ライフサイエンスコーパス: cancer pain

1 ncer-related pain encounter (advanced cancer/cancer pain).

2 mn is a biased agonist of PAR(2) that evokes cancer pain.

3 pain and morphine tolerance in treating bone cancer pain.

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

5 frequently prescribed for moderate to severe cancer pain.

6 blocks this ectopic sprouting and attenuates cancer pain.

7 promising therapeutic tool in treating bone cancer pain.

8 cannabinoids may be effective in attenuating cancer pain.

9 romising strategy for the management of bone cancer pain.

10 mechanical hyperalgesia in a murine model of cancer pain.

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

12 wal assay, supporting a role for exosomes in cancer pain.

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

14 nous opioids in the modulation of pancreatic cancer pain.

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

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

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

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

19 mproved survival in patients with refractory cancer pain.

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

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

22 tes neuropathic involvement in this model of cancer pain.

23 nvolved in the generation and maintenance of cancer pain.

24 ique opportunity to study mechanisms of oral cancer pain.

25 development of more effective treatments for cancer pain.

26 rithmic decision making in the management of cancer pain.

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

28 ly using or had used opioids for chronic non-cancer pain.

29 barriers can lead to suboptimal treatment of cancer pain.

30 to severe acute pain and alleviating chronic cancer pain.

31 men), including 1283 with advanced cancer or cancer pain.

32 for people living with chronic cancer or non-cancer pain.

33 These findings indicate poor control of cancer pain.

34 s and thereby promoting PDAC progression and cancer pain.

35 g may offer a promising therapy for PDAC and cancer pain.

36 nnel ORAI1 is an important regulator of oral cancer pain.

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

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

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

40 nd mechanical hyperalgesia in rats with bone cancer pain.

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

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

43 pering opioids in patients with chronic, non-cancer pain.

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

45 the use of nonopioid analgesia for stronger cancer pain.

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

47 economic level, and nonspecific setting for cancer pain.

48 some of the molecular components involved in cancer pain.

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

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

51 also exhibiting elements that seem unique to cancer pain.

52 s pain hypersensitivity associated with bone cancer pain.

53 or treating neuropathic pain, including bone cancer pain.

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

55 acute cancer pain and prevention of chronic cancer pain.

56 and CCR2 antagonism effectively reduced bone cancer pain.

57 r the development and maintenance of chronic cancer pain.

58 py in the management of chronic uncontrolled cancer pain.

59 unct to opioids and standard coanalgesics in cancer pain.

60 nts compared with alternative analgesics for cancer pain?

61 reatment (68.6% [2160 of 3148]), followed by cancer pain (6.0% [190 of 3148]), insomnia (4.8% [152 of

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

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

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

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

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

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

68 Cancer pain and headache with a logical step ladder mana

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

70 scale was used to evaluate the magnitude of cancer pain and its impact on the patients' lifestyle.

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

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

73 er medical conditions (primarily chronic non-cancer pain and multiple sclerosis; SMD -0.25 [95% CI -0

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 valuated in patients with moderate-to-severe cancer pain, and they effectively reduce pain in this po

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

94 ber 2020 with 2 cases: patient with advanced cancer, pain, and OUD treated with buprenorphine-naloxon

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

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

97 90% of patients (66 of 73) had cancer pain as a presenting symptom at diagnosis.

98 Patients with terminal cancer suffer from cancer pain as a result of bone metastasis and bone dest

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

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

101 significant prevention and reversal of bone cancer pain behaviour.

102 nces in opioid prescribing practices for non-cancer pain between jurisdictions.

103 genes) confer remarkable protection against cancer pain, bone destruction, and local tumor burden.

104 commonly experienced by people with advanced cancer: pain, breathlessness, nausea and vomiting, and f

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

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

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

108 enting bone destruction and alleviating bone cancer pain by suppressing osteoclastogenesis.

109 viders involved in management of chronic non-cancer pain can include reduction or elimination of opio

110 -scale uptake of the fundamental elements of cancer pain care.

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

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

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

114 rexone, including thermally stimulated pain, cancer pain, constipation, sedation, psychological depen

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

116 The primary outcome was the median score of cancer pain control.

117 ociation studies for OPRM1 A118G in advanced cancer pain demonstrate the importance of taking ancestr

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

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

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

121 Cancer pain, especially pain caused by metastasis to bon

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

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

124 they had cancer and were taking opioids for cancer pain for at least 1 week.

