ライフサイエンスコーパス: neoplastic

1 HCV+ (18%), liver biopsy (9%), HBsAg+ (6%), neoplastic (6%), or infective risk (5%).Most recipient a

2 N lesions that were ultimately resected were neoplastic (adenomas or serrated lesions), of which 43%

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

4 mouse prostate epithelium, which may promote neoplastic alterations in the prostate.

5 ic mice, histopathologically confirmed to be neoplastic and epithelial in origin.

6 n the medical management of individuals with neoplastic and inflammatory conditions have resulted in

7 that gliomas are complex tumors composed of neoplastic and non-neoplastic cells, which each individu

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

9 te cytotoxic T cells, whereas macrophages in neoplastic and parasitic diseases express anti-inflammat

10 Instead, the ECM is an active participant in neoplastic and physiologic invasion, and acts as an info

11 found that the average elastic moduli of non-neoplastic and tumor-bearing optic nerves were approxima

12 Similarly, MMP9 inhibition reduced neoplastic angiogenesis and significantly decreased loca

13 al features, patchy skin manifestations, and neoplastic association previously led to the suggestion

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

15 s increase genomic instability in normal and neoplastic B cells by an AID-dependent mechanism.

16 inositol 3-kinase can induce mobilization of neoplastic B cells from the lymphoid tissues into the bl

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

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

19 the amplification loop strongly reduces the neoplastic behavior of these cells and significantly imp

20 ancer stem cells exert enormous influence on neoplastic behavior, in part by governing asymmetric cel

21 ortant dermoscopic features for detection of neoplastic behavior.

22 significantly in CCA cells compared with non-neoplastic biliary epithelial cells.

23 was elevated in GBM tumors compared with non-neoplastic brain tissues, portended a worse prognosis, a

24 with stem cell maintenance in the normal and neoplastic brain.

25 imensional breast organoids derived from pre-neoplastic BRCA1(mut/+) tissue attenuated progesterone-i

26 Redox switches are important mediators in neoplastic, cardiovascular and neurological disorders.

27 croglia, that create a supportive stroma for neoplastic cell expansion and invasion.

28 in human tumours and its ability to promote neoplastic cell survival and growth.

29 h of the published literature has focused on neoplastic cell-autonomous processes for these adaptatio

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

31 rations driven by increased proliferation of neoplastic cells and angiogenesis in the cancer microenv

32 ils are rapidly diverted from a wound to pre-neoplastic cells and these interactions lead to increase

33 s NCTC cells against radiation, whilst HepG2 neoplastic cells are sensitized.

34 The majority of the non-neoplastic cells are tumor-associated macrophages (TAMs)

35 s aimed at inducing programmed cell death in neoplastic cells by re-engaging the proapoptotic activit

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

37 It is conceivable that neoplastic cells exhibit differential drug sensitivity b

38 Neoplastic cells express only low endogenous levels of t

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

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

41 Loss of CD37 on neoplastic cells in patients with diffuse large B cell l

42 he Trx and GSH systems synergistically kills neoplastic cells in vitro and in mice and decreases resi

43 However, the mechanisms by which neoplastic cells induce an immunosuppressive state to ev

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

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

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

47 novel molecular mechanism by which cervical neoplastic cells shape their local microenvironment by i

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

49 cancer-cell-intrinsic mechanisms that enable neoplastic cells to invade the local microenvironment, r

50 modification levels are tightly regulated in neoplastic cells to maintain cellular processes known as

51 s on using epigenetic therapies to reprogram neoplastic cells toward a normal state.

