ライフサイエンスコーパス: neoplastic

1 ies in addition to those necessary to become neoplastic.

2 framework for how ceramides exert their anti-neoplastic activity.

3 se findings demonstrate low probability of a neoplastic aetiology of the examined pathologies in the

4 Cisplatin, a commonly used anti-neoplastic agent for solid tumors causes significant hea

5 l-Th biochemically modulates various anti-neoplastic agents by increasing their bioavailability in

6 s significantly impairs the proliferation of neoplastic AKT1 cells.

7 o offer the potential for early detection of neoplastic alterations.

8 issues to defend against cancer, by removing neoplastic and aneuploid cells.

9 aberrant intergenic CpG methylation to human neoplastic and developmental overgrowth.

10 hat DDR1 regulates tissue homeostasis in the neoplastic and injured pancreas.

11 ese tumors are composed of numerous distinct neoplastic and non-neoplastic cell populations, which co

12 When ZIAQ was applied to the comparison of neoplastic and non-neoplastic cells from a human gliobla

13 mary cilia in multiple cell types, including neoplastic and non-neoplastic cells.

14 CD47 is expressed at different levels by neoplastic and normal cells.

15 fferences in the cytokine milieu between the neoplastic and the surrounding non-neoplastic tissue, wh

16 digm for future studies of colchicinoids for neoplastic and various other diseases.

17 on dose-limiting side effect of several anti-neoplastics and a main cause of sensory disturbances in

18 decrease the risk of autoimmune, metabolic, neoplastic, and infectious diseases of the intestine and

19 itiating cells, but hardly detectable in non-neoplastic astrocytes, neural stem cells or normal brain

20 of ILT3 in CLL was a distinctive feature of neoplastic B cells and hematopoietic stem cells, thus id

21 treatment of diseases involving activated or neoplastic B cells or activated T cells.

22 ession and genomic instability in normal and neoplastic B cells.

23 ated signalling is a hallmark feature of the neoplastic B lymphocytes in chronic lymphocytic leukaemi

24 liferative capacity of MYC-driven normal and neoplastic B lymphoid cells depends on MNT, a MYC-relate

25 a synergistic interaction of MYC and MNT in neoplastic B-cell development, but the underlying mechan

26 strategies are urgently sought to breach the neoplastic barriers that prevent effective drug delivery

27 ) or their first endoscopic therapy of early neoplastic BE, from April 2015 through June 2018.

28 GERD in identifying individuals at risk for neoplastic BE.

29 ration of NTRK splice variants in normal and neoplastic brain provides an intersection of these two r

30 aster) that develop invasive or non-invasive neoplastic brain tumors.

31 RTs compared with other brain tumors and non-neoplastic brain.

32 histological subtypes of lung cancer and non-neoplastic bronchial mucosa as in vitro models represent

33 damage of the basement membrane (BM) in all neoplastic, but not hyperplastic, models examined.

34 nificant fraction of patients with CTCL, the neoplastic CD4(+) lymphocytes acquire extracutaneous tro

35 gainst these pathogens and were cytotoxic to neoplastic cell lines, suggesting their potential as lea

36 an dermal fibroblast NHDF cell lines, and on neoplastic cell lines: acute monocytic leukemia THP-1 an

37 and identified three shared and five private neoplastic cell populations, offering insight into the o

38 osed of numerous distinct neoplastic and non-neoplastic cell populations, which could each influence

39 ing a differentially expressed in normal and neoplastic cells (DENN) domain have emerged as the large

40 n developed to understand the effects of non-neoplastic cells and extracellular matrix (ECM) on drug

41 reased proliferation and survival in thyroid neoplastic cells and highlights a novel ceRNA circuitry

42 uman model demonstrated the influence of non-neoplastic cells and matrix on chemoresistance of GBM ce

43 , these tumours are composed of a mixture of neoplastic cells and non-neoplastic cells, including tum

44 read of a disease-producing agent, including neoplastic cells and pathogens such as certain viruses,

45 is regulated by a complex interplay between neoplastic cells and the tumor microenvironment.

46 t, which upon expression, recognizes CD19 on neoplastic cells and triggers T-cell activation and tumo

47 tifying subclones from the transcriptomes of neoplastic cells collected from patients.

