ライフサイエンスコーパス: tumor stem cell

1 y and high-resolution monitoring of AC133(+) tumor stem cells.

2 in human glioblastoma multiforme (GBM) brain tumor stem cells.

3 minin did not induce cFLIP expression in GBM tumor stem cells.

4 d it to be markedly downregulated in mammary tumor stem cells.

5 from neural stem cells and appear to contain tumor stem cells.

6 cells, we examined its expression in mammary tumor stem cells and found it to be markedly downregulat

7 a panel of human glioma cell lines and brain tumor stem cells and found that Tie2 activation was sign

8 NF-kappaB contributes to expansion of breast tumor stem cells and heterotypic signals that enhance TA

9 the self-renewal and growth of mouse mammary tumor stem cells and sensitizes MCF-7 human breast cance

10 n is heterogeneous across the spectrum of MM tumor stem cells and their more differentiated progeny.

11 tration of PGE2 to Apc(Min/+) mice increased tumor stem cells and tumor burden, compared with control

12 Our data demonstrate that characteristics of tumor stem cells are separable, and highlight ABCG2 as a

13 ides a rationale for detecting and analyzing tumor stem cells as one of the most effective ways to tr

14 ritical signaling pathways involved in brain tumor stem cell biology and discuss how targeting these

15 erarchy with self-renewing tumorigenic brain tumor stem cells (BTSCs) at the apex.

16 or STAT3 in mouse astrocytes and human brain tumor stem cells (BTSCs).

17 RNA-based therapies that specifically target tumor stem cells, but spare normal stem cells.

18 successful noninvasive detection of AC133(+) tumor stem cells by PET and near-infrared fluorescence m

19 ng the notion that transformation of a solid tumor stem cell can occur at distinct stages of maturati

20 In this study, we report that brain tumor stem cells can be identified from adult GBMs.

21 cs that can inhibit the growth of Drosophila tumor stem cells can paradoxically promote the hyperprol

22 stinguishing feature from normal NSCs, these tumor stem cells can reform spheres even after the induc

23 activity is markedly concentrated within the tumor stem cell compartment.

24 Brain tumor stem cells contribute to therapeutic resistance an

25 d contrast, clearly delineating subcutaneous tumor stem cell-derived xenografts from surrounding tiss

26 However, the impact immune responses have on tumor stem cell differentiation or expansion is not well

27 tiated tumor cells that inhibits the rate of tumor stem cell division.

28 These findings suggest that the bulk of tumor stem cell divisions serve only to replace stem cel

29 py with approaches that limit the process of tumor stem cell enrichment.

30 These tumor stem cells form neurospheres, possess the capacity

31 efflux of androgen, protecting the putative tumor stem cells from androgen deprivation, hypoxia, or

32 fore, BCRP expression isolates prostate stem/tumor stem cells from the prostate tissue microenvironme

33 Putative prostate stem cells and prostate tumor stem cells in benign and malignant human prostate

34 role of p21(CIP1) in regulating features of tumor stem cells in vivo is unknown.

35 This population possesses characteristics of tumor stem cells including quiescence, therapy resistanc

36 s possess many traits of tumor-initiating or tumor stem cells including self-renewal capacity, high t

37 nsfected with miR-378 acquired properties of tumor stem cells, including cell self-renewal.

38 nd-healing response that mobilizes quiescent tumor stem cells into active proliferation.

39 In several tumors, stem cell-like and more-differentiated cancer ce

40 3 currently is one of the best-characterized tumor stem cell markers for many intra- and extracranial

41 IkappaBalphaSR inhibited breast tumor stem cell markers in transgenic tumors, reduced st

42 A workshop "Targeting Oncolytic Viruses to Tumor Stem Cells," organized by the Division of Cancer B

43 nalysis showed that IkappaBalphaSR inhibited tumor stem cell pathways.

44 l barrier against the unchecked expansion of tumor stem cell pools; however, little is known about th

45 ll division promotes a permanent rise of the tumor stem cell population over time, both in the absenc

46 sion caused by HAF also promotes an enriched tumor stem cell population, resulting in highly aggressi

47 Tumor stem cells, postulated to be the source cells for

48 response in association with distorted skin tumor stem cell signaling and population dynamics, impli

49 essed in teratoma-susceptible germ cells and tumor stem cells, suggesting that retention of pluripote

50 oint to the existance of a common progenitor tumor stem cell that gives rise to genomically unstable

51 Putative prostate tumor stem cells that express BCRP but not AR protein in

52 show that radiation must induce apoptosis in tumor stem cells to be effective.

53 now well established that a subpopulation of tumor stem cells (TSCs) are present within cancer tissue

54 ontribute to the formation of the so-called 'tumor stem cells' (TSCs) that are currently hypothesized

55 pically heterogeneous cells, no evidence for tumor stem cells was found.

56 Furthermore, only these tumor stem cells were able to form tumors and generate b

57 y partly due to an increase in the number of tumor stem cells, which typically respond to chemotherap

58 A technology that visualizes tumor stem cells with clinically relevant tracers could

59 The identification of tumor stem cells within adult GBM may represent a major