52 During the course of cancer progression, neoplastic cells undergo dynamic and reversible transiti

53 In response, neoplastic cells utilize NF-kappaB to suppress this kill

54 PD-L1 expression by neoplastic cells was significantly associated with commo

55 racellular domain to the apical cytoplasm of neoplastic cells with the expansion of IPMN lesions in A

56 Neoplastic cells within individual carcinomas often exhi

57 situ (DCIS) is defined as a proliferation of neoplastic cells within the duct of the mammary gland th

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

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

60 eting defects in the DNA repair machinery of neoplastic cells, for example, those due to inactivating

61 In neoplastic cells, however, autophagic responses constitu

62 branching, was decreased in E2f7/8-deficient neoplastic cells, indicating that E2F7/8 might inhibit i

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

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

65 that contrast with those of actively growing neoplastic cells, such as the expression of cell-cycle i

66 omplex tumors composed of neoplastic and non-neoplastic cells, which each individually contribute to

67 ulation of CAFs, located more distantly from neoplastic cells, which lacked elevated alphaSMA express

68 ered by the inability to specifically target neoplastic cells.

69 anism to suppress invading microorganisms or neoplastic cells.

70 verse impact of MTOR and EIF4A inhibitors on neoplastic cells.

71 ther enhancement in the growth properties of neoplastic cells.

72 cells drawn to a wound, and to adjacent pre-neoplastic cells.

73 s lead to increased proliferation of the pre-neoplastic cells.

74 ticipate in immune surveillance to eliminate neoplastic cells.

75 mas, but the molecular mechanisms underlying neoplastic changes in schwannoma cells remain unclear.

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

77 pendent on the maturation stage at which the neoplastic clone arose.

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

79 ncies generated immunophenotypically defined neoplastic clones capable of long-term, multi-lineage re

80 a method of choice in the diagnostics of all neoplastic CNS lesions.

81 nts with PMF harbors an abundance of clonal, neoplastic collagen- and fibronectin-producing fibrocyte

82 of the "field change" milieu permissive for neoplastic colon growth.

83 cells are dispensable in both the normal and neoplastic colonic epithelium, as ablation of Lgr5(+) st

84 ul for treating chronic viral infections and neoplastic conditions.

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

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

87 ids of 18 patients with benign tumors or non-neoplastic cysts.

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

89 the alteration of this balance can result in neoplastic development.

90 nt translation deregulation that would favor neoplastic development.

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

92 ssociated processes important for normal and neoplastic development.

93 for the pathogenesis of multiple myeloma, a neoplastic disease characterized by abnormal proliferati

94 Primary myelofibrosis (PMF) is a fatal neoplastic disease characterized by clonal myeloprolifer

95 Progression of neoplastic disease in the remnant pancreas following res

96 hangioleiomyomatosis, a rare and progressive neoplastic disease that predominantly affects women in t

97 ents diagnosed at autopsy or with additional neoplastic disease were excluded.

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

99 nhibitors are therapeutically useful against neoplastic disease, in particular refractory multiple my

100 y inflammatory condition to that of a clonal neoplastic disease.

101 rek's disease virus (MDV), is a lymphotropic neoplastic disease.

102 MS have been widely used in the treatment of neoplastic disease.

103 ing such pathways to modulate autoimmune and neoplastic disease.

104 overall small-bowel diseases (P = .0159) and neoplastic diseases (P = .0412) but not for the detectio

105 to investigate infectious, inflammatory and neoplastic diseases and develop novel drug regimes and v

106 enterography was more accurate in detecting neoplastic diseases in particular.

107 molecular contribution and functionality in neoplastic diseases remain to be established.

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

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

110 mpullary neoplasms, and 51 patients with non-neoplastic diseases who underwent pancreatic resection a

111 ctivity has been linked to immunological and neoplastic diseases.

112 pathogenesis of allergic, inflammatory, and neoplastic diseases.

113 al target for the treatment of metabolic and neoplastic diseases.

114 tes genes involved in normal development and neoplastic diseases.

115 as evolved into a neoplastic-like or overtly neoplastic disorder, perhaps contributing to its relativ

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

117 background, complicating the acquisition of neoplastic DNA without extensive background contaminatio

118 vered that doxorubicin, a commonly used anti-neoplastic drug, significantly decreased neuronal surviv

119 (nRTKI), is one of the most successful anti-neoplastic drugs in clinical use.

