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Добірка наукової літератури з теми "Bone cancer pain"

Автор: Grafiati

Опубліковано: 13 квітня 2024

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Статті в журналах з теми "Bone cancer pain"

Koyyalagunta, Dhanalakshmi, BCarolina Hernández-Porras, Ricardo Plancarte, and JuanMiguel Jimenez Andrade. "Bone cancer pain." Indian Journal of Pain 35, no. 1 (2021): 4. http://dx.doi.org/10.4103/ijpn.ijpn_4_21.

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Clohisy, Denis R., and Patrick W. Mantyh. "Bone Cancer Pain." Clinical Orthopaedics and Related Research 415 (October 2003): S279—S288. http://dx.doi.org/10.1097/01.blo.0000093059.96273.56.

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Mantyh, Patrick W. "Bone cancer pain." Current Opinion in Supportive and Palliative Care 8, no. 2 (June 2014): 83–90. http://dx.doi.org/10.1097/spc.0000000000000048.

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Jimenez-Andrade, Juan Miguel, William G. Mantyh, Aaron P. Bloom, Alice S. Ferng, Christopher P. Geffre, and Patrick W. Mantyh. "Bone cancer pain." Annals of the New York Academy of Sciences 1198, no. 1 (June 2010): 173–81. http://dx.doi.org/10.1111/j.1749-6632.2009.05429.x.

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Clohisy, Denis R., and Patrick W. Mantyh. "Bone cancer pain." Cancer 97, S3 (January 23, 2003): 866–73. http://dx.doi.org/10.1002/cncr.11144.

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Ungard, Robert G., Eric P. Seidlitz, and Gurmit Singh. "Oxidative stress and cancer pain." Canadian Journal of Physiology and Pharmacology 91, no. 1 (January 2013): 31–37. http://dx.doi.org/10.1139/cjpp-2012-0298.

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Анотація:

Breast cancers are the most common source of metastases to bone, of which cancer-induced bone pain is a frequent pathological feature. Cancer-induced bone pain is a unique pain state with multiple determinants that remains to be well understood and managed. Current standard treatments are limited by dose-dependent side effects that can reduce the quality of life of patients. Glutamate is a neurotransmitter and bone cell-signalling molecule that is released via the system [Formula: see text] cystine/glutamate antiporter from cancer cell types that frequently metastasize to bone, including breast cancers. In cancer cells, glutamate release is understood to be a side effect of the cellular response to oxidative stress that upregulates the expression and activity of system [Formula: see text] to promote the increased import of cystine. Attenuation of glutamate release from cancer cells has been demonstrated to result in reductions in associated cancer-induced bone pain in animal models. This review examines the clinical implications of attenuating cystine uptake and glutamate release in the treatment of cancer-induced bone pain.

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Feller, Liviu, Razia Abdool Gafaar Khammissa, Michael Bouckaert, Raoul Ballyram, Yusuf Jadwat, and Johan Lemmer. "Pain: Persistent postsurgery and bone cancer-related pain." Journal of International Medical Research 47, no. 2 (January 11, 2019): 528–43. http://dx.doi.org/10.1177/0300060518818296.

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The generation of neuropathic pain is a complex dynamic process. Factors involved include one or more dysregulated sensory neural pathways; dysregulated activity of specific neurotransmitters, synapses, receptors and cognitive and emotional neural circuits; and the balance between degenerative and regenerative neural events. Risk factors include age, sex, cognition, emotions, genetic polymorphism, previous or ongoing chronic pain conditions and the use of certain drugs. Intense pain experienced before, during and after surgery is a risk factor for the development of central sensitization with consequent persistent postsurgery neuropathic pain. Blockade of N-methyl-D-aspartate receptors with appropriate drugs during and immediately after surgery may prevent persistent postsurgical pain. Most cancers, but particularly malignant metastases in bone, can induce persistent pain. Local factors including direct damage to sensory nerve fibres, infiltration of nerve roots by cancer cells and algogenic biological agents within the microenvironment of the tumour bring about central sensitization of dorsal horn neurons, characterized by neurochemical reorganization with persistent cancer pain. In this article, the clinical features, pathogenesis and principles of management of persistent postsurgery pain and cancer pain are briefly discussed.

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Erdmann, A. "Cancer-related Bone Pain." British Journal of Anaesthesia 101, no. 1 (July 2008): 132–33. http://dx.doi.org/10.1093/bja/aen142.

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Kane, C. M., P. Hoskin, and M. I. Bennett. "Cancer induced bone pain." BMJ 350, jan29 7 (January 29, 2015): h315. http://dx.doi.org/10.1136/bmj.h315.

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Mohsin, Intikhab. "Cancer induced bone pain." Public Health and Emergency 1 (August 23, 2016): 29. http://dx.doi.org/10.21037/phe.2016.08.10.

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Дисертації з теми "Bone cancer pain"

Sukhtankar, Devki. "Mechanisms Underlying Cancer-Induced Bone Pain." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/202718.

