ライフサイエンスコーパス: nonsmall-cell lung cancer

1 maintenance therapy of colorectal cancer and nonsmall cell lung cancer.

2 , including ovarian, breast, pancreatic, and nonsmall cell lung cancer.

3 of involvement for patients with metastatic nonsmall cell lung cancer.

4 ts with a variety of solid tumors, including nonsmall cell lung cancer.

5 been shown to be a hot spot (67%) for LOH in nonsmall cell lung cancer.

6 as well as cytokines such as IL-6, in human nonsmall cell lung cancers.

7 s, leading to the emergence of resistance in nonsmall cell lung cancer and other tumor types.

8 impact on the clinical care of patients with nonsmall-cell lung cancer and squamous cell carcinoma of

9 ceptor (EGFR) inhibitors in the treatment of nonsmall-cell lung cancer and the treatment of squamous

10 Here we demonstrate that multiple nonsmall cell lung cancer cell lines demonstrate constit

11 between breast, esophageal, colorectal, and nonsmall cell lung cancer cell lines, as well as heterog

12 e CACNA2D2 gene transfer in 3p21.3-deficient nonsmall cell lung cancer cell lines.

13 es have been detected with high frequency in nonsmall cell lung cancer cells (NSCLC) and contribute t

14 ions was observed in pancreatic (PANC-1) and nonsmall cell lung cancer cells (NSCLC, NCI-H460) of 80-

15 to previous studies in other cell types, in nonsmall cell lung cancer cells survivin was expressed i

16 ues for USP1/UAF1 inhibition and activity in nonsmall cell lung cancer cells, specifically increased

17 In experiments with NCI-H1299 human nonsmall cell lung cancer cells, the cytotoxicity of the

18 izes filamentous actin in vitro and in A549 (nonsmall cell lung cancer) cells, inhibits growth of can

19 De novo nonsmall cell lung cancer, colon cancer, breast cancer,

20 onstrated to induce a significant portion of nonsmall cell lung cancer-derived angiogenic activity an

21 ients with first, primary, clinical stage IA nonsmall cell lung cancer from a large cohort undergoing

22 Recurrent gene rearrangements in nonsmall cell lung cancer fuse EML4 to anaplastic lympho

23 The management of skeletal metastases from nonsmall cell lung cancer is evolving as biochemical mar

24 ment of skeletal metastases in patients with nonsmall cell lung cancer is evolving as improved treatm

25 datory to perform MLNR when screen-diagnosed nonsmall cell lung cancer manifests as a subsolid nodule

26 profiling for miRNAs in a cohort of stage 1 nonsmall cell lung cancers (n = 81) and determined that

27 e antifolate used for therapy of nonsquamous nonsmall cell lung cancer (NS-NSCLC).

28 at the expression of FUT8 is up-regulated in nonsmall cell lung cancer (NSCLC) and correlates with tu

29 and women, and the majority of patients with nonsmall cell lung cancer (NSCLC) are over 65 years of a

30 function to be approved for the treatment of nonsmall cell lung cancer (NSCLC) by the FDA, demonstrat

31 ssion and its overexpression is critical for nonsmall cell lung cancer (NSCLC) cell growth in vitro a

32 d 13b was further tested against a series of nonsmall cell lung cancer (NSCLC) cell lines in which it

33 In vitro cytotoxicity toward a number of nonsmall cell lung cancer (NSCLC) cell lines revealed on

34 ll cell lung cancer cell lines (SCLC), 13/14 nonsmall cell lung cancer (NSCLC) cell lines, and 1/2 br

35 n to be highly effective in the treatment of nonsmall cell lung cancer (NSCLC) harboring oncogenic EG

36 Treatment of advanced nonsmall cell lung cancer (NSCLC) has rapidly changed ov

37 to standard treatment paradigms for advanced nonsmall cell lung cancer (NSCLC) have been successful,

38 the 5-year recurrence with localized stage I nonsmall cell lung cancer (NSCLC) is 18.4%-24%.

39 Nonsmall cell lung cancer (NSCLC) is one of the leading

40 Because resection of early stage nonsmall cell lung cancer (NSCLC) is primary therapy, we

41 Nonsmall cell lung cancer (NSCLC) is the leading cause o

42 r, has the potential to improve outcomes for nonsmall cell lung cancer (NSCLC) patients.

43 Advanced nonsmall cell lung cancer (NSCLC) remains a therapeutic

44 in various cancer xenograft models including nonsmall cell lung cancer (NSCLC), liver, breast, head a

45 ficant improvement in the disease outcome of nonsmall cell lung cancer (NSCLC).

46 practice in treating patients with advanced nonsmall cell lung cancer (NSCLC).

47 ith or without known effective therapies for nonsmall cell lung cancer (NSCLC).

48 antial proportion of the tumor mass in human nonsmall cell lung cancers (NSCLC), but the precise comp

49 smoking pack-years in a large collection of nonsmall-cell lung cancer (NSCLC) tumors.

50 ) and induces dramatic clinical responses in nonsmall cell lung cancers (NSCLCs) with activating muta

51 utations in the BRAF kinase occur in 6-8% of nonsmall cell lung cancers (NSCLCs), accounting for more

52 ients, silent changes were identified in one nonsmall cell lung cancer, one prostate cancer, and one

53 duction of Ab, CD8(+), and CD4(+) T cells in nonsmall cell lung cancer patients vaccinated with MAGE-

54 e EGFR inhibitors erlotinib and gefitinib in nonsmall cell lung cancer patients.

55 nt population for colon cancer (all stages), nonsmall cell lung cancer (stage II), breast cancer (sta

56 It indicates that in advanced nonsmall-cell lung cancer survival, symptom control and

57 In nonsmall cell lung cancer, the presence of spontaneous U

58 In the nonsmall cell lung cancer xenograft model studied, a lin