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

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

122 Rho GTPases may paradoxically result in pro-neoplastic effects.

123 r and to elucidate how RK-33 exerts its anti-neoplastic effects.

124 negatives) and two biopsied lesions were non-neoplastic entities on pathological review (false positi

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

126 whereas GSTA4 was strongly expressed in the neoplastic epithelia of invasive carcinomas.

127 r capture microdissection was used to obtain neoplastic epithelial tissue from 17 tumors which were e

128 ture microdissection was used to isolate the neoplastic epithelial tissue in 20 cases.

129 In response to signals elicited by the neoplastic epithelium, CCL8 production is enhanced in st

130 expanding opportunities for studies of early neoplastic events near this critical interface and poten

131 s and result in pathogenesis contributing to neoplastic events.

132 Vascular malformations are non-neoplastic expansions of blood vessels that arise due to

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

134 Early neoplastic features in oral epithelial dysplasia are fir

135 Collectively, our data suggest that neoplastic fibrocytes contribute to the induction of BM

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

137 lization of endogenous SK1, reduced in vitro neoplastic growth and tumor growth in mice, and suppress

138 For instance, tissue repair and neoplastic growth are greater in anterior than in poster

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

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

141 mponent in a pathway well described to drive neoplastic growth.

142 with increased proliferation, survival, and neoplastic growth.

143 Neoplastic hematologic disorders of the myeloid lineage

144 C-seq) was performed in MFD-1, OE33, and non-neoplastic HET1A cells.

145 RNA-Seq libraries covering 30 different non-neoplastic human tissues and cells as well as 15 mouse t

146 conditions were hematologic, prothrombotic, neoplastic, immune, and exposure to toxins.

147 Local immune-neoplastic interactions have been intensively investigat

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

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

150 UDH is most appropriately viewed as an early neoplastic intraductal proliferation.

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

152 Neoplastic involvement of the sternum is extremely unusu

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

154 ction of high-grade cervical intraepithelial neoplastic lesions and invasive cancer (cervical intraep

155 Agr2 induction preceded the formation of pre-neoplastic lesions and their development was largely inh

156 uation by diagnostic pathologists, describes neoplastic lesions associated with them, and discusses f

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

158 Pancreatic cancer (PC) and associated pre-neoplastic lesions have been reported to be hypoxic, pri

159 disorder characterized by the development of neoplastic lesions in kidney, lung, brain, heart, and sk

160 n CXCR2 levels were associated with advanced neoplastic lesions in tissue from human pancreatic speci

161 resulting system allowed the reproduction of neoplastic lesions in vitro at 27 days post-infection (P

162 Neoplastic lesions that developed with either MYC activa

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

164 terns are able to identify many sites in pre-neoplastic lesions, which display progression in invasiv

165 JNK inhibition reduced cholangiocellular pre-neoplastic lesions.

166 and 100 control patients with benign or non-neoplastic lesions.

167 number of deregulated miRNAs shared by both neoplastic lesions.

168 non-transformed cells neighbouring these pre-neoplastic lesions.

169 ed in human breast cancer, the most frequent neoplastic lethality among women.

170 toimmune T cell expansion has evolved into a neoplastic-like or overtly neoplastic disorder, perhaps

171 X9 overexpression may be responsible for the neoplastic-like phenotype observed in our model.

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

173 of Hippo pathway components in tumor and non-neoplastic liver tissue from 7 pediatric patients with m

174 issue and compared it to non-transformed and neoplastic low-grade and high-grade prostate epithelial

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

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

177 K3CA(H1047R) on mammary cell fate in the pre-neoplastic mammary gland and show that the cell of origi

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

179 ayloads such as radionuclides and drugs into neoplastic masses.