48 tion using scRNA-seq of 59,915 tumor and non-neoplastic cells from 8 primary and 3 metastatic samples

49 lied to the comparison of neoplastic and non-neoplastic cells from a human glioblastoma dataset, the

50 ere, to reveal mechanisms by which different neoplastic cells generate this dominant 'don't eat me' s

51 Here, we show that neoplastic cells hijack mechanisms that are usually empl

52 n (alphaSMA) located immediately adjacent to neoplastic cells in mouse and human PDA tissue.

53 cer cells can influence the phenotype of non-neoplastic cells in the tumor microenvironment.

54 te tracing revealed that lactate produced by neoplastic cells leads to increased production of alpha-

55 ng to the line of differentiation that these neoplastic cells most closely resemble: the endothelial

56 had a median absolute number of circulating neoplastic cells of 4.6 (IQR 2-12) cells per muL.

57 in the infiltrate except in 1 case in which neoplastic cells of chronic myelogenous leukemia were in

58 In conclusion, neoplastic cells repurpose the endogenous neuron to micr

59 f nodal metastasis involves the extension of neoplastic cells through the lymph node capsule into the

60 tic role of PUFA-ePLs can be extended beyond neoplastic cells to other cell types, including neurons

61 Leptin sensitizes non-neoplastic cells to proliferative stimuli, causes mitoti

62 s and colocalized with phosphorylated Sqh in neoplastic cells undergoing mitosis and cytokinesis, con

63 Co-culture of neoplastic cells with CAFs led to increased invasiveness

64 Co-injection of neoplastic cells with TET-deficient MSCs inhibited tumor

65 Neoplastic cells within individual carcinomas often exhi

66 netic vulnerabilities specifically affecting neoplastic cells without similarly affecting normal cell

67 DENN (differentially expressed in normal and neoplastic cells) domains(7), and WDR41 is a beta-propel

68 en (Ag) is expressed at high copy numbers on neoplastic cells, absent on normal tissues, and contribu

69 ras oncogenes when transfected with DNA from neoplastic cells, but they failed to do so in 80 to 90%

70 GBM cells coexist with normal non-neoplastic cells, including endothelial cells, astrocyte

71 sed of a mixture of neoplastic cells and non-neoplastic cells, including tumour-associated macrophage

72 ction margin, (2) intraparenchymal spread of neoplastic cells, leading to an anatomically separate bu

73 ity of tumor samples that contain normal and neoplastic cells, limit reliable and accurate detection

74 the mechanisms underlying ASM in normal and neoplastic cells, remain to be clarified.

75 impacts of NAMPT inhibition extended beyond neoplastic cells, shaping surrounding immune effectors.

76 tional neural network to identify regions of neoplastic cells, then aggregates those classifications

77 ust responses against invading pathogens and neoplastic cells.

78 ccumulation of tumor-initiating cells in pre-neoplastic cells.

79 exclusively of differentiated neuronal-like neoplastic cells.

80 Sox2 upregulation in a subset of pancreatic neoplastic cells.

81 clones from one another, or from admixed non-neoplastic cells.

82 anism to suppress invading microorganisms or neoplastic cells.

83 ticipate in immune surveillance to eliminate neoplastic cells.

84 ple cell types, including neoplastic and non-neoplastic cells.

85 cer immunity upon genomic destabilization of neoplastic cells.

86 tic lesions, and constitute up to 30% of all neoplastic cells.

87 tion factor binding sites in both normal and neoplastic cells.

88 form intuitive visualizations of normal and neoplastic cellular distribution and differentiation.

89 are rare outcomes of a pervasive process of neoplastic change across morphologically normal colorect

90 ysiology-and indicate that the procession of neoplastic change that leads to endometrial cancer is in

91 firming minimal proliferation and absence of neoplastic change within the grafts during the time eval

92 nstability are detectable in CLDs before any neoplastic changes occur.

93 tanding of the earliest phases of colorectal neoplastic changes-which may occur in morphologically no

94 olymerase chain reaction was used to map the neoplastic clone in 20 adults with LCH, ECD, and HCL.

95 tes, the OC precursors, are derived from the neoplastic clone, we wondered whether decreased OC numbe

96 e mutations and chromosomal abnormalities of neoplastic clones.

97 While SBTS in neoplastic colon obstruction may reduce morbidity and ne

98 Incomplete resection of neoplastic colorectal polyps can result in postcolonosco

99 mal CAF content and MYC protein level in the neoplastic compartment, and identify CAFs as the specifi

100 reasing recognition of the importance of non-neoplastic components, the ability to breakdown the gene

101 ough multicentric Castleman disease is not a neoplastic condition, it is an emerging precursor to neo

102 Here, we review the different neoplastic conditions observed in patients with APDS and

103 c MC contributions to other inflammatory and neoplastic conditions were suggested by studies in tradi

104 s, as well as cardiovascular, autoimmune and neoplastic conditions.

