ライフサイエンスコーパス: invasive cancer

1 epithelial characteristics in progressively invasive cancer.

2 4.3%-10.1%) of the women had a diagnosis of invasive cancer.

3 lastic lesions, which display progression in invasive cancer.

4 ssociated with risk of progression to muscle invasive cancer.

5 changes associated with tissue distortion by invasive cancer.

6 Primary outcome was time to first invasive cancer.

7 areas, areas of hyperplasia, and in situ and invasive cancer.

8 ssion levels in ductal carcinoma in situ and invasive cancer.

9 ysplasia, any dysplastic serrated lesion, or invasive cancer.

10 ee synchronous IPMNs (10%) had an associated invasive cancer.

11 before histological or anatomic evidence of invasive cancer.

12 ivity was not associated with progression to invasive cancer.

13 of p53 are not sufficient for progression to invasive cancer.

14 terns were similar for advanced adenomas and invasive cancer.

15 oderate dysplasia, high-grade dysplasia, and invasive cancer.

16 ive effects of both young age and high-grade invasive cancer.

17 1.8%) of the patients, 58 of whom (0.6%) had invasive cancer.

18 rsors to ductal carcinoma in situ (DCIS) and invasive cancer.

19 rated histology, high-grade dysplasia, or an invasive cancer.

20 ly thought to be dysregulated secondarily to invasive cancer.

21 1), respectively] and with DCIS but not with invasive cancer.

22 s that MPA prevented CIN from progressing to invasive cancer.

23 (LGD) through high-grade dysplasia (HGD) to invasive cancer.

24 of bronchiectasis, anogenital dysplasia, or invasive cancer.

25 tic changes during development of tumors and invasive cancer.

26 biological mechanism of DCIS progressing to invasive cancer.

27 luence the mortality of patients with muscle-invasive cancer.

28 east event defined as DCIS recurrence or new invasive cancer.

29 l strategies to intercept the development of invasive cancers.

30 en considered a vital therapeutic target for invasive cancers.

31 s, 56% had branch duct (BD)-IPMN and 21% had invasive cancers.

32 helial cells and is significantly reduced in invasive cancers.

33 es that carry a higher risk of transition to invasive cancers.

34 e for cytoplasmic E-cadherin localization in invasive cancers.

35 ating this system as a therapeutic target in invasive cancers.

36 cancer is one of the most commonly diagnosed invasive cancers.

37 way signaling for prevention or treatment of invasive cancers.

38 ction rate and enabled the detection of more invasive cancers.

39 pothesis that IPBN and VMC are precursors to invasive cancers.

40 ly confirmed at histologic examination to be invasive cancers.

41 t significant trend was seen for ER-negative invasive cancers.

42 rentiated breast cancers but not in advanced invasive cancers.

43 gression of a subset of recurring non-muscle-invasive cancers.

44 ractive therapeutic target for many types of invasive cancers.

45 ), but no change in the detection of grade 3 invasive cancers.

46 y a comparable reduction in the incidence of invasive cancers.

47 s, but no change in the detection of grade 3 invasive cancers.

48 s, as candidate targets for the treatment of invasive cancers.

49 d will remain indolent, never progressing to invasive cancers.

50 eatment had similar risk of developing total invasive cancer (101.1/10,000 person-years for the activ

51 screening MR imaging were more likely to be invasive cancer (118 of 167 [71%]; P < .0001).

52 diate or high grade [seven of eight]) and 18 invasive cancers (14 T1a-c and four T2+ cancers, 89% Not

53 Increased sensitivity was largest for invasive cancers: 15% and 22% in studies 1 and 2 versus

54 A total of 379 women developed invasive cancer (187 in the active treatment group and 1

55 Among invasive cancers, 25% were late stage (stage 2B, 3, or 4

56 Thirty-seven additional invasive cancers (36 cancers with complete subtypes and

57 pathological testing, 54 patients (23%) had invasive cancer, 45 (19%) had ductal carcinoma in situ,

58 ata System category 4 or 5 breast masses (35 invasive cancers, 74 benign) from 2013 through 2017.

59 (4.21 +/- 1.16), DCIS (15.95 +/- 1.31), and invasive cancer (78.1 +/- 6.31) and highly correlated wi

60 %; minimal cancers, 57.7%; and node-negative invasive cancers, 79.4%.