180 is expressed abundantly in the cytoplasm of neoplastic mast cells (MCs) in patients with advanced sy

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

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

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

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

185 D30(+) MC lines tested as well as in primary neoplastic MCs in patients with CD30(+) SM, but did not

186 CD30(+) SM, but did not induce apoptosis in neoplastic MCs in patients with CD30(-) SM.

187 ent types of epithelium is a hotspot for pre-neoplastic metaplasia and malignancy, but the cells of o

188 atopoietic cell interactions contributing to neoplastic myeloid disease.

189 to age-related, cardiovascular, infectious, neoplastic, neurodegenerative, and metabolic pathologies

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

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

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

193 classified for LOH, because of insufficient neoplastic nuclei in the sample.

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

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

196 eveloped a system called DNN-CAD to identify neoplastic or hyperplastic colorectal polyps less than 5

197 DNN-CAD classified polyps as neoplastic or hyperplastic in 0.45 +/- 0.07 seconds-shor

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

199 ed to classify the images of the test set as neoplastic or hyperplastic.

200 PD-L1 expression by either neoplastic or intratumoral inflammatory cells is related

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

202 Neoplastic pancreatic epithelial cells are believed to d

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

204 Despite documentation of various types of neoplastic pathologies encountered in the vertebrate fos

205 ated focal adhesion kinase (FAK) activity in neoplastic PDAC cells as an important regulator of the f

206 ting BMX with ibrutinib selectively targeted neoplastic pericytes and disrupted the BTB, but not the

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

208 estigated a role for this pathway in the pre-neoplastic phase of BRCA1-mutation carriers.

209 ole in the initiation and maintenance of the neoplastic phenotype and in cancer stem cells, which may

210 roduction was a common feature of normal and neoplastic plasma cells in mice, and IL-10 levels increa

211 ate flow cytometric evaluation of normal and neoplastic plasma cells, since the therapeutic antibody

212 f CD19 expression in 99.95% of the patient's neoplastic plasma cells.

213 of IL-10 during conditions of polyclonal and neoplastic plasmacytosis for the regulation of immunity

214 We collected 1476 images of neoplastic polyps and 681 images of hyperplastic polyps,

215 ravenous GE-137 enabled visualization of all neoplastic polyps that were visible with white light (38

216 required to differentiate hyperplastic from neoplastic polyps with high levels of accuracy.

217 test set of images (96 hyperplastic and 188 neoplastic polyps, smaller than 5 mm), obtained from pat

218 HCV and concurrently eliminating cells with neoplastic potential during chronic liver diseases, incl

219 develop a fully-penetrant myeloproliferative neoplastic process.

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

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

222 s are at the crossroads of developmental and neoplastic processes.

223 cilitates differentiation into heterogeneous neoplastic progeny when necessary.

224 tients and/or the difference in incidence of neoplastic progression among patients diagnosed with LGD

225 Intratumor heterogeneity (ITH) drives neoplastic progression and therapeutic resistance.

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

227 gulation of all three PPs appears central to neoplastic progression for melanoma, and the customary r

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

229 enetic and evolutionary principles governing neoplastic progression that has come from application of

230 sets derived from the W12 model of cervical neoplastic progression, for which high quality phenotype

231 lutionary model simulating genetic drift and neoplastic progression.

232 erexpression is the bypass of senescence and neoplastic progression.

233 ic or epigenetic alterations may account for neoplastic progression.

234 nd thereby generates the cells that initiate neoplastic progression.

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

236 tory elements driving cancer development and neoplastic progression.

237 ymmetric cell division resulting in dramatic neoplastic proliferation of neuroblasts and massive larv

238 mpletely severed without affecting normal or neoplastic proliferation, even under the most demanding

239 vity nor showed any cytotoxicity against non-neoplastic prostate epithelial PWR-1E cells.

240 g of laser capture microdissected normal non-neoplastic prostate epithelial tissue and compared it to

241 nes and pathways involved in both normal and neoplastic prostate epithelium are largely unknown.

242 se nuclear positions are robustly altered in neoplastic prostate tissues.

