ライフサイエンスコーパス: cancer pain

1 drugs for moderate to severe acute pain and cancer pain.

2 , the most common being anemia, fatigue, and cancer pain.

3 the calcaneus bone, an established model of cancer pain.

4 ly modulates early and late-stage pancreatic cancer pain.

5 nous opioids in the modulation of pancreatic cancer pain.

6 in patients with prostate tumor-induced bone cancer pain.

7 k of self-care can improve the management of cancer pain.

8 irst-line strong opioid for the treatment of cancer pain.

9 wth factor (PDGF) was used to alleviate bone cancer pain.

10 hasis to the 20th century and to chronic and cancer pain.

11 mproved survival in patients with refractory cancer pain.

12 ty in the management of bone cancer and bone cancer pain.

13 icant bone remodeling, bone destruction, and cancer pain.

14 tes neuropathic involvement in this model of cancer pain.

15 nvolved in the generation and maintenance of cancer pain.

16 development of more effective treatments for cancer pain.

17 rithmic decision making in the management of cancer pain.

18 ative care and hospice concept used to treat cancer pain.

19 r Endothelial Growth Factor (VEGF) family in cancer pain.

20 ed constipation in patients with chronic non-cancer pain.

21 the use of nonopioid analgesia for stronger cancer pain.

22 ical hypersensitivity in a rat model of bone cancer pain.

23 economic level, and nonspecific setting for cancer pain.

24 some of the molecular components involved in cancer pain.

25 level in the spinal cord is reduced in bone cancer pain.

26 al anti-inflammatory drugs (NSAIDs) for mild cancer pain.

27 also exhibiting elements that seem unique to cancer pain.

28 s pain hypersensitivity associated with bone cancer pain.

29 or treating neuropathic pain, including bone cancer pain.

30 ics for the management of moderate to severe cancer pain.

31 acute cancer pain and prevention of chronic cancer pain.

32 ed constipation in patients with chronic non-cancer pain.

33 nd mechanical hyperalgesia in rats with bone cancer pain.

34 r the development and maintenance of chronic cancer pain.

35 py in the management of chronic uncontrolled cancer pain.

36 unct to opioids and standard coanalgesics in cancer pain.

37 pain and morphine tolerance in treating bone cancer pain.

38 tes to analgesic efficacy in a model of bone cancer pain.

39 frequently prescribed for moderate to severe cancer pain.

40 blocks this ectopic sprouting and attenuates cancer pain.

41 promising therapeutic tool in treating bone cancer pain.

42 cannabinoids may be effective in attenuating cancer pain.

43 romising strategy for the management of bone cancer pain.

44 mechanical hyperalgesia in a murine model of cancer pain.

45 nts compared with alternative analgesics for cancer pain?

46 tions directed at improving the treatment of cancer pain across an institution or nursing unit.

47 femur and that, in an in vivo model of bone cancer pain, acute or chronic administration of a TRPV1

48 Using a well-established rat model of bone cancer pain, AF-353, a recently described potent and sel

49 ecommends that current standards of care for cancer pain, analgesics and local radiation therapy, not

50 barachnoidale of animals suffering from bone cancer pain and animals in the negative group.

51 l oncology practices involved in the Indiana Cancer Pain and Depression (INCPAD) trial.

52 Cancer pain and headache with a logical step ladder mana

53 suggest a potential target for treating bone cancer pain and improving analgesic effect of morphine c

54 ight into the evolving mechanisms that drive cancer pain and lead to more effective control of this c

55 cord is critical to the development of bone cancer pain and morphine tolerance in treating bone canc

56 trials supporting the value of hypnosis for cancer pain and nausea; relaxation therapy, music therap

57 controlled trials in adults with chronic non-cancer pain and opioid-induced constipation.

58 quality evidence-based management of general cancer pain and pain syndromes.

59 cer and as a conduit for the transmission of cancer pain and perineural invasion.

60 promising approach to the treatment of acute cancer pain and prevention of chronic cancer pain.

61 Patient education is effective in reducing cancer pain and should be standard practice in all setti

62 ssment, treatment, and follow-up for general cancer pain and specific pain syndromes.

