ライフサイエンスコーパス: invasive cancer

1 of bronchiectasis, anogenital dysplasia, or invasive cancer.

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

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

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

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

6 before histological or anatomic evidence of invasive cancer.

7 ivity was not associated with progression to invasive cancer.

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

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

10 terns were similar for advanced adenomas and invasive cancer.

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

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

13 1.8%) of the patients, 58 of whom (0.6%) had invasive cancer.

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

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

16 at high levels in both precursor lesions and invasive cancer.

17 ) had pCR+DCIS, and 2,025 (88%) had residual invasive cancer.

18 ted the early response and persisted through invasive cancer.

19 ology, adenoma with high-grade dysplasia, or invasive cancer.

20 neoplasia, compared with treatment given for invasive cancer.

21 from the inception of preinvasive disease to invasive cancer.

22 stologically defined complete eradication of invasive cancer.

23 %); 18 of the 30 specimens were positive for invasive cancer.

24 n DCIS, with several of them present only in invasive cancer.

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

26 ion that, in humans, typically progresses to invasive cancer.

27 eatures, and not all necessarily progress to invasive cancer.

28 illous histology or high-grade dysplasia, or invasive cancer.

29 event progression of premalignant lesions to invasive cancer.

30 n four (27%) were upgraded to either DCIS or invasive cancer.

31 epithelial characteristics in progressively invasive cancer.

32 4.3%-10.1%) of the women had a diagnosis of invasive cancer.

33 lastic lesions, which display progression in invasive cancer.

34 tic changes during development of tumors and invasive cancer.

35 ssociated with risk of progression to muscle invasive cancer.

36 biological mechanism of DCIS progressing to invasive cancer.

37 changes associated with tissue distortion by invasive cancer.

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

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

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

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

42 way signaling for prevention or treatment of invasive cancers.

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

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

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

46 ly confirmed at histologic examination to be invasive cancers.

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

48 rentiated breast cancers but not in advanced invasive cancers.

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

50 lism with the ability of tumor cells to form invasive cancers.

51 progression mechanism, resulting in immortal invasive cancers.

52 embryos and a key step in the progression of invasive cancers.

53 l strategies to intercept the development of invasive cancers.

54 en considered a vital therapeutic target for invasive cancers.

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

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

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

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

59 Of 171 patients with invasive cancer, 131 (77%) underwent preoperative CRT.

60 ma in situ [11 of 19 (57.9%), P = 0.018] and invasive cancer [14 of 30 (46.7%), P = 0.0023] tissues.

61 In those patients with invasive cancers, 15% had invasive cancer at the final s

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

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

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

65 diagnoses in the PI group were IPMN without invasive cancer (30%), cystadenoma (17%), and pancreatic

66 hylation of ASC/TMS1 is also associated with invasive cancers (41 of 152 or 27.0% of all lung cancer

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

68 42.0%; percentage of axillary node-negative invasive cancers, 73.6%; and percentage of stage 0 and I

69 tter than the rate of patients with residual invasive cancer (74.4%; P < .001).

70 (4.21 +/- 1.16), DCIS (15.95 +/- 1.31), and invasive cancer (78.1 +/- 6.31) and highly correlated wi

71 %; minimal cancers, 57.7%; and node-negative invasive cancers, 79.4%.

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

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

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

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

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

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

78 much lower prevalence of concomitant occult invasive cancer among high-grade dysplasia patients unde

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

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

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

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

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

84 We estimated the frequency of DCIS and invasive cancer and time to breast events from birth usi

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

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

87 nancy was identified in 52 (61%) lesions: 35 invasive cancers and 17 ductal carcinoma in situ (DCIS)

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

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

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

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

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

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

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

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

96 nent: 12 were minimally or noninvasive (<10% invasive cancer) and 13 had an invasive component rangin

97 s, high-grade dysplasia, size > or =1 cm, or invasive cancer) and adenoma multiplicity (0, 1-2, or >

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

99 ion from self-limited premalignant growth to invasive cancer, and, therefore, that this transition ma

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

101 s of minimal cancers, axillary node-negative invasive cancers, and stage 0 and I cancers.

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

103 % confidence interval: 0.73, 0.96) for total invasive cancer; and 4.17 (95% confidence interval: 2.68

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

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

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

107 Invasive cancer arises over many years, even decades, in

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

109 None of the invasive cancers arising from mucinous cysts was <3 cm.

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

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

112 24%) of the 17 DCIS lesions were upgraded to invasive cancer at excisional biopsy or mastectomy.