243 pronounced improvement in selectivity toward neoplastic relative to normal cells compared to its pare

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

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

246 5-hmC at enhancer regions in the majority of neoplastic samples.

247 In human early neoplastic skin and breast tissue, hTERT expression was

248 fic response to the forced transition from a neoplastic state to terminal differentiation.

249 t of human hematopoietic cells in normal and neoplastic states.

250 che, nerves help to regulate both normal and neoplastic stem cell dynamics.

251 t of RNA helicase inhibition as a novel anti-neoplastic strategy.

252 g CD5, a common surface marker of normal and neoplastic T cells, undergo only limited fratricide and

253 ell antigen receptor (TCR) repertoire of the neoplastic T-cells in 108 PTCL samples.

254 They have been proposed to be useful anti-neoplastic targets for over two decades, especially in R

255 esions, the highest accuracy (77%) to detect neoplastic tissue (19/26 patients) was obtained when the

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

257 study was to evaluate the alterations in the neoplastic tissue of GIST following Imatinib treatment.

258 DNA methylation field defects in normal pre-neoplastic tissue represent infrequent stochastic "outli

259 ariability was orders of magnitude less than neoplastic tissue transformation.

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

261 gical malignancies, and the accessibility of neoplastic tissue, the study of MPNs has provided a wind

262 by the expansion and accumulation of clonal (neoplastic) tissue mast cells in various organs.

263 We collected colorectal tumor and non-neoplastic tissues from 31 patients with IBD and colorec

264 of TTK protein are significantly elevated in neoplastic tissues from a cohort of liver cancer patient

265 When multiple samples are taken from the neoplastic tissues of a single patient, it is natural to

266 hesizes GABA, are significantly increased in neoplastic tissues.

267 and revealed strikingly altered patterns in neoplastic tissues.

268 ellular stresses, many of which occur during neoplastic transformation and in the tumor microenvironm

269 ential role of cellular reprogramming during neoplastic transformation and the major players involved

270 27M) and Trp53 loss alone are sufficient for neoplastic transformation if introduced in utero.

271 strate GSTA4 activation during 4-HNE-induced neoplastic transformation in colorectal carcinogenesis.

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 Neoplastic transformation is driven by oncogenic lesions

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

276 ole of TGF-beta deficiency in BWS-associated neoplastic transformation is unexplored.

277 at invasive capacity was altered even before neoplastic transformation occurred, as triggered by miR-

278 iral oncogene expression is insufficient for neoplastic transformation of human cells, so human papil

279 ow that targeted disruption of PTEN leads to neoplastic transformation of human neural stem cells (NS

280 constitutive Wnt activation, which leads to neoplastic transformation of the epithelial hair matrix.

281 ronic Helicobacter pylori infection triggers neoplastic transformation of the gastric mucosa in a sma

282 n the early stages of Kras-driven pancreatic neoplastic transformation was associated with decreased

283 trated for the first time a role for CIB1 in neoplastic transformation, and revealed a novel mechanis

284 tumors affect cell identity, cell state and neoplastic transformation, as well as addressing the pot

285 hat elevated levels of CIB1 resulted in full neoplastic transformation, in a manner dependent on SK1.

286 In some cases, the pagetic tissue undergoes neoplastic transformation, resulting in osteosarcoma and

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

288 Upon neoplastic transformation, the role of PDX1 changes from

289 ed regulation of ion channels is part of the neoplastic transformation, which suggests that ion chann

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

291 at CIN impairs cellular fitness and prevents neoplastic transformation.

292 ways, cancer cell proliferation and cellular neoplastic transformation.

293 rrounding tissue that in turn promotes their neoplastic transformation.

294 Cdh1 would exhibit a phenotype indicative of neoplastic transformation.

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

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

297 fects of tumor on neutrophil responses, anti-neoplastic treatment, including surgery, chemotherapy, a

298 nuclei without any direct information about neoplastic tumor cells.

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

300 Here, we show through analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila