ライフサイエンスコーパス: severe dysplasia

コーパス検索結果 (１語後でソート)

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1 One fifth of the adenomas exhibited severe dysplasia.

2 D1 immunoreactivity is associated with more severe dysplasia.

3 Fifteen patients were found to have severe dysplasia.

4 nt to the CLIC4-suppressed RPE cells display severe dysplasia.

5 ens were characterized as mild, moderate, or severe dysplasia; 52% were classified as carcinoma in si

6 ontinue surveillance who display moderate-to-severe dysplasia alone.

7 nd predisposes this gland to hyperplasia and severe dysplasia analogous to prostatic intraepithelial

8 Adenomas with severe dysplasia and carcinomas showed an equal, diffuse

9 high risk" because of their association with severe dysplasia and cervical carcinoma.

10 n of phosphorylated Akt were associated with severe dysplasia and each other.

11 H. pylori infection induced severe dysplasia and gastric cancer classified as high-g

12 n parallel in proliferating keratinocytes in severe dysplasias and carcinomas suggesting that IL-1alp

13 oses of mild dysplasia, 26 % had moderate to severe dysplasia, and 2% presented with carcinoma in sit

14 A extracted from normal squamous epithelium, severe dysplasia, and corresponding carcinoma specimens

15 Overexpressed EpCAM was detected in severe dysplasia, but negative in mild to moderate dyspl

16 omas with a villous component or moderate-to-severe dysplasia, carcinoma in situ, or frank carcinoma)

17 ping to p13.3 was involved in progression of severe dysplasia/carcinoma in situ to invasive bladder c

18 mmunoreactivity was concentrated in areas of severe dysplasia/carcinoma or invasion, where K-ras muta

19 3), from mild (n = 4), moderate (n = 6), and severe dysplasias/carcinomas in situ (CIS) (n = 13), and

20 al genetic aberration at the transition from severe dysplasia/CIS to invasive cervical carcinoma.

21 f chromosome 3q became visible in one of the severe dysplasias/CIS.

22 n was stronger for adenomas with moderate or severe dysplasia compared with mild dysplasia.

23 Of 50 ACF, 3 (6%) contained focal areas with severe dysplasia, ie, carcinoma in situ, 4 (8%) containe

24 regional homozygous deletion of Alk1 induces severe dysplasia in the adult mouse brain, akin to human

25 nt signaling, and genes associated with more severe dysplasia included those encoding members of the

26 The likelihood of Dukes' A cancer or severe dysplasia increased from 4% (3/70) in small flat

27 dividuals also contained foci of moderate to severe dysplasia (intraepithelial neoplasia grade II/III

28 s 1 cm or larger or with villous features or severe dysplasia located beyond sigmoidoscopic view.

29 Helicobacter pylori infection causes severe dysplasia manifested as gastrointestinal intraepi

30 detected in 15.4% and 11.5% of patients with severe dysplasia of the oral epithelium.

31 splasia, and 89% (8/9) of MCN epithelia with severe dysplasia or carcinoma.

32 54% (20/37) lesions containing severe dysplasia or Dukes' A carcinoma were flat or depr

33 increase in CN in preinvasive lesions graded severe dysplasia or higher.

34 cm; OR 2.4, 95% CI 1.2-4.8), had moderate to severe dysplasia (OR 2.1, 95% CI 1.1-3.8), or were in th

35 a polyp with villous histologic features or severe dysplasia, or a cancer.

36 cm or larger or one with villous histology, severe dysplasia, or cancer) was measured for each score

37 r or with tubulovillous or villous features, severe dysplasia, or invasive cancer), the respective re

38 an adenoma > or = 1 cm and none had cancer, severe dysplasia, or villous or tubulovillous histology.

39 the stomach and preventing progression from severe dysplasia to gastric cancer in H. pylori-infected

40 Areas of mild, moderate, or severe dysplasia were microdissected from paraffin-embed

41 rn fetuses with congenital renal agenesis or severe dysplasia would possess mutations in RET, GDNF, o

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