105 re classified by the study team as vascular, neoplastic, congenital, other neurologic, or non-neurolo

106 l panels cannot reliably distinguish between neoplastic conjunctival myxomas and other myxoid lesions

107 artment of the mammary epithelium, and their neoplastic counterparts, mammary TICs (MaTICs), are thou

108 ring a clonal growth advantage on normal and neoplastic (cutaneous squamous cell carcinoma, cSCC) hum

109 s sufficient on its own to increase rates of neoplastic development in the prostate by upregulating c

110 etic selection is the major driving force of neoplastic development.

111 sified into groups containing those with non-neoplastic disease and those with high-grade dysplasia/c

112 Neurofibromatosis type 2 is an inherited, neoplastic disease associated with schwannomas, meningio

113 te application to inflammatory, fibrotic and neoplastic disease in multiple organs, including the det

114 Marek's disease (MD) is a neoplastic disease of chickens caused by Marek's disease

115 th Marek's disease (MD), a highly contagious neoplastic disease of chickens.

116 tic ductal adenocarcinoma is the predominant neoplastic disease of the pancreas and it represents the

117 Marek's disease (MD) is a highly neoplastic disease primarily affecting chickens, and rem

118 ransforms CD4(+) T cells and causes a deadly neoplastic disease that is associated with metabolic dys

119 pathway, we first generated mouse models of neoplastic disease with TGFbeta receptor deficiencies.

120 we discuss the role of AHR in autoimmune and neoplastic diseases of the central nervous system, with

121 ated polyamine metabolism is associated with neoplastic diseases such as colon cancer, prostate cance

122 wel inflammation (including complications of neoplastic diseases such as leukemia and Hodgkins'diseas

123 s (CI) instigate anticancer immunity in many neoplastic diseases, albeit only in a fraction of patien

124 ighly sought as treatments for metabolic and neoplastic diseases, and RJW100 has one of the few scaff

125 mune, cardiometabolic, neuropsychiatric, and neoplastic diseases.

126 of immunity to infection, inflammation, and neoplastic diseases.

127 utations in clonal hematopoiesis and diverse neoplastic diseases.

128 susceptibility to metabolic, autoimmune, and neoplastic diseases.

129 ctivity has been linked to immunological and neoplastic diseases.

130 scular dystrophy, epilepsy, chronic pain and neoplastic diseases.

131 sociated with rheumatic, cardiovascular, and neoplastic diseases.

132 ch in treating several conditions, including neoplastic diseases.

133 heim-Chester disease (ECD) are heterogeneous neoplastic disorders marked by infiltration of pathologi

134 s of cardiovascular diseases, lower rates of neoplastic disorders no differences in mortality for res

135 be suppressed pharmacologically to treat for neoplastic disorders with Galphaq pathway mutations.

136 pathogenesis of inflammatory, autoimmune and neoplastic disorders.

137 riving proliferation in UM and several other neoplastic disorders.

138 sions in which a colectomy was performed for neoplastic, diverticular, or inflammatory bowel disease

139 ivation of T cells, apoptosis of Kras mutant neoplastic ductal cells and pancreatic regeneration afte

140 n and metabolic homeostasis in Yap-deficient neoplastic ductal cells, which gradually re-differentiat

141 Herein, the anti-neoplastic effects of the electrophilic fatty acid nitro

142 livers and HCC, allowing us to identify pre-neoplastic epigenetic and transcriptional events.

143 Genetic analyses showed that the neoplastic epithelium at the margin was independent from

144 rapidly activated PI3K-Akt signaling in the neoplastic epithelium to promote nuclear translocation o

145 tor in the cross-talk between the stroma and neoplastic epithelium, functioning to promote fibrosis a

146 re best known for their pathological role in neoplastic evasion of chemotherapeutics and antibiotics.

