ライフサイエンスコーパス: cancer cachexia

1 ion of a glycoprotein factor associated with cancer cachexia.

2 lammatory response during the development of cancer cachexia.

3 that IL-6 trans-signaling may be targeted in cancer cachexia.

4 thways causes skeletal muscle wasting during cancer cachexia.

5 l muscle mass in naive conditions and during cancer cachexia.

6 rcinoma (LLC) and Apc(Min/+) mouse models of cancer cachexia.

7 mass and strength and for protection against cancer cachexia.

8 rapeutic approach for at least some types of cancer cachexia.

9 es and contributes to the broader aspects of cancer cachexia.

10 cidating the causes and treatment options of cancer cachexia.

11 such as fasting, denervation, diabetes, and cancer cachexia.

12 bo for appetite improvement in patients with cancer cachexia.

13 role in the pathogenesis of endotoxemic and cancer cachexia.

14 lpain, and caspase) in muscle wasting during cancer cachexia.

15 dramatic resistance to the muscle wasting of cancer cachexia.

16 ork for the definition and classification of cancer cachexia.

17 f the ActRIIB pathway and the development of cancer cachexia.

18 approved for the prevention or treatment of cancer cachexia.

19 clinical settings, including denervation and cancer cachexia.

20 reduced tolerance to chemotherapy induced by cancer cachexia.

21 inflammation may contribute to the effect of cancer cachexia.

22 t potentially be useful for the treatment of cancer cachexia.

23 tumors, indicating a possible role of NMU in cancer cachexia.

24 nisms of immunometabolic response in AT from cancer cachexia.

25 it from single agent EPA in the treatment of cancer cachexia.

26 clinical states such as anorexia nervosa or cancer cachexia.

27 sing therapeutic target in the management of cancer cachexia.

28 in the substantial reduction of adiposity of cancer cachexia.

29 in ligase, and its functional involvement in cancer cachexia.

30 ed peptides derived from tumors in producing cancer cachexia.

31 rexpression by tumors has been implicated in cancer cachexia.

32 addition to its previously described role in cancer cachexia.

33 abnormalities in the liver of patients with cancer-cachexia.

34 ork for the definition and classification of cancer cachexia a panel of experts participated in a for

35 Severe weight loss is characteristic for cancer cachexia, a condition that significantly impairs

36 aling in progressive stages of clinical lung cancer cachexia and assessed whether circulating factors

37 been major advances in the understanding of cancer cachexia and asthenia.

38 pproach with combined therapy to manage both cancer cachexia and asthenia.

39 se the underlying metabolic abnormalities of cancer cachexia and have limited long-term impact on pat

40 of PTHrP might hold promise for ameliorating cancer cachexia and improving patient survival.

41 duced in muscle in three different models of cancer cachexia and in glucocorticoid-treated mice.

42 uble lipid-mobilizing factor associated with cancer cachexia and is a novel adipokine.

43 ated with clinical and biological markers of cancer cachexia and is associated with a shorter surviva

44 al role for myostatin in the pathogenesis of cancer cachexia and link this condition to tumor growth,

45 To investigate the pathophysiology of cancer cachexia and pursue treatment options, we develop

46 ssary for normal muscle fiber atrophy during cancer cachexia and sepsis, and further suggest that bas

47 p3 and inhibited muscle fiber atrophy during cancer cachexia and sepsis.

48 ant role in muscle protein catabolism during cancer cachexia and suggest that E3alpha-II is a potenti

49 n may improve the prognosis of patients with cancer cachexia and systemic inflammation (i.e., those w

50 yeloma, rheumatoid arthritis, hypercalcemia, cancer cachexia, and Castleman's disease.

51 necrosis factor-alpha and interleukin-6 with cancer cachexia, and the weight loss induced by leukaemi

52 tant for tumorigenicity, lung metastasis and cancer cachexia, and thus a promising therapeutic target

53 ing and pathological conditions ranging from cancer, cachexia, and diabetes to denervation and immobi

54 Cancer cachexia/anorexia is a complex syndrome that invo

55 Whereas, the abundance of cancer cachexia associated bacteria, such as Dysgonomona

56 ing beneficial bacteria, and down-regulating cancer-cachexia associated bacteria.