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

126 y of patients with cancer taking opioids for cancer pain found that 19% of patients developed NMOU be

127 pensed for antidepressants, opioids (for non-cancer pain), gabapentinoids, benzodiazepines, or Z-drug

128 Antidepressants, opioids for non-cancer pain, gabapentinoids (gabapentin and pregabalin),

129 Eligible patients had cancer, pain >=4/10 on a 0-10 numerical rating scale, re

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

131 e in neuropathic pain, their contribution to cancer pain has not been established.

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

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

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

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

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

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

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

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

140 s (TIRFs), indicated solely for breakthrough cancer pain in opioid-tolerant patients, are subject to

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

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

143 ng literature does not address how to manage cancer pain in patients with OUD.

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

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

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

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

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

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

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

151 Cancer pain is a complex problem that, when left unaddre

152 Cancer pain is a debilitating disorder and a primary det

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

154 Undertreated cancer pain is a major public health concern among older

155 Poor control of cancer pain is a major public health problem worldwide.

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

157 Chronic cancer pain is associated with elevated serine proteases

158 Cancer pain is attributed to cancer-derived mediators th

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

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

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

162 Oral cancer pain is initiated and maintained in the cancer mi

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

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

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

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

167 Cancer pain is the most feared symptom at end of life.

168 The contribution of Schwann cells to oral cancer pain is unclear.

169 The role of Lgmn in PAR(2)-dependent cancer pain is unknown.

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

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

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

173 Worldwide, cancer pain management follows the World Health Organiza

174 This may reflect a shift in cancer pain management from first-line opioids to tramad

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

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

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

178 ing pain-related ED visits suggests that EOL cancer pain management may be worsening.

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

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

181 An evidence-practice gap exists for cancer pain management, and cancer pain remains prevalen

182 st opioid medications are the cornerstone of cancer pain management, but the existing literature does

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

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

185 The opioid crisis creates challenges for cancer pain management.

186 o-step approach is an alternative option for cancer pain management.

187 vice use and their treatment efficacy in non-cancer pain management.

188 ectiveness of patient education in improving cancer pain management.

189 possible interventions, underlies effective cancer pain management.

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

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

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

193 Bone cancer pain most commonly occurs when tumors originating

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

195 with the greatest daily burden included skin cancer, pain/neuropathy, skin issues, kidney disease, me

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

197 Patients using opioids to treat chronic non-cancer pain often experience side effects that may affec

198 r acupressure may be recommended for general cancer pain or musculoskeletal pain.

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

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

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

202 ern when treating patients with chronic, non-cancer pain, patients with active opioid use disorder, a

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

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

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

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

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

208 For women, a mental health/cancer/pain-related conditions cluster at ages 40-59 (Ha

209 University of Miami, USA; Cancer Pain Relief Committee; Medical Research Council;

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

211 tumor microenvironment, providing long-term cancer pain relief.

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

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

214 e gap exists for cancer pain management, and cancer pain remains prevalent and disabling.

215 truction, but how PD-1 blockade affects bone cancer pain remains unknown.

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

217 vates PAR(2) by biased mechanisms that evoke cancer pain.SIGNIFICANCE STATEMENT Oral squamous cell ca

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

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

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

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

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

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

224 is Review, we examine the role of opioids in cancer pain, the risk of substance use disorder and meth

225 elines recommend acupuncture and massage for cancer pain, their comparative effectiveness is unknown.

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

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

228 ovides unique advantages in controlling bone cancer pain through distinct and synergistic actions on

229 Schwann cell TRPA1 sustains cancer pain through release of M-CSF and oxidative stres

230 ich have been shown to be less effective for cancer pain treatment.

231 agement of moderate to severe acute pain and cancer pain, use of oxycodone imposes a risk of adverse

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

233 ain sensitivity, but the development of bone cancer pain was compromised in Pd1-/- mice.

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

235 hronic prescription opioid treatment for non-cancer pain was infrequent overall (3-4% within five yea

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

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

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

239 Episodes of prescription opioid use for non-cancer pain were identified based on drugs dispensed bet

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

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

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

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