147 er hallmark, but how it unfolds during early neoplastic events and its role in carcinogenesis and can

148 uartile range, 3.9-6.3 years), there were 14 neoplastic events with tamoxifen and 28 with placebo (11

149 nal interplay between tumour cells and their neoplastic extracellular matrix plays a decisive role in

150 We find no evidence of neoplastic features in BPH: no evidence of driver genomi

151 30 of the GHPs with neoplastic formation had a "strawberry-like" appearance

152 O mice had a significant delay in developing neoplastic gastric lesions.

153 transformation with 39 patients who had non-neoplastic GHPs.

154 Accurate discrimination of IPMN-associated neoplastic grade is an unmet clinical need.

155 Within the non-neoplastic group, aspirin users had lower EMF (p = 0.001

156 ce of quantitative parameters for evaluating neoplastic growth and aggressiveness.

157 oting activation of beta-catenin and driving neoplastic growth in mice lacking intact adaptive immuni

158 1AK55me2 loss dramatically reduce Ras-driven neoplastic growth in mouse models and in patient-derived

159 deterioration in lung function is driven by neoplastic growth of atypical smooth muscle-like LAM cel

160 we found that targeting CIB1 also inhibited neoplastic growth of cells induced by oncogenic Ras, sug

161 LAM is characterized by neoplastic growth of smooth muscle-alpha-actin-positive

162 upregulated by mutant KRAS, is essential for neoplastic growth.

163 tion of pancreatic ducts led to two types of neoplastic growth: exophytic lesions that expanded outwa

164 athway, Yap levels, and growth of normal and neoplastic hepatocytes.

165 ic condition, it is an emerging precursor to neoplastic high-grade B-cell lymphoproliferation among p

166 We further examined a non-neoplastic human primary cell line (lung lymphatic endot

167 mouse lung tumors at seven stages, from pre-neoplastic hyperplasia to adenocarcinoma.

168 he decision between normal injury repair and neoplastic initiation are unclear.

169 ariably detected in leukocyte DNA and/or non-neoplastic intestinal mucosa of these patients.

170 ound no evidence for mosaicism in APC in non-neoplastic intestinal mucosa.

171 ters expression of EMT markers and abrogates neoplastic invasion in breast cancer cells.

172 The sternum is an uncommon site for neoplastic involvement and metastases are far commoner t

173 Therefore, we aimed to improve neoplastic lesion detection by employing a fluorescence-

174 to identify the conjunctival margins of the neoplastic lesion.

175 proportion of subjects with resection of non-neoplastic lesions (26.0% in the CADe group vs 28.7% of

176 ypes in the setting of Pten loss, with early neoplastic lesions (high-grade prostatic intraepithelial

177 ammary gland homeostasis, evolution of early neoplastic lesions and cancer dissemination.

178 pression of ACLY, ACC1, and FASN proteins in neoplastic lesions and increased circulating levels of t

179 Kras mutations occur early in pre-neoplastic lesions but are insufficient to cause PDA.

180 tational discrimination between early breast neoplastic lesions for which pathologists often disagree

181 groups (83 [23.31%] of 356 patients with non-neoplastic lesions in the MB-MMX vs 97 [29.75%] of 326 p

182 -MMX vs 97 [29.75%] of 326 patients with non-neoplastic lesions in the placebo group).

183 Ducts with neoplastic lesions showed higher inflammation, wall thic

184 lt to resect recurrent / residual colorectal neoplastic lesions treated by EFTR.

185 A minority of animals with CI developed pre-neoplastic lesions, but cancer was not observed in any T

186 , and increases detection and delineation of neoplastic lesions.

187 acebo, without increasing the removal of non-neoplastic lesions.

188 number of deregulated miRNAs shared by both neoplastic lesions.

189 cell associated transcription factor, to the neoplastic-like properties of human lung epithelial cell

190 s, although the potential role of YAP in non-neoplastic liver diseases remains largely unknown.

191 t of ovine pulmonary adenocarcinoma (OPA), a neoplastic lung disease of sheep.

192 isregulation of PRC2 is linked to a range of neoplastic malignancies, which is believed to involve me

193 ic fungi, antibiotic-resistant bacteria, and neoplastic mammalian cells.

194 cell surfaceome, we used mouse models of pre-neoplastic mammary epithelial and cancer stem cells to r

195 henotypic and genetic changes within the pre-neoplastic mammary epithelium of mice with and without s

196 sts after exclusion of infectious causes and neoplastic masquerades of uveitis.