57 These results shed new light on cancer cachexia by revealing that wasting does not resul

58 Using an established mouse model of cancer cachexia (C26 adenocarcinoma), we determined how

59 udy was to determine whether colon-26 (C-26) cancer cachexia causes diaphragm muscle fiber atrophy an

60 These data demonstrate that C-26 cancer cachexia causes profound respiratory muscle atrop

61 In models of muscular dystrophy and cancer cachexia, combined inhibition of activins and myo

62 tophagic-lysosomal proteolytic system during cancer cachexia development in humans.

63 atrophy induced by denervation as well as by cancer cachexia, diabetes, and renal failure.

64 In two different animal models of cancer cachexia, E3alpha-II was significantly induced at

65 of MeAT from patients and an animal model of cancer cachexia enabled us to identify early disruption

66 With no effective treatment of cancer cachexia, future therapies directed at preserving

67 Experimental models of cancer cachexia have indicated that systemic inflammatio

68 mmobilization, aging, catabolic steroids, or cancer cachexia, however, are poorly understood.

69 cytokines have been shown to be mediators of cancer cachexia; however, the role of cytokines in dener

70 n1/MAFbx and muscle wasting are hallmarks of cancer cachexia; however, the underlying mechanism is un

71 Moreover, depletion of TRAF6 prevents cancer cachexia in an experimental mouse model.

72 anations include negative effects related to cancer cachexia in patients with low BMI, increased drug

73 P mice die within 6 weeks of age from severe cancer cachexia induced by large, activin-secreting ovar

74 the IKK complex are cardioprotective against cancer cachexia-induced cardiac atrophy and systolic dys

75 Cancer cachexia involves the loss of weight, mainly in s

76 Cancer cachexia is a complex metabolic condition charact

77 Muscle protein wasting in cancer cachexia is a critical problem.

78 Cancer cachexia is a devastating metabolic syndrome char

79 Cancer cachexia is a life-threatening syndrome that affe

80 Cancer cachexia is a multifactorial syndrome characteriz

81 Cancer cachexia is a multifactorial syndrome that is poo

82 Cancer cachexia is a severe wasting syndrome characteriz

83 Cancer cachexia is a syndrome of progressive wasting whi

84 Cancer cachexia is an unmet medical need and our data su

85 Cancer cachexia is characterized by a continuous loss of

86 Cancer cachexia is mediated in part by TNF-alpha.

87 es to levels approximating those observed in cancer cachexia models induced a more rapid and profound

88 Here, we show that in several cancer cachexia models, pharmacological blockade of ActR

89 lly, we observed that in an in vivo model of cancer cachexia, Mstn expression coupled with downregula

90 In cancer cachexia, muscle depletion is related to morbidit

91 However, the mechanisms of cancer cachexia remain poorly understood.

92 The role of hypermetabolism in cancer cachexia remains unclear.We studied the relation

93 d in various biological functions, including cancer cachexia, renal and heart failure, atherosclerosi

94 cle during systemic wasting states (fasting, cancer cachexia, renal failure, diabetes).

95 ogenesis in a plethora of diseases including cancer cachexia, sarcopenia, and muscular dystrophy.

96 from the tumor, phenotypes that resemble the cancer cachexia seen in human patients.

97 rule pathway, the same pathway activated in cancer cachexia, sepsis, and hyperthyroidism.

98 red muscles from fasted mice, from rats with cancer cachexia, streptozotocin-induced diabetes mellitu

99 rnover induces immunometabolic modulation in cancer cachexia syndrome.

100 In a model of cancer cachexia, they significantly reduce muscle atroph

101 Cancer cachexia was defined as a multifactorial syndrome

102 Here, using a Lewis lung carcinoma model of cancer cachexia, we show that tumour-derived parathyroid

103 Using this model, and a model of cancer cachexia, we test the hypothesis that CD4(+)CD44(

104 bute to increased muscle proteolysis in lung cancer cachexia, whereas the absence of downstream chang

105 undescribed mechanism for the development of cancer cachexia, whereby progressive MDSC expansion cont

106 ism is a promising new approach for treating cancer cachexia, whose inhibition per se prolongs surviv