate-risk.

194 Follicular lymphoma (FL) is an indolent malignancy of germinal center B cells.

195 rt-solid nodules (PSNs), have a high risk of indolent malignancy.

196 In 16 of 22 patients, a diagnosis of indolent mastocytosis could be established, and 1 patien

197 er ammonium and glutamate than patients with indolent monoclonal gammopathies.

198 types of renal cancer, including tumors with indolent, multifocal presentation and solitary tumors wi

199 Essential thrombocythemia (ET) is an indolent myeloproliferative neoplasm that may be complic

200 e effect of cediranib from the intrinsically indolent nature of ASPS.

201 n was limited to certain subtypes, mostly of indolent nature.

202 Follicular lymphoma (FL), an indolent neoplasm caused by a t(14;18) chromosomal trans

203 ncreatic neuroendocrine tumors (GEPNETs) are indolent neoplasms presenting unpredictable and unusual

204 nifest itself in multiple ways, ranging from indolent nephropathy and inflammation to proteinuria wit

205 % of DCIS lesions are benign and will remain indolent, never progressing to invasive cancers.

206 e B-cell lymphoma and relapsed or refractory indolent NHL into indication-specific cohorts.

207 Indolent NHL is highly susceptible to immunologic graft-

208 fuse large B-cell lymphoma, seven of 15 with indolent NHL, and two with mantle-cell lymphoma) and sev

209 Indolent non-Hodgkin lymphoma (iNHL) remains largely inc

210 the expansion phase (n = 179), patients with indolent non-Hodgkin lymphoma (iNHL), chronic lymphocyti

211 a phase I study in 64 patients with relapsed indolent non-Hodgkin lymphoma (iNHL).

212 hemotherapy agent increasingly used to treat indolent non-Hodgkin lymphoma (iNHL).

213 t relevant data regarding transplantation in indolent non-Hodgkin lymphoma and highlights the issues

214 Follicular lymphoma (FL) is the most common indolent non-Hodgkin lymphoma in the Western hemisphere.

215 ith histologically documented, CD20-positive indolent non-Hodgkin lymphoma refractory to rituximab we

216 l dynamic randomisation scheme stratified by indolent non-Hodgkin lymphoma subtype, rituximab-refract

217 Patients with indolent non-Hodgkin lymphoma who fail to achieve adequa

218 mphoma (FL) is the most frequently occurring indolent non-Hodgkin lymphoma, with generally favorable

219 herapy in rituximab-refractory patients with indolent non-Hodgkin lymphoma, with manageable toxicity,

220 lar lymphoma (FL) is the most common form of indolent non-Hodgkin lymphoma, yet it remains only parti

221 ial for patients with relapsed CD37-positive indolent non-Hodgkin lymphoma.

222 ation trial for patients with relapsed CD37+ indolent non-Hodgkin lymphoma.

223 lar lymphoma (FL) is the most common form of indolent non-Hodgkin lymphoma.

224 nt, is effective as monotherapy for relapsed indolent non-Hodgkin lymphoma.

225 b in patients with untreated, advanced stage indolent non-Hodgkin lymphoma.

226 d and highly active as initial treatment for indolent non-Hodgkin lymphoma.

227 Standard treatments for indolent non-Hodgkin lymphomas are often toxic, and most

228 ade in the overall survival of patients with indolent non-Hodgkin lymphomas, these lymphomas remain l

229 Subtypes of indolent non-Hodgkin's lymphoma included follicular lymp

230 e [R-CVP]) for treatment-naive patients with indolent non-Hodgkin's lymphoma or mantle cell lymphoma.

231 n acceptable safety profile in patients with indolent non-Hodgkin's lymphoma who had received extensi

232 e rates were observed across all subtypes of indolent non-Hodgkin's lymphoma, though the numbers were

233 Indolent non-Hodgkin's lymphomas (iNHLs) are incurable w

234 open-label, phase 2 study, 125 patients with indolent non-Hodgkin's lymphomas who had not had a respo

235 activity in patients with previously treated indolent non-Hodgkin's lymphomas.

236 Indolent non-progressive forms of ductal carcinoma in si

237 Marginal zone lymphomas (MZLs) are indolent nonfollicular B-cell lymphomas (INFLs) and have

238 LymphoCare Study by Casulo et al to include indolent nonfollicular B-cell lymphomas (INFLs).

239 NET fostered the progression of the indolent NPM1-driven myeloproliferation toward an exacer

240 s arise from various tissues and they may be indolent or aggressive, as is the case with skin basal c

241 sive non-Hodgkin lymphoma (n=83), and 37% in indolent or mantle-cell lymphoma (n=65).

242 , we enrolled adults (aged 18-75 years) with indolent or smouldering systemic mastocytosis, according

243 nt for the treatment of severely symptomatic indolent or smouldering systemic mastocytosis.