197 816V mutation and pathologic accumulation of neoplastic mast cells (MCs) in various tissues, leading

198 ed against KIT and other relevant targets in neoplastic mast cells and will hopefully receive recogni

199 is characterized by abnormal accumulation of neoplastic mast cells harboring the activating KIT mutat

200 Furthermore, knockdown of CCL2 in neoplastic mast cells resulted in reduced microvessel de

201 ession of the proangiogenic cytokine CCL2 in neoplastic mast cells.

202 ias, lamin A/C helps distinguish normal from neoplastic mature T cells, and VAMP-7 recapitulates ligh

203 (TME), and tackling spatial heterogeneity in neoplastic metabolic aberrations is critical for tumor t

204 development in vivo, considering the complex neoplastic microenvironment.

205 heterogeneous cellular ecosystems, where non-neoplastic monocytic cells have emerged as key regulator

206 followed by tuberculosis (n = 30, 28.0%) and neoplastic (n = 11, 10.3%).

207 associated with diseases, including genetic, neoplastic, nervous and reproductive system disorders.

208 loss of STAT3 activation, a decrease in the neoplastic neuroendocrine cell population, and impaired

209 oncogenesis, likely via direct signaling to neoplastic neuroendocrine cells capable of trophic influ

210 tification of miRNAs discriminating CNs from neoplastic nodules may have relevant translational impli

211 Neoplastic onset and the PanIN lesion progression were s

212 at characterize these tumors relative to non-neoplastic optic nerve tissue.

213 murine optic gliomas relative to normal non-neoplastic optic nerve.

214 Neoplastic or dysplastic neuronal tissue in the brain st

215 In the test set, the DNN-CAD identified neoplastic or hyperplastic polyps with 96.3% sensitivity

216 Drosophila imaginal discs is known to cause neoplastic overgrowth fueled by mis-regulation of signal

217 induced in ER-stressed and inflammatory pre-neoplastic pancreas is a potential marker of cancer prog

218 Here, we show that neoplastic pancreatic epithelium, as well as a subset of

219 lecular profiles and diagnoses of benign and neoplastic pancreatic lesions.

220 In neoplastic PanIN cells, pERK was not necessary for eithe

221 ome congenital, inflammatory, traumatic, and neoplastic pathologies of the duodenum along with the co

222 ax) >= 5 typically indicates tuberculosis or neoplastic pericarditis except in just one case of autoi

223 ighlight the clinical potential of targeting neoplastic pericytes to significantly improve treatment

224 In summary, PGC-1alpha modifies the neoplastic phenotype of glioblastoma cells toward more a

225 False-positive (resection rate for non-neoplastic polyps) and adverse events were assessed as s

226 /macrophages (TAM) are the most numerous non-neoplastic populations in the tumour microenvironment in

227 n and pre-emptive cancer treatment using the neoplastic precursor lesion Barrett's esophagus as an ex

228 lti-omics and immunity - basic tenets of the neoplastic process.

229 n pressure in the continuum of ERG dependent neoplastic process.

230 ntal cues encountered by the cell during the neoplastic process.

231 cal implications for inflammation-associated neoplastic processes.

232 tion is associated with an increased risk of neoplastic progression and may also lead to screening fo

233 p62 accumulation promotes neoplastic progression by controlling the NRF2-mediated

234 d to the development of unique biomarkers of neoplastic progression for patients with early stage bre

235 coccus aureus (SA) can inadvertently enhance neoplastic progression in models of skin cancer and cuta

236 ions, assessed here for their correlation to neoplastic progression in the gastro-oesophageal reflux

237 systematic study was made of the dynamics of neoplastic progression in various concentrations of CS i

238 ory may better define those most at risk for neoplastic progression.

239 tory elements driving cancer development and neoplastic progression.

240 ic or epigenetic alterations may account for neoplastic progression.

241 ollow-up intervals vary, which may result in neoplastic progression.

242 croenvironment combine to drive unrestricted neoplastic proliferation and metastasis.

243 s exhibited reduced nuclear beta-catenin and neoplastic proliferation but increased apoptosis.

244 were adenomas detected per colonoscopy, non-neoplastic resection rate, and withdrawal time.

245 mportance of epithelial SLC7A2 in abrogating neoplastic risk.

246 ncing efforts, suggesting both pro- and anti-neoplastic roles.

247 te units and HERV-K copies) were observed in neoplastic samples as compared to healthy counterparts.

248 in 18,430 samples, including tumors and non-neoplastic samples, across 31 cancer types.

249 vestibular schwannomas (VS) that arise from neoplastic Schwann cells (SCs).

