戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ould not screen average-risk individuals for pancreas cancer.
2  skin cancer, breast cancer, lung cancer and pancreas cancer.
3 iffness and epithelial cell contractility in pancreas cancer.
4 s primary sources of treatment resistance in pancreas cancer.
5 on provides the only possibility of cure for pancreas cancer.
6 s favorably with published data for resected pancreas cancer.
7 or (EGFR) signaling pathway in patients with pancreas cancer.
8 mycin improves the survival of patients with pancreas cancer.
9 nt of patients with colorectal, gastric, and pancreas cancer.
10 ne in patients with newly diagnosed advanced pancreas cancer.
11 ptoms in patients with advanced, symptomatic pancreas cancer.
12 iclovir (GCV) for peritoneal metastases from pancreas cancer.
13  a novel approach to treatment of metastatic pancreas cancer.
14 primary mechanism of treatment resistance in pancreas cancers.
15 uding prostate, breast, small cell lung, and pancreas cancers.
16 ironment of patients with invasive breast or pancreas cancers.
17 t is frequently lost in squamous, colon, and pancreas cancers.
18 g exosomes bring it closer for patients with pancreas cancer?
19 iver cancer (14 RCTs [2%] and 8% of deaths), pancreas cancer (14 RCTs [2%] and 5% of deaths), and cer
20  in late-stage metastatic orthotopic KPC-Luc pancreas cancer, 4T1-Luc2 triple negative breast cancer,
21             Their near-universal presence in pancreas cancer and ostensible support of disease progre
22       Current protocols for the treatment of pancreas cancer are not as effective as we desire.
23  the control of growth and invasion of human pancreas cancer because of the independent activation of
24 els are elevated in breast, colon, lung, and pancreas cancers, but not correlated with EGFR mRNA leve
25 nalyzed the inactivation of p53 in the human pancreas cancer cell line Hs766T, which harbors a struct
26 sected pancreas cancer tissues (n = 14), and pancreas cancer cell lines (n = 8), and was hybridized t
27 ative indirect immunofluorescence imaging of pancreas cancer cells and tumors and mutual information
28 tudies leveraging orthotopic implantation of pancreas cancer cells into wild-type and KLF10 KO mice r
29                                              Pancreas cancer cells were transduced in vitro with HS-t
30 DA-MB-231 (breast), H460 (lung), and BxPC-3 (pancreas) cancer cells were pretreated with 15 to 30 mic
31 ; Moffitt Lung Cancer Cohort (n=60); Moffitt Pancreas Cancer Cohort (n=40); and The Cancer Genome Atl
32 wenty-six patients with advanced symptomatic pancreas cancer completed a lead-in period to characteri
33 es experimental opportunities to investigate pancreas cancer development, progression and early-stage
34                  Most patients with advanced pancreas cancer experience pain and must limit their dai
35 arly studies with gemcitabine, patients with pancreas cancer experienced an improvement in disease-re
36 t of lung, breast, prostate, colorectal, and pancreas cancers from 2000 to 2007.
37 o describe the indications for screening for pancreas cancer in high-risk individuals.
38 hly aggressive drug-resistant human lung and pancreas cancers in mice, but also to prevent the emerge
39                                    Localized pancreas cancer includes resectable, borderline resectab
40 d tumor suppressor activity of Smad4/DPC4 in pancreas cancer, including a short C-terminal truncation
41 ndromes associated with an increased risk of pancreas cancer, including all patients with Peutz-Jeghe
42 s for the treatment of advanced prostate and pancreas cancer, including those targeting prostate stem
43 e (TGFBR2) were identified in 4 of 97 (4.1%) pancreas cancers, including a homozygous deletion in a r
44 velopment of esophageal, gastric, liver, and pancreas cancer is heterogenous with studies showing eit
45                                              Pancreas cancer is one of the most lethal malignancies a
46                                              Pancreas cancer is the fourth and fifth leading cause of
47                                              Pancreas cancer is the seventh leading cause of cancer d
48                 The desmoplastic reaction of pancreas cancer may begin as a wound healing response to
49 h patients in previous prognostic studies of pancreas cancer may explain the failure of histological
50 ral HS-tk vectors is effective treatment for pancreas cancer metastatic to the peritoneal cavity; fur
51 ete tumor regressions in a therapy-resistant pancreas cancer model, but only when combined with immun
52  PSCA-CAR T cells in metastatic prostate and pancreas cancer models, with no observed toxicities in n
53 nate process, cancer of the body and tail of pancreas, cancer of the extrahepatic bile duct, cancer o
54 The same TRM-driven fibrosis, however, drove pancreas cancer pathogenesis and progression.
55          In breast cancer patients (n = 35), pancreas cancer patients (n = 30), and normal donors (n
56 her in breast cancer patients (p < 0.01) and pancreas cancer patients (p < 0.01) when compared with n
57 Het to 84 tumor samples from 14 prostate and pancreas cancer patients, we identify subclonal CNAs and
58                                In a panel of pancreas cancers preselected for loss of heterozygosity
59                       Patients with advanced pancreas cancer present with disease that is poorly resp
60  impact of gene perturbation at any stage of pancreas cancer progression.
61 uals when they are more likely to die of non-pancreas cancer-related causes due to comorbidity and/or
62 counseling should be considered for familial pancreas cancer relatives who are eligible for surveilla
63     In the last decade, continued efforts in pancreas cancer research have led to the development of
64  smoking and obesity are known and suspected pancreas cancer risk factors, and have been associated w
65                      BEST PRACTICE ADVICE 6: Pancreas cancer screening in high-risk individuals shoul
66 12: Clinicians should consider discontinuing pancreas cancer screening in high-risk individuals when
67                      BEST PRACTICE ADVICE 1: Pancreas cancer screening should be considered in patien
68                      BEST PRACTICE ADVICE 2: Pancreas cancer screening should be considered in patien
69 E 13: The limitations and potential risks of pancreas cancer screening should be discussed with patie
70 reviewed in this work is based on reports of pancreas cancer screening studies in high-risk individua
71 reening modalities in individuals undergoing pancreas cancer screening.
72 n possible for high-risk patients undergoing pancreas cancer screening.
73 ing fivefold or greater expression levels in pancreas cancer specimens as compared to normal tissue,
74 as having > or = 3-fold expression levels in pancreas cancer specimens as compared with nonneoplastic
75 he analysis of mass spectrometry data from a pancreas cancer study biological relevant and statistica
76                                  The Ontario Pancreas Cancer Study enrolls consenting participants wi
77       An international survey of high-volume pancreas cancer surgeons revealed wide variations in man
78                    In patients with advanced pancreas cancer, the anti-EGFR monoclonal antibody cetux
79            For the majority of patients with pancreas cancer, the high metastatic proclivity is life
80 , including breast cancer, glioblastoma, and pancreas cancer, this report is to our knowledge the fir
81 l gastrointestinal mucosa (n = 22), resected pancreas cancer tissues (n = 14), and pancreas cancer ce
82 s of chronic pancreatitis, and 39 samples of pancreas cancer tissues or cancer cell lines and hybridi
83 on therapy in patients with locally advanced pancreas cancer to determine the maximum-tolerated dose
84         Seven patients with locally advanced pancreas cancer were treated with planned doses of radia
85 elop an undifferentiated and more aggressive pancreas cancer with agents commonly prescribed to manag
86 ding first-degree relatives of patients with pancreas cancer with at least 2 affected genetically rel
87 s with 1 or more first-degree relatives with pancreas cancer with Lynch syndrome, and mutations in BR