61 ation of AIM1 from the actin cytoskeleton in invasive cancers, advanced prostate cancers often harbor

62 Patients who have extensive residual invasive cancer after neoadjuvant chemotherapy are at a

63 ter SIFU and in three (25%; 95% CI: 5%, 57%) invasive cancers after RTAS.

64 were found in seven (44%; 95% CI: 20%, 70%) invasive cancers after SIFU and in three (25%; 95% CI: 5

65 rs (four ductal carcinomas in situ and seven invasive cancers; all T1N0 intermediate or high grade) w

66 cross normal, intra-epithelial neoplasia and invasive cancer allows the identification of CpG sites t

67 tivation significantly declined from CIN3 to invasive cancer, also when compared in the same clinical

68 rveillance files to identify newly diagnosed invasive cancers among female workforce members during 1

69 We obtained incidence data for invasive cancers among people aged 25-84 years diagnosed

70 We identified 78 invasive cancers among treated patients: rituximab 33 (i

71 st tomosynthesis detected 7 of 17 women with invasive cancer and 2 of 6 women with DCIS.

72 viated breast MRI detected all 17 women with invasive cancer and 5 of 6 women with DCIS.

73 The smallest invasive cancer and DCIS detected were both 1 mm.

74 For detection of invasive cancer and DCIS, sensitivity was 95.7% (95% CI,

75 tive predictive value (PPV) of biopsy, using invasive cancer and ductal carcinoma in situ (DCIS) to d

76 paraffin-embedded histology, for identifying invasive cancer and ductal carcinoma in situ versus beni

77 re is in equipoise, with half progressing to invasive cancer and half regressing or remaining static.

78 patients with recurrent high-grade nonmuscle invasive cancer and patients undergoing radical cystopro

79 t by promoting development of differentiated invasive cancer and reducing prevalence of noninvasive c

80 the specimen that was removed in the case of invasive cancer and tumor that was within 1 mm of the ed

81 entially determine which lesions progress to invasive cancer and which could remain as pre-invasive D

82 immediate postmastectomy reconstruction for invasive cancer and/or carcinoma in situ were enrolled a

83 g enables desirable detection rates of small invasive cancers and DCIS.

84 n rate, recall rate, and proportion of small invasive cancers and ductal carcinoma in situ (DCIS).

85 ) and the separate cancer detection rate for invasive cancers and for DCIS was assessed.

86 ustment for numbers of small screen-detected invasive cancers and for numbers of grade 3 invasive scr

87 motes tumor development, including growth of invasive cancers and lymph node metastasis.

88 tor associations are similar for in situ and invasive cancers and may influence early stages of tumor

89 lated with both the cancer detection rate of invasive cancers and the cancer detection rate of DCIS (

90 cers detected at MR imaging, there were nine invasive cancers and three cases of ductal carcinoma in

91 Of the nine biopsy-proved cancers, six were invasive cancers and three were ductal carcinoma in situ

92 cases of ductal carcinoma in situ [DCIS], 43 invasive cancers) and 287 (81.3%) were false-positive.

93 lator of the transition from premalignant to invasive cancer, and may lead to the development of uniq

94 arly detection and prompt treatment of early invasive cancers, and palliative care.

95 Moreover, MKP3 expression is reduced in invasive cancers, and reduced p63 expression increases m

96 in cancer detection rates, particularly for invasive cancers, and the reduction in false-positive ra

97 % confidence interval: 0.73, 0.96) for total invasive cancer; and 4.17 (95% confidence interval: 2.68

98 d estrogen receptor alpha-positive papillary invasive cancers appeared in efatutazone-treated mice.

99 ts of detecting nonprogressive and nonlethal invasive cancer are considered.

100 e interleukin signaling profiles observed in invasive cancers are absent or weakly expressed in healt

101 Invasive cancer arising in BD-IPMN was found in 23 patie

102 ening are related to high detection rates of invasive cancers, as well as DCIS.

103 To examine the risk of invasive cancer associated with ADH diagnosed using core

104 RRs for concordant CIS-invasive cancer associations were lower than CIS-CIS ass

105 enage participants, 120 of their parents had invasive cancer before the Young-HUNT study according to

106 teristics, we found no difference in risk of invasive cancer between rituximab, natalizumab, and the

107 rum and plasma and hold promise as minimally invasive cancer biomarkers, potentially for assessing di

108 e higher rates of detection of grade 1 and 2 invasive cancers (both ductal and lobular), but no chang

109 (HSILs) ablation may reduce the incidence of invasive cancer, but few data exist on treatment efficac

110 ells (CTCs) are shed into the bloodstream by invasive cancers, but the difficulty inherent in identif

111 eptive use, we assessed associations for all invasive cancers by histology.

112 Among women with invasive cancer, CAD was associated with greater likelih

113 on criteria were applied after including all invasive cancer cases based on age group and diagnosis y

114 ignant features in 65% of in situ and 98% of invasive cancer cases, respectively, suggesting that the

115 vector can measure the dynamic signature of invasive cancer cell activity and cell-migration-induced

116 any, selective events to transform a highly invasive cancer cell into one with the capacity to metas

117 P-resistant homotrimers were produced by all invasive cancer cell lines tested, both in culture and i

118 h the ability of detecting a few human colon invasive cancer cells (SW48) in a mixed cell culture of

119 eutic target to selectively eliminate highly invasive cancer cells and improve the disease-free and o

120 trix metalloproteinase (MT1-MMP) anchored on invasive cancer cells and its proteolytic activity simul

121 he contrast MRI-enhancing edge of the tumor, invasive cancer cells are protected by the intact blood-

122 oncoproteins induces NM23-H1 degradation in invasive cancer cells by increasing cysteine cathepsin t

123 in transportability and may be a feature of invasive cancer cells by promoting cell perfusion throug

124 ng the increased cell plasticity inherent to invasive cancer cells for transdifferentiation therapy.

125 Invasive cancer cells form dynamic adhesive structures a

126 al (3D) organoid assays to identify the most invasive cancer cells in primary breast tumors.

127 vitro and the growth and migration of highly invasive cancer cells in vivo.

128 Invasive cancer cells interact with the surrounding extr

129 The conversion of invasive cancer cells into adipocytes repressed primary

130 Therefore, targeting the locally invasive cancer cells is more important than preventing

131 In summary, our findings suggest that invasive cancer cells may use homotrimers for building M

132 d an enhanced proliferation and migration of invasive cancer cells on the surface of homotrimeric ver

133 e during transendothelial migration (TEM) of invasive cancer cells remain elusive.

134 ment of prostatic (PC-3) and ovarian (SKOV3) invasive cancer cells resembled the response to MDA-MB-2

135 ce of noninvasively and sequentially sampled invasive cancer cells suitable for propagation in vitro.

136 reduced friction may be a factor in enabling invasive cancer cells to efficiently squeeze through tig

137 As a consequence, invasive cancer cells were no longer able to form leadin

138 ted cell types (fibroblasts, leukocytes, and invasive cancer cells) that we report here indicates the

139 ly migratory stem cell population likened to invasive cancer cells, as a model for physiological epit

140 s filopodia formation and bundling in highly invasive cancer cells, leading to attenuated cancer cell

141 eficient contact inhibition is a hallmark of invasive cancer cells, yet surprisingly the vascular inv

142 Syk negatively regulates motility of highly invasive cancer cells.

143 rtain cancers, PDLIM2 is highly expressed in invasive cancer cells.

144 eas hMENADeltav6 expression is restricted to invasive cancer cells.

145 dia, matrix-degrading protrusions present in invasive cancer cells.

146 ) was defined as when there were no residual invasive cancer cells.

147 the silenced state of Snai1 target genes in invasive cancer cells.

148 tor of NPY in hepatocytes and induced Y5R in invasive cancer cells.

149 and miR200 microRNAs in invasive versus non-invasive cancer cells.

150 iptionally active MT1-MMP and MMP-2 genes in invasive cancer cells.

151 invading capacity, including fibroblasts and invasive cancer cells.

152 umor (<5 mm), and 19 of 25 (76.0%) exhibited invasive cancer cellularity of <=10%.

153 vical intraepithelial neoplastic lesions and invasive cancer (cervical intraepithelial neoplasia grad

154 or prognosis of patients with aggressive and invasive cancers combined with toxic effects and short h

155 agement of high-risk patients with nonmuscle invasive cancer continues to be controversial, with a nu

156 in situ (DCIS) is largely extrapolated from invasive cancer data, but robust evidence specific to DC

157 Kinetic curve performance for identifying invasive cancer decreased after compression (area under

158 CI: 0.47, 0.83; P = .001), particularly for invasive cancers detected at a rescreening examination,

159 The percentage of invasive cancers detected was significantly higher with

160 The invasive cancer detection rate was 11.8 (95% CI, 7.4-18.

161 The primary end point was the invasive cancer detection rate.

162 ce, 1.2 (95% CI, 0.8-1.6; P < .001); and for invasive cancer detection, 2.9 (95% CI, 2.5-3.2) with di

163 der cancer, noninvasive papillary and muscle-invasive cancer, develop through independent pathologic

164 Invasive cancer developed in 10 patients (3%) by the 12-

165 er 5 years in 20 of 363 patients (5.5%), and invasive cancer developed in 16 of 363 patients (4.4%).

166 Cholangiocarcinoma (CCA) is a highly invasive cancer, diagnosed at an advanced stage, and ref

167 g the past 5 years including advances in non-invasive cancer diagnosis, monitoring of neurotransmitte

168 rous exosome detection towards potential non-invasive cancer diagnosis.

169 nitrosamine, Stat3-transgenic mice developed invasive cancer directly from carcinoma in situ (CIS), b

170 but 9 patients (41%) with HGD progressed to invasive cancer during endotherapy.

171 Approximately 40% of adults develop invasive cancer during their lifetimes, many of whom req

172 s we assessed the same interactions, but for invasive cancer, estrogen receptor (ER) positive cancer

173 opment of better methods to predict risk for invasive cancer, evaluation of a strategy of active surv

174 Consistent with this, we observe that invasive cancers exhibit increased covariation in DNA me

175 otential use in a clinical setting to detect invasive cancer foci and for individualized cancer thera

176 analysis confirmed associations with serous invasive cancers for two correlated (r(2) = 0.62) SNPs:

177 Invasive cancers from controls were uniformly estrogen r

178 recommended chemotherapy for all women with invasive cancer greater than 1 centimeter.

179 c genetic drivers that are likely to set-off invasive cancer growth.

180 role in oncogenesis, tumor progression, and invasive cancer growth.

181 ological states, including wound healing and invasive cancer growth.

182 oma in situ and 95% of resected BD-IPMN with invasive cancer had high-risk stigmata or worrisome feat

183 ients included in our analysis, 2,024 had an invasive cancer history.

184 y escape immune surveillance and progress to invasive cancer; however, the mutational landscape that

185 demonstrated significantly increased risk of invasive cancer (HR, 2.73; 95% CI, 1.66 to 4.49) but not

186 ncidence of estrogen receptor (ER) -positive invasive cancers (HR, 0.70; 95% CI, 0.52 to 0.94, P = .0

187 vestigated as a therapeutic platform for non-invasive cancer hyperthermia therapy.

188 Results Among 653 invasive cancers identified in 629 women, a total of 532

189 p53 and Pten in bladder epithelium leads to invasive cancer in a novel mouse model.

190 ete response (pCR; defined as the absence of invasive cancer in breast and nodes) and RFS, overall an

191 e factors associated with underestimation of invasive cancer in patients with a clinical diagnosis of

192 he is found to have several foci of residual invasive cancer in the breast (largest focus, 0.3 cm), l

193 mplete response (pCR), defined as absence of invasive cancer in the breast and axillary lymph nodes.

194 onstrated a complete pathologic response (no invasive cancer in the breast or axillary nodes) to chem

195 n) as the standard for an adequate margin in invasive cancer in the era of multidisciplinary therapy

196 or as the standard for an adequate margin in invasive cancer in the era of multidisciplinary therapy

197 ve progression was defined as development of invasive cancer in the remnant pancreas or metastatic di

198 fat reduction delays transition from mPIN to invasive cancer in this Myc-driven transgenic mouse mode

199 s cytology-based screening for prevention of invasive cancer in women who undergo regular screening,

200 ilial intestinal cancer can develop frequent invasive cancers in the absence of overt genomic instabi

201 ses; in turn, MR imaging depicted additional invasive cancers in three women with false-positive find

202 ted prospectively to total and site-specific invasive cancer incidence (1993-2005).

203 ally higher detection of grade 1 and grade 2 invasive cancers, including both ductal and lobular canc

204 good prognosis, its profile of expression in invasive cancer is consistent with a role in breast tumo

205 gression from normal prostatic epithelium to invasive cancer is driven by molecular alterations, tumo

206 oment of lesion development nor the onset of invasive cancer is observed.

207 did not reduce percentage of mice developing invasive cancer, it significantly reduced prevalence of

208 ough such cells have been identified in many invasive cancers, it is not clear whether they emerge du

209 reast cancer risk, and interval cancer rate (invasive cancer </=12 months after a normal mammography

210 the size of MR imaging-detected multicentric invasive cancers (median, 0.6 cm; range, 0.1-6.3 cm) was

211 es responses to TGF-beta that are needed for invasive cancer migration and metastasis.

212 (n = 11), high-grade dysplasia (n = 4), and invasive cancer (n = 5).

213 ial tumors can often be treated effectively, invasive cancers not only require invasive surgery, but

214 In 535 earlier-stage (T1-2, N0) invasive cancers, nuclear pSmad2 was associated with imp

215 However, progression from HGPIN to invasive cancer occurs slowly, suggesting that tumorigen

216 Primary end points were invasive cancer of any type and major cardiovascular eve

217 ke, or death from cardiovascular causes) and invasive cancer of any type.

218 5-99 years) diagnosed with a first, primary, invasive cancer of the breast (women), colon, rectum, or

219 pression has been documented in a variety of invasive cancers of epithelial origin.

220 hed with up to five women with no history of invasive cancer on the index date (date of EC diagnosis)

221 nodal status, between the screening-detected invasive cancers on DM versus DBT (P = .09-.99).

222 Analyzing invasive cancers only, 5-year relapse-free survival for

223 significant effect on overall risk of total invasive cancer or breast cancer among women during the

224 min D did not result in a lower incidence of invasive cancer or cardiovascular events than placebo.

225 pCR was defined as absence of any residual invasive cancer or DCIS.

226 pCR) as the complete absence of any residual invasive cancer or ductal carcinoma in situ (DCIS).

227 A total of 2963 were diagnosed with invasive cancer or ductal carcinoma in situ within 12 mo

228 d with unilateral BC since 1970 and no other invasive cancer or tamoxifen use before first BC.

229 was histologically confirmed breast cancer (invasive cancers or non-invasive ductal carcinoma in sit

230 Restricting the analysis to ER+ cancers or invasive cancers or using samples from all ethnic groups

231 (hazard ratio for disease recurrence, second invasive cancer, or death, 0.72; 95% confidence interval

232 (hazard ratio for disease recurrence, second invasive cancer, or death, 0.83; 95% confidence interval

233 (SLNB) performed by high-volume surgeons in invasive cancers (P = 0.005).

234 eneral population; invasive cancer patients; invasive cancer patients diagnosed or treated at UPCI-af

235 data from 2000 to 2004: general population; invasive cancer patients; invasive cancer patients diagn

236 human tissues is strongly correlated with an invasive cancer phenotype.

237 witch in splicing, towards a more aggressive invasive cancer phenotype.

238 ne the evolutionary dynamics that promote an invasive cancer phenotype.

239 sed mitochondrial activities associated with invasive cancer phenotypes and circulating tumor cells.

240 .9] years) without experiencing an in-breast invasive cancer prior to death.

241 ell population and EMT, hence suppressed the invasive cancer progression, which is similar with the r

242 ic monoclonal antibodies (mAbs) for both non-invasive cancer radioimmunodetection (RID) and radioimmu

243 The invasive cancer rate was 1.5 per 1000 examinations after

244 g the course of tumor development over time, invasive cancer, reactive stroma, and infiltration of in

245 elates of RT receipt among all patients with invasive cancer receiving breast-conserving surgery (BCS

246 The DBT group had a higher proportion of invasive cancers relative to in situ cancers (81.1% vs 7

247 agement of high-risk patients with nonmuscle-invasive cancer remains a challenge, with continued cont

248 theless, the risk of harboring malignancy or invasive cancer remains a significant matter of conseque

249 t were localized or targeted for biopsy were invasive cancers, representing 23% of the 22 malignancie

250 ive cancer than CIS-CIS suggest that CIS and invasive cancers share only partially risk factors that

251 ant to identify those at risk for submucosal invasive cancer (SMIC).