250 owever, MHC-E also binds diverse foreign and neoplastic self-peptide antigens for presentation to CD8

251 DO1 and KP metabolites interact with pivotal neoplastic signaling pathways of the colon epithelium.

252 These results reveal a pre-neoplastic stage in human lymphomagenesis and a cascade

253 Also, it can present a profile from neoplastic states of different regions of a tumor.

254 The neoplastic stromal cells of giant cell tumor of bone (GC

255 are significantly higher in purified CD4(+) neoplastic T cells from patients with CTCL than from hea

256 -FnIII interaction as a novel method of anti-neoplastic targeting in the tumor microenvironment.

257 arly in infection, sterile inflammation, and neoplastic tissue and then extending to more targeted pr

258 sign of effective targeted therapies against neoplastic tissue growth.

259 r the spectral difference between normal and neoplastic tissue is not well understood.

260 nce is provided for morphologic selection of neoplastic tissue, testing algorithms, scoring methods,

261 tween the neoplastic and the surrounding non-neoplastic tissue, which may have further influenced NKp

262 ous specimens compared to tumor-adjacent non-neoplastic tissues (P = 0.009).

263 and distinctive presence of fusion genes in neoplastic tissues and their involvement in multiple pat

264 Yet, many non-neoplastic tissues are more prolific compared with typic

265 nous administration, ss-CyFaP accumulates in neoplastic tissues of mice and rats bearing orthotopic m

266 To study somatic mutations in non-neoplastic tissues, we developed a series of protocols t

267 and revealed strikingly altered patterns in neoplastic tissues.

268 out mouse studies revealed that stromal, not neoplastic, TLR7 is requisite for R848-mediated response

269 as a risk factor for GHPs which demonstrated neoplastic transformation (odds ratio [OR], 3.729; 95% c

270 es; earlier during oncogenesis it suppresses neoplastic transformation and tumor growth, but later it

271 Neoplastic transformation in a Drosophila genetic model

272 have recently shown that Caspase-8 sustains neoplastic transformation in vitro in human GBM cell lin

273 Notably, stepwise neoplastic transformation is accompanied by a gradual in

274 f the most highly upregulated enzymes during neoplastic transformation is MTHFD2, a mitochondrial met

275 gene expression of hypergastrinemia-induced neoplastic transformation of enterochromaffin-like (ECL)

276 mutations in AIS/MIA/ADC than AAH suggesting neoplastic transformation of lung preneoplasia is predom

277 metabotropic glutamate receptor 1 (GRM1) in neoplastic transformation of melanocytes in vitro and sp

278 extracellular vesicles (TEVs) results in the neoplastic transformation of nonmalignant human SV-HUC u

279 not all types of colitis seem to have equal neoplastic transformation potential.

280 arcinoma (HCC) and are highly susceptible to neoplastic transformation triggered by activation of Erb

281 We compared 16 patients who had GHPs showing neoplastic transformation with 39 patients who had non-n

282 astic polyps (GHPs) have a potential risk of neoplastic transformation, but the responsible mechanism

283 cription and processing of genes involved in neoplastic transformation, including CCND1 (the cyclin D

284 These epigenetic events occur before neoplastic transformation, resulting in what may be a ph

285 rmine the cellular origins and mechanisms of neoplastic transformation, we studied highly fractionate

286 rt these miRNAs role in suppression of HCSCs neoplastic transformation.

287 nder (P = 0.146) in the GHP patients who had neoplastic transformation.

288 on in cancer tissues and different models of neoplastic transformation.

289 ansduction networks of melanoma cells during neoplastic transformation.

290 tors of muscle development and implicated in neoplastic transformation.

291 in cellular energetics, stress defense, and neoplastic transformation.

292 uced apoptosis and inhibition of Ras-induced neoplastic transformation.

293 ish risk factors that may be associated with neoplastic transformation.

294 one of the risk factors for GHPs to undergo neoplastic transformation.

295 d to protect against genomic instability and neoplastic transformation.

296 capable of dysregulating gene expression for neoplastic transformation.

297 hylation of REX1 was closely associated with neoplastic transition and advanced tumor stage in humans

298 s provide mechanistic insight into why human neoplastic translocation fragile DNA sequences are more

299 ugh caspases are activated in a well-studied neoplastic tumor model in Drosophila, oncogenic mutation

300 tent upregulation of Notch signaling induces neoplastic tumorigenesis in a transition zone between th