244 Some are indolent; others quickly progress to glioblastoma.

245 ght distinguish aggressive lesions from more indolent pathology.

246 l decision-making and avoid overtreatment of indolent PC and undertreatment of aggressive disease are

247 conclusion, CLL can evolve gradually during indolent phases, and undergo rapid changes following the

248 th CK and +12,+19 displayed an exceptionally indolent profile.

249 After decades of indolent progression, such plaques may suddenly cause li

250 Overdiagnosis and overtreatment of indolent prostate cancer (PCA) is a serious health issue

251 ncing produces the opposite result in a more indolent prostate cancer cell line.

252 ts on the outgrowth of distant and otherwise indolent prostate cancer cells.

253 The inability to distinguish aggressive from indolent prostate cancer is a longstanding clinical prob

254 Many men with indolent prostate cancer often opt for radical prostatec

255 ased use of radiotherapy among patients with indolent prostate cancer with limited to no correlation

256 dimethyl transferase WHSC1 critically drives indolent PTEN-null tumors to become metastatic PCa.

257 higher compared to surrounding epithelia in indolent samples but lower in aggressive LSCC.

258 however, some patients appear to have a more indolent, skin-limited disease.

259 subgroups: cutaneous mastocytosis (0.042%), indolent SM (0.285%), smoldering SM (5.991%), aggressive

260 analyzed 39 KIT D816V mutated patients with indolent SM (n = 10), smoldering SM (n = 2), SM with ass

261 eoplastic MCs in 3 of 25 patients (12%) with indolent SM, 4 of 7 patients (57%) with aggressive SM, a

262 ginal zone lymphoma (NMZL) is a rare form of indolent small B-cell lymphoma which has only been clear

263 omatic MM, and was negative in patients with indolent smoldering MM and monoclonal gammopathy of unkn

264 hat cause actively growing cells to enter an indolent state, thereby enabling them to survive for ext

265 eparate clinical entities, ranging from very indolent (subset 4) to aggressive disease (subsets 1 and

266 Follicular lymphoma, the most common indolent subtype of non-Hodgkin lymphoma, is associated

267 Up to 10% of CLL patients transform from an indolent subtype to an aggressive form of B cell lymphom

268 h frequency in type A thymomas, a relatively indolent subtype.

269 n future lymphoma patients, mainly driven by indolent subtypes.

270 Indolent systemic mastocytosis (ISM) patients have a nor

271 16V mutation is present in a subset of adult indolent systemic mastocytosis (ISM) patients in associa

272 Indolent systemic mastocytosis (ISM) without skin lesion

273 teoporosis occur frequently in patients with indolent systemic mastocytosis (ISM), even before 50 yea

274 In indolent systemic mastocytosis (ISM), several risk facto

275 Two of these individuals had indolent systemic mastocytosis (ISM).

276 marrow biopsy in patients suspected to have indolent systemic mastocytosis (ISM).

277 ystemic mastocytosis is further divided into indolent systemic mastocytosis and advanced systemic mas

278 its KIT and LYN kinases that are involved in indolent systemic mastocytosis pathogenesis.

279 Indolent systemic mastocytosis, including the subvariant

280 oL impairment in patients with cutaneous and indolent systemic mastocytosis, the Mastocytosis Quality

281 63% female cohort of 164 adult patients with indolent systemic mastocytosis.

282 nnaire for adult patients with cutaneous and indolent systemic mastocytosis.

283 Indolent T-cell lymphoproliferative disorder is usually

284 After the diagnosis of indolent T-cell lymphoproliferative disorder of the gast

285 Indolent T-cell lymphoproliferative disorder of the gast

286 gression to identify factors associated with indolent (TDT > 365 days) and rapid (TDT < 90 days) tumo

287 An indolent threshold (ultralow risk) of the US Food and Dr

288 eening that results in the identification of indolent thyroid cancers, and treatment of these overdia

289 A vast range of disorders--from indolent to fast-growing lesions--are labelled as cancer

290 The transition of a subset of tumors from indolent to invasive disease is associated with a poor c

291 pectrum of illnesses that vary from the most indolent to the most aggressive malignancies.

292 Better tools to identify indolent tumors are needed to avoid overtreatment.

293 ristic features of human FLs, explaining how indolent tumors arise from GC B cells.

294 Follicular lymphomas (FLs) are slow-growing, indolent tumors containing extensive follicular dendriti

295 which TECs confer stem cell-like activity to indolent tumors is unknown.

296 ific host factor promoting the transition of indolent tumors to an angiogenic malignant state through

297 malignancy potential ranging from virtually indolent tumors to rapidly progressing cancers.

298 uld be used on a prostatic biopsy to predict indolent versus aggressive behavior of the cancer after

299 ) is a rare genodermatosis in which numerous indolent, well-differentiated basal cell carcinomas deve

300 Follicular lymphoma (FL) is an indolent, yet incurable B cell malignancy.