252 east cancer within 1 year after mammography, invasive cancer stage, and diagnostic testing within 90

253 Lower risks for CIS-invasive cancer than CIS-CIS suggest that CIS and invasi

254 tic intraepithelial lesions and more foci of invasive cancer than pancreata of unexposed mice (contro

255 Gliomas are invasive cancers that resist all forms of attempted ther

256 s would become promising next-generation non-invasive cancer theranostic techniques and improve our a

257 individual lung cancer CTCs toward minimally invasive cancer therapy prediction and disease monitorin

258 In patients with nonmuscle invasive cancer, there is a need for enhanced visualizat

259 Since certain cyst types are precursors to invasive cancer, this situation presents an opportunity

260 %, and treatment of pre-invasive lesions and invasive cancer to 90%.

261 carcinogenesis, screening, and precancer and invasive cancer treatment.

262 The high demand in effective and minimally invasive cancer treatments, namely thermal ablation, lea

263 Detection of invasive cancers up to 10 mm for DR photon counting was

264 Invasive cancers use pericellular proteolysis to breach

265 atus (OR, 1.9 [95% CI: 1.3, 2.6]; P < .001), invasive cancer versus ductal carcinoma in situ (OR, 1.6

266 The proportions of screening-detected invasive cancers, versus in situ cancers, were similar (

267 Ib, III, IV) versus early (ie, I, IIa) stage invasive cancer was calculated according to BIRADS densi

268 rsistent DCIS remained in 50 patients (85%), invasive cancer was detected in six patients (10%), and

269 Invasive cancer was diagnosed in 820 participants in the

270 six patients (10%), and no residual DCIS or invasive cancer was seen in nine patients (15%).

271 se-modifying therapies, no increased risk of invasive cancer was seen with rituximab and natalizumab,

272 The median tumor size of invasive cancers was 10 mm; 88% were node negative.

273 45.6% were minimal cancers, the mean size of invasive cancers was 21.2 mm, and 69.6% of invasive canc

274 as identified with asymmetry, one (6%) in 16 invasive cancers was identified with architectural disto

275 Overall, one (5%) in 20 invasive cancers was identified with asymmetry, one (6%)

276 architectural distortion, one (21%) in five invasive cancers was identified with calcifications, and

277 Rates of histologic grade 1 invasive cancer were 0.5 per 1000 screened women (study

278 eoplasia (advanced adenomas and cancer), and invasive cancer were seen in 3.8% (55 of 1429), 2.8% (40

279 ly 13%, only 9.8% of patients diagnosed with invasive cancers were African American.

280 The invasive cancers were all less than 2 cm in size.

281 Tumor characteristics were obtained, and invasive cancers were classified according to St Gallen

282 Twenty-five additional invasive cancers were detected with mammography plus tom

283 No invasive cancers were found.

284 Additional invasive cancers were identified in three women with fal

285 with calcifications, and two (68%) in three invasive cancers were identified with a mass.

286 Five percent of invasive cancers were identified with asymmetry, and asy

287 t screening with mammography and MR imaging, invasive cancers were more likely to be detected at MR i

288 Most of these small invasive cancers were multifocal (66%), less than 10 mm

289 f invasive cancers was 21.2 mm, and 69.6% of invasive cancers were node negative.

290 USS) of 58 (48.3%; 95% CI 35.0-61.8) of the invasive cancers were stage I/II, with no difference (p=

291 3 (16 ductal carcinoma in situ [DCIS] and 67 invasive cancers) were malignant.

292 ding on why only some DCIS lesions evolve to invasive cancer whereas others appear not to do so durin

293 quamous epithelium progresses to early-stage invasive cancer will help formulate rational surveillanc

294 The reference standard was positive for invasive cancer with or without DCIS in 17 women and for

295 Nasopharyngeal carcinoma (NPC) is an invasive cancer with particularly high incidence in Sout

296 (GBM) is a highly proliferative and locally invasive cancer with poor prognosis and a high recurrenc

297 y and distinguished IPMN LGD or IPMN HGD and invasive cancer with up to 90.06% accuracy.

298 sensitivity and specificity and reveals more invasive cancers with fewer nodal or distant metastases.

299 Pathology demonstrated a 1.9-cm grade 2 invasive cancer without lymphatic vascular invasion; cle

300 ch show aberrant expression in several other invasive cancers, would also predict HBL tumor invasiven