113 hose patients with invasive cancers, 15% had invasive cancer at the final surgical margin, 23% had IP

114 final surgical margin, 23% had IPMN without invasive cancer at the margin, and 54% had lymph node me

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

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

117 esponse [pCR]) and patients with no residual invasive cancer but persistent in situ disease (pCR+DCIS

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

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

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

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

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

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

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

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

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

127 ssion levels were similar in preinvasive and invasive cancer cells and significantly lower than adjac

128 members of this enzyme class up-regulated in invasive cancer cells and to evaluate the selectivity of

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

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

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

132 Invasive cancer cells form dynamic adhesive structures a

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

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

135 Invasive cancer cells interact with the surrounding extr

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

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

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

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

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

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

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

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

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

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

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

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

148 eas hMENADeltav6 expression is restricted to invasive cancer cells.

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

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

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

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

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

154 with a matrix degradation activity formed by invasive cancer cells.

155 Syk negatively regulates motility of highly invasive cancer cells.

156 invading capacity, including fibroblasts and invasive cancer cells.

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

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

159 carriers, 48 (37%) had DCIS (with or without invasive cancer) compared with 92 noncarriers (34%).

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

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

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

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

164 The percentage of invasive cancers detected was significantly higher with

165 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

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

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

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

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

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

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

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

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

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

175 Invasive cancers from controls were uniformly estrogen r

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

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

178 inhibit Met signaling and potentially block invasive cancer growth.

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

180 ity of dual time point imaging was 90.1% for invasive cancer >10 mm, 82.7% for invasive breast cancer

181 nivariate analysis showed that both DCIS and invasive cancer had an earlier onset in mutation carrier

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

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

186 -MMP expression within in situ dysplasia and invasive cancer in 61 samples of human colon cancer.

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

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

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

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

191 pCR was defined as no residual invasive cancer in the breast and axillary lymph nodes.

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

193 juvant chemotherapy (no evidence of residual invasive cancer in the breast and lymph nodes at the tim

194 s who experience complete eradication of the invasive cancer in the breast and lymph nodes does not a

195 nificantly improved the ability to eradicate invasive cancer in the breast and lymph nodes.

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

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

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

199 N function is required in the development of invasive cancer in the model.

200 Patients with in situ or invasive cancer in the same breast or patients without f

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

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

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

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

205 t-treatment disease (ie, CIN of any grade or invasive cancer) in relation to completeness of excision

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

207 The NCI benchmark did not reflect the actual invasive cancer incidence rate in African American patie

208 was strengthened in a subgroup of women with invasive cancers infected by high-risk human papillomavi

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

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

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

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

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

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

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

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

217 ts, lesions were upgraded to DCIS (n = 4) or invasive cancer (n = 2).

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

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

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

221 No residual invasive cancer occurred in tumors 17 mm or smaller or i

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

223 5-99 years) diagnosed with a first, primary, invasive cancer of the breast (women), colon, rectum, or

224 There were 631 confirmed cases of invasive cancer of the colon or rectum.

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

226 Papillary and invasive cancers of the urinary bladder appear to evolve

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

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

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

230 ntified patients subsequently diagnosed with invasive cancer or adenoma with high-grade dysplasia.

231 were at higher risk of being diagnosed with invasive cancer or adenoma with high-grade dysplasia.

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

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

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

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

236 Diagnosis of invasive cancer or ductal carcinoma in situ within 24 mo

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

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

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

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

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

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

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

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

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

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

247 The DNA panel detected 29 of 71 invasive cancers plus adenomas with high-grade dysplasia

248 .9] years) without experiencing an in-breast invasive cancer prior to death.

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

250 tegrity was positively correlated to size of invasive cancers (r = 0.48; P < .0001) and significantly

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

252 The invasive cancer rate was 1.5 per 1000 examinations after

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

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

255 urvival following resection of IPMNs without invasive cancer (regardless of degree of dyplasia) is go

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

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

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

259 ced neoplasms were found, including 14 and 4 invasive cancers, respectively.

260 No differences were found for other invasive cancer sites, for ischemic heart disease events

261 diagnosis rate, 25.3 per 1000 examinations; invasive cancer size, 20.2 mm; percentage of minimal can

262 nd biopsy performed), cancer diagnosis rate, invasive cancer size, and the percentages of minimal can

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

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

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

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

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

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

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

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

271 Invasive cancers use pericellular proteolysis to breach

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

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

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

275 rate was 4.7 per 1000, and the mean size of invasive cancers was 13 mm.

276 45.6% were minimal cancers, the mean size of invasive cancers was 21.2 mm, and 69.6% of invasive canc

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

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

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

280 with noninvasive neoplasms was 100% and, for invasive cancer, was 63%.

281 ing examination and tumor stage and size for invasive cancer were determined through linkage to patho

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

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

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

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

286 No invasive cancers were found.

287 Additional invasive cancers were identified in three women with fal

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

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

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

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

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

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

294 3 (16 ductal carcinoma in situ [DCIS] and 67 invasive cancers) were malignant.

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

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

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

298 a-carotene and breast cancer was greater for invasive cancers with nodal metastasis.

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