63 utic potential for VEGFR1-modifying drugs in cancer pain and suggest a palliative effect for VEGF/VEG

64 echanism underlying the pathogenesis of bone cancer pain and suggest a potential target for treating

65 demonstrate a direct role for PAR2 in acute cancer pain and suggest that PAR2 upregulation may favor

66 sensitization of WDR neurons contributes to cancer pain and supports the notion that the mechanisms

67 uction is involved in the generation of bone cancer pain and that osteoprotegerin may provide an effe

68 indicators that psychological factors affect cancer pain and that psychological and behavioral treatm

69 ew is to explore the current studies on oral cancer pain and their implications in clinical managemen

70 bone destruction of the injected femur, bone cancer pain, and a stereotypic set of neurochemical chan

71 ial for use as an antiemetic, for refractory cancer pain, and as an antitumor agent.

72 asic science, chronic pain, myofascial pain, cancer pain, and therapeutic options.

73 hyperalgesia developed in the rats with bone cancer pain, and these effects were accompanied by bone

74 ling, neuroinflammation, glaucoma, epilepsy, cancer, pain, and obesity.

75 This "neurochemical signature" of bone cancer pain appears unique when compared to changes that

76 More than half of all chronic cancer pain arises from metastases to bone, and bone can

77 other strategies for overcoming barriers to cancer pain assessment and management.

78 reagent EphB2-Fc prevents and reverses bone cancer pain behaviors and the associated induction of c-

79 significant prevention and reversal of bone cancer pain behaviour.

80 In this review I focus on chronic and cancer pain, but many of the principles apply in acute p

81 ndisputed in acute (e.g., postoperative) and cancer pain, but their long-term use in chronic pain has

82 (IDDSs) have been used to manage refractory cancer pain, but there are no randomized clinical trial

83 and above, elderly, and aged along with non-cancer pain, chronic pain, persistent pain, pain managem

84 appear to be more effective than placebo for cancer pain; clear evidence to support superior safety o

85 s (music, n = 2; massage, n = 2) in reducing cancer pain compared with a control arm.

86 Treating bone cancer pain continues to be a clinical challenge and und

87 High-quality management of cancer pain depends on evidence-based standards for scre

88 ts the notion that the mechanisms underlying cancer pain differ from those that contribute to inflamm

89 subcutaneous morphine (SCM) to treat severe cancer pain episodes.

90 Cancer pain, especially pain caused by metastasis to bon

91 To improve the management of cancer pain, every practitioner involved in the care of

92 pass this and address the chronic effects of cancer (pain, fatigue, premature menopause, depression/a

93 based sample of Australians with chronic non-cancer pain for which opioids have been prescribed.

94 est that, for more than 20 years, a focus on cancer pain has not adequately addressed the perception

95 We propose that oral cancer pain has underlying biologic mechanisms that are

96 er ATP and P2X3 receptors contribute to bone-cancer pain in a mouse model, immunohistochemical techni

97 erine proteases such as trypsin induce acute cancer pain in a PAR2-dependent manner.

98 d by the development of neuropathic and bone cancer pain in animal models.

99 umor-induced nerve remodeling and attenuated cancer pain in diverse mouse models in vivo.

100 heir implications in clinical management for cancer pain in general.

101 teristics of acute and chronic head and neck cancer pain in humans.

102 to attenuate nociception in a model of bone cancer pain in mice.

103 have long appreciated the ability to manage cancer pain in patients for months on stable opioid dose

104 appears to have the potential to reduce bone cancer pain in patients with advanced tumor-induced bone

105 midline myelotomy at T10 can relieve pelvic cancer pain in patients.

106 reverses morphine tolerance in treating bone cancer pain in rats and defensive pain in mice.

107 amorphine remain the stronghold for treating cancer pain in the United Kingdom.

108 n greatly reduces the severity of persistent cancer pain in wild-type mice, but most strikingly, the

109 Additional expressions of orofacial cancer pain include distant tumor effects, involving par

110 terventions in the management of chronic non-cancer pain, including pharmacological, interventional,

111 (ie, showed greatest symptom burden) in lung cancer (pain interference, 55.5; fatigue, 57.3; depressi

112 Cancer pain is a debilitating disorder and a primary det

113 Bone cancer pain is a major clinical problem and remains diff

114 Cancer pain is an ever-present public health concern.

115 Chronic cancer pain is associated with elevated serine proteases

116 Bone cancer pain is common among cancer patients and can have

117 ropriate use of opioids for the treatment of cancer pain is complex.

