ライフサイエンスコーパス: malignant conversion

1 K(er)-mediated (p-Mypt1/tenascin C/rigidity) malignant conversion.

2 nchymal transition (EMT), a critical step in malignant conversion.

3 may be important in preventing or reverting malignant conversion.

4 enic, and IKK activities might contribute to malignant conversion.

5 tributes to tumor formation, progression and malignant conversion.

6 ls, thereby increasing their risk to undergo malignant conversion.

7 of alterations specifically associated with malignant conversion.

8 action of human cancers and can occur before malignant conversion.

9 ic characteristics of transformation or true malignant conversion.

10 ng cervical carcinogenesis and increase with malignant conversion.

11 s and carcinomas associated with accelerated malignant conversion.

12 rly germ cell-like phenotype advantageous in malignant conversion.

13 e incidence of adenomas by 65% and prevented malignant conversion.

14 gene-induced skin tumors undergo accelerated malignant conversion.

15 ularly for selecting tumors at high risk for malignant conversion.

16 rance of preneoplastic lesions and prevented malignant conversion.

17 gned to yield tumors at low or high risk for malignant conversion.

18 stimulation, which may have significance for malignant conversion.

19 dysplastic stage in all animals well before malignant conversion.

20 tional alterations appear to be required for malignant conversion.

21 evidence that loss of p73 can contribute to malignant conversion and support a role for TAp73alpha i

22 or IGF-IR signaling suppresses IL-6-mediated malignant conversion and the associated invasive phenoty

23 oncogenic insults p53 loss was required for malignant conversion, and following p53 loss persistent,

24 ing early tumor progression, at the onset of malignant conversion, and that these cells preferentiall

25 that are recruited to the tumor just before malignant conversion are essential for the angiogenic sw

26 Benign tumours that are at a risk of malignant conversion are primarily derived from cells lo

27 ced the percent of papillomas that underwent malignant conversion as well as the number of mice devel

28 e c-myc/TGF-beta1 mice showed a high rate of malignant conversion associated with a reduced expressio

29 ntiation, and induced keratin 8, a marker of malignant conversion, but did not cause tumor formation.

30 t capture the multi-hit initiation-promotion-malignant-conversion hypothesis of carcinogenesis.

31 is down-regulated at initiation and lost at malignant conversion in a clonal model of epidermal carc

32 We explored the role of p73 in malignant conversion in a clonal model of epidermal carc

33 stration that Smad7 overexpression can cause malignant conversion in a multistage cancer model and su

34 romotes spontaneous premalignant changes and malignant conversion in mammary glands of transgenic mic

35 forms of RCC and PICTs might play a role in malignant conversion in this disease.

36 A stepwise model for malignant conversion in VHL disease is herein proposed.

37 uestion related to the tissue-specificity of malignant conversion in VHL disease, a problem not easil

38 ss of p73 protein expression associates with malignant conversion in vivo and ionizing radiation (IR)

39 Ron signaling augments papilloma growth and malignant conversion in vivo.

40 evelopment, including initiation, promotion, malignant conversion, invasion, and metastasis.

41 In addition, malignant conversion occurred more rapidly, and the SCCs

42 V-induced skin tumorigenesis and reduced the malignant conversion of benign papillomas to SCCs.

43 s, and progression, the step involved in the malignant conversion of benign tumors to frank cancer.

44 on that the cph oncogene plays a role in the malignant conversion of chemically transformed hamster f

45 on of collagen fibrils, but does not inhibit malignant conversion of dysplasias into carcinomas or de

46 mechanisms of wtp53 protein inactivation in malignant conversion of epithelial cells by comparing cl

47 sis and the number of mutations that precede malignant conversion of healthy cell lineages.

48 These data indicate that malignant conversion of HPV-immortalized oral keratinocy

49 changes to changes in gene expression during malignant conversion of keratinized epithelium.

50 hat suppression of TM1 expression during the malignant conversion of mammary epithelium as a contribu

51 f the head and neck and of trials to prevent malignant conversion of oral premalignant lesions and th

52 s of p21WAF1 do not account for the enhanced malignant conversion of p53 null epidermal tumors.

53 on signature is strongly associated with the malignant conversion of preneoplastic liver lesions.

54 skin carcinogenesis but rather promotes the malignant conversion of skin papillomas.

55 MYC oncogene as a plausible driver gene for malignant conversion of the DNs.

56 ted expression of C/EBPbeta-2 contributes to malignant conversion of the human breast.

57 tumor suppressors function to constrain the malignant conversion of these PanIN lesions into lethal

58 r p73 contributes directly to the process of malignant conversion or whether aberrant p73 expression

59 overexpression can dramatically increase the malignant conversion rate of benign tumors, suggesting t

60 hyperplasia, cysts and papillomas, and while malignant conversion required p53 loss, elevated p21 exp

61 was found to be aberrantly expressed at the malignant conversion stage in a clonal epidermal model o

62 ecific times during promotion but not during malignant conversion to carcinomas.

63 nocyte transformation that parallels in vivo malignant conversion to squamous cell carcinoma, we show

64 helial hyperplasias, but did not inhibit the malignant conversion to squamous cell carcinomas.

65 TEN(flx) papillomatogenesis was accelerated, malignant conversion was delayed and tumours exhibited w

66 Matriptase-induced malignant conversion was preceded by progressive interfo

67 ed, their proliferation was lower, and their malignant conversion was profoundly inhibited (7% in tra

68 Spontaneous HK1.ras/Delta5PTEN malignant conversion was rare, whereas TPA promotion res

69 However, the frequency of malignant conversion was similar among all three genotyp

70 e models support a role for p53 mutations in malignant conversion, we found that each of three Schwan

71 Similar frequencies of malignant conversion were also observed in an in vitro a