ライフサイエンスコーパス: pancreas cancer

1 skin cancer, breast cancer, lung cancer and pancreas cancer.

2 on provides the only possibility of cure for pancreas cancer.

3 s favorably with published data for resected pancreas cancer.

4 or (EGFR) signaling pathway in patients with pancreas cancer.

5 mycin improves the survival of patients with pancreas cancer.

6 iffness and epithelial cell contractility in pancreas cancer.

7 nt of patients with colorectal, gastric, and pancreas cancer.

8 ne in patients with newly diagnosed advanced pancreas cancer.

9 ptoms in patients with advanced, symptomatic pancreas cancer.

10 s primary sources of treatment resistance in pancreas cancer.

11 iclovir (GCV) for peritoneal metastases from pancreas cancer.

12 a novel approach to treatment of metastatic pancreas cancer.

13 uding prostate, breast, small cell lung, and pancreas cancers.

14 ironment of patients with invasive breast or pancreas cancers.

15 t is frequently lost in squamous, colon, and pancreas cancers.

16 primary mechanism of treatment resistance in pancreas cancers.

17 g exosomes bring it closer for patients with pancreas cancer?

18 Current protocols for the treatment of pancreas cancer are not as effective as we desire.

19 the control of growth and invasion of human pancreas cancer because of the independent activation of

20 els are elevated in breast, colon, lung, and pancreas cancers, but not correlated with EGFR mRNA leve

21 nalyzed the inactivation of p53 in the human pancreas cancer cell line Hs766T, which harbors a struct

22 sected pancreas cancer tissues (n = 14), and pancreas cancer cell lines (n = 8), and was hybridized t

23 Pancreas cancer cells were transduced in vitro with HS-t

24 DA-MB-231 (breast), H460 (lung), and BxPC-3 (pancreas) cancer cells were pretreated with 15 to 30 mic

25 ; Moffitt Lung Cancer Cohort (n=60); Moffitt Pancreas Cancer Cohort (n=40); and The Cancer Genome Atl

26 wenty-six patients with advanced symptomatic pancreas cancer completed a lead-in period to characteri

27 es experimental opportunities to investigate pancreas cancer development, progression and early-stage

28 Most patients with advanced pancreas cancer experience pain and must limit their dai

29 arly studies with gemcitabine, patients with pancreas cancer experienced an improvement in disease-re

30 t of lung, breast, prostate, colorectal, and pancreas cancers from 2000 to 2007.

31 d tumor suppressor activity of Smad4/DPC4 in pancreas cancer, including a short C-terminal truncation

32 e (TGFBR2) were identified in 4 of 97 (4.1%) pancreas cancers, including a homozygous deletion in a r

33 Pancreas cancer is one of the most lethal malignancies a

34 Pancreas cancer is the fourth and fifth leading cause of

35 h patients in previous prognostic studies of pancreas cancer may explain the failure of histological

36 ral HS-tk vectors is effective treatment for pancreas cancer metastatic to the peritoneal cavity; fur

37 nate process, cancer of the body and tail of pancreas, cancer of the extrahepatic bile duct, cancer o

38 In breast cancer patients (n = 35), pancreas cancer patients (n = 30), and normal donors (n

39 her in breast cancer patients (p < 0.01) and pancreas cancer patients (p < 0.01) when compared with n

40 In a panel of pancreas cancers preselected for loss of heterozygosity

41 Patients with advanced pancreas cancer present with disease that is poorly resp

42 impact of gene perturbation at any stage of pancreas cancer progression.

43 In the last decade, continued efforts in pancreas cancer research have led to the development of

44 smoking and obesity are known and suspected pancreas cancer risk factors, and have been associated w

45 ing fivefold or greater expression levels in pancreas cancer specimens as compared to normal tissue,

46 as having > or = 3-fold expression levels in pancreas cancer specimens as compared with nonneoplastic

47 he analysis of mass spectrometry data from a pancreas cancer study biological relevant and statistica

48 The Ontario Pancreas Cancer Study enrolls consenting participants wi

49 In patients with advanced pancreas cancer, the anti-EGFR monoclonal antibody cetux

50 For the majority of patients with pancreas cancer, the high metastatic proclivity is life

51 , including breast cancer, glioblastoma, and pancreas cancer, this report is to our knowledge the fir

52 l gastrointestinal mucosa (n = 22), resected pancreas cancer tissues (n = 14), and pancreas cancer ce

53 s of chronic pancreatitis, and 39 samples of pancreas cancer tissues or cancer cell lines and hybridi

54 on therapy in patients with locally advanced pancreas cancer to determine the maximum-tolerated dose

55 Seven patients with locally advanced pancreas cancer were treated with planned doses of radia