118 Adding an NSAID to an opioid for stronger cancer pain is efficacious, but the risk of long-term ad

119 The most common etiology of cancer pain is local tumor invasion (primary or metastat

120 ain arises from metastases to bone, and bone cancer pain is one of the most difficult of all persiste

121 most strikingly, the development of chronic cancer pain is prevented in PAR2-deficient mice.

122 problem in designing new therapies for bone cancer pain is that it is unclear what mechanisms drive

123 As a presenting symptom of orofacial cancer, pain is often of low intensity and diagnosticall

124 splantation in conditions of neuropathic and cancer pain, it is proposed that the neuroactive substan

125 Corticosteroids are frequently used in cancer pain management despite limited evidence.

126 We implemented clinical guidelines for cancer pain management in the community setting and eval

127 ctor that seems to contribute to ineffective cancer pain management is poor adherence to the analgesi

128 The use of morphine for cancer pain management may be beneficial through its eff

129 The WHO guidelines on cancer pain management recommend a sequential three-step

130 alth Care Policy and Research Guidelines for Cancer Pain Management was compared with standard-practi

131 as the most important barrier to outpatient cancer pain management, little is known about pain asses

132 nd three phone calls on how to improve their cancer pain management.

133 ectiveness of patient education in improving cancer pain management.

134 possible interventions, underlies effective cancer pain management.

135 Until recently, knowledge of cancer pain mechanisms was poor compared with understand

136 r specialty highly for the ability to manage cancer pain (median, 7; interquartile range [IQR], 6 to

137 The development of rodent cancer pain models has provided the opportunity to inves

138 Bone cancer pain most commonly occurs when tumors originating

139 al in a wide range of diseases, ranging from cancer, pain, neurodegenerative, and cardiovascular dise

140 es in recommendations for the use of IDD for cancer pain, nonmalignant pain, and spasticity, as well

141 e mechanisms that give rise to advanced bone cancer pain, osteolytic 2472 sarcoma cells or media were

142 s might decrease the clinical disparities in cancer pain outcomes.

143 planted intrathecally to relieve intractable cancer pain, patients obtained significant and long-last

144 he WHO analgesic ladder for the treatment of cancer pain provides a three-step sequential approach fo

145 reduction in both early and late stage bone cancer pain-related behaviors that was greater than or e

146 ice develop ongoing and movement-evoked bone cancer pain-related behaviors, extensive tumor-induced b

147 Pain-free survival and time to first cancer pain-related opioid intake were comparable.

148 first appearance of pain), and time to first cancer pain-related opioid intake.

149 Oxycodone was not associated with superior cancer pain relief or fewer adverse effects compared wit

150 challenge and underlying mechanisms of bone cancer pain remain elusive.

151 Adequate treatment of cancer pain remains a significant clinical problem.

152 the WHO three-step ladder for management of cancer pain, several controversies have arisen, which ar

153 ce as a beneficial tool for the treatment of cancer pain, spasticity, and chronic nonmalignant pain.

154 ffected a sensitive body area), or a fear of cancer (pain, suffering, and death), or both.

155 Data generated in a murine model of bone cancer pain suggest that a disturbance of local endocann

156 ent models of inflammatory, neuropathic, and cancer pain, suggesting their utility as analgesics.

157 ial research conducted on arthritis pain and cancer pain that addresses both psychosocial factors rel

158 In an experimental model of cancer pain, the hyperalgesia that occurs with osteolyti

159 lore the endogenous opioid systems and novel cancer pain therapeutics that target these systems, whic

160 nalgesics, which is crucial to the relief of cancer pain, there is a lack of evidence to support many

161 ity that it is an important mediator of bone cancer pain via its capacity to detect osteoclast- and t

162 The rat model of bone cancer pain was induced by implanting rat mammary gland

163 n to define the mechanisms that give rise to cancer pain, we examined the neurochemical changes that

164 define the role COX-2 plays in driving bone cancer pain, we used an in vivo model where murine osteo

165 mized controlled study, adults with moderate cancer pain were assigned to receive either a weak opioi

166 nuated both ongoing and movement-evoked bone cancer pain, whereas chronic inhibition of COX-2 signifi

167 of the neurobiological mechanisms underlying cancer pain will likely lead to the development of more

168 opioid regimen for treatment of chronic non-cancer pain with a total daily dose averaging at least 3

169 tional RCTs evaluating CAM interventions for cancer pain with adequate power, duration, and sham cont