ライフサイエンスコーパス: severe dysplasia

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 th late disease (i.e., higher proportions in severe dysplasia and carcinoma than in less severe lesio

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

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

11 While all mice developed severe dysplasia and cystic papillary neoplasms, there e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

31 Helicobacter pylori infection causes severe dysplasia manifested as gastrointestinal intraepi

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

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

34 54% (20/37) lesions containing severe dysplasia or Dukes' A carcinoma were flat or depr

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

36 in 45 percent of GPR68(-/-) mice developing severe dysplasia or squamous cell carcinoma compared to

37 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

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

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

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

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

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

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

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