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Pain from bone metastases is multifaceted with clinical descriptors including ongoing pain, hypersensitivity to external stimuli and intermittent episodes of breakthrough pain characterized as a sudden and abrupt onset of severe pain on a background of well-controlled pain. Moreover, cancer-induced bone pain remains inadequately managed due to a myriad of side effects associated with the current pain relieving regimens, which primarily rely on administration of opiates. Despite advances made in cancer therapeutics, these patients experience an inferior quality of life with incapacitating pain with limited daily activities. Development of long-term novel, non-opiate mechanism-based therapeutics with limited side effects is considered beneficial in elevating the patients' quality of life. First part of this dissertation encompasses the role of p38 MAPK in a mouse model of cancer-induced bone pain in which breast cancer cells were injected and sealed into the femur. Our data demonstrated that both acute and prolonged inhibition of p38 MAPK blocked cancer-induced spontaneous pain but had no effect on the evoked pain indicating important differences in mechanisms mediating ongoing pain as opposed to evoked pain. Undermanaged control of breakthrough pain is attributed to poor understanding of underlying mechanisms and how they may differ from ongoing pain due, in part, to lack of a pre-clinical model in which these mechanisms can be studied. We have established a rat model of cancer-induced bone pain to examine ongoing pain and pain relief using conditioned place preference paradigm as well as breakthrough pain using palpation-induced conditioned place aversion. We have shown that while peripheral afferent input from the tumor-bearing tibia mediates cancer-induced ongoing pain and initiation of breakthrough pain, it does not contribute to the maintenance of breakthrough pain. These data suggest that molecular targets mediating these two mechanisms may be different. This hypothesis was confirmed by our findings in this model that acute blockade of interleukin-6 blocked movement-evoked breakthrough pain in tumor-bearing rats, but failed to block tumor-induced ongoing pain. Hence, we provide a platform to manipulate treatments that can be given alone or in combination with opiates in such a way that patients receive adequate control of breakthrough pain.

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Currie, Gillian Laura. "Novel analgesic interventions in cancer-induced bone pain." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6515.

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Cancer-induced bone pain (CIBP), due to bony metastases, is a major clinical problem, significantly reducing quality of life in cancer patients. Current therapies often provide inadequate analgesia or unacceptable side effects. The aim of this thesis was to characterise behaviours of a preclinical model of CIBP and test novel analgesic interventions in this model. A secondary aim was to investigate the involvement of the N-methyl-D-Aspartate (NMDA) receptors and TRP channels (TRPM8, TRPV1 and TRPV4) in CIBP. Investigation of CIBP in a preclinical model may lead to better pain management in CIBP patients. The results presented here demonstrate that this model of CIBP develops behaviours that may be indicative of mechanical allodynia, thermal sensitivity, movement-evoked pain, ongoing pain and spontaneous pain. This suggests that this model reflects the clinical condition of CIBP, where patients suffer from constant background pain with spontaneous and movement-related breakthrough pain. In this study it was found that radiotherapy significantly attenuated movement-evoked pain and thermal sensitivity to 20°C and 40°C. XRT also significantly reduced anxiety and risk assessment behaviours (grooming behaviour and number of protected stretch attends) compared to untreated CIBP. Duloxetine attenuated CIBP-induced mechanical allodynia, thermal sensitivity to 40°C and movement-evoked pain, whereas S,S-reboxetine attenuated thermal sensitivity to 40°C but did not effect CIBP-induced mechanical allodynia or movement-evoked pain. In addition, CB 65 attenuated movement-evoked pain and thermal sensitivity to 40°C. A single dose of gabapentin did not attenuate CIBP-induced mechanical allodynia, thermal sensitivity to 40°C or movement-evoked pain. These studies confirm that the CIBP model shows characteristics and pharmacological sensitivities consistent with known and predicted mechanisms and validate it as a useful model for assessing potential new treatments proposed for use in patients. Behavioural results suggest that NMDA receptors containing the NR2A subunit are involved in CIBP-induced movement-evoked pain. This suggests that NR2A antagonists may be useful for treating CIBP-induced movement-evoked pain. Additionally, results show that there is increased expression of NR2A in the laminae I, II and III in the dorsal horn of the spinal cord. XRT treated animals also showed increased expression of NR2A in laminae I and II. The selective involvement of NR2A in CIBP is different to other chronic pain states, for example, neuropathic pain states that appear to involve the NR2B subunit. The TRPV1 antagonist AMG 9810 did not attenuate mechanical allodynia, thermal sensitivity to 40°C or movement-evoked pain. Interestingly, the TRPM8 agonist icilin attenuated movement-evoked pain, which suggests that icilin might be useful in the treatment of movement-evoked pain. The TRPV4 antagonist RN 1734 attenuated mechanical allodynia, thermal sensitivity to 40°C and movement-evoked pain in CIBP. This suggests RN 1734 may be useful in the treatment of mechanical allodynia, thermal sensitivity to 40°C and movement-evoked pain in CIBP. Results show that the expression of TRPV4 is increased in DRG ipsilateral to the cancerbearing tibia. In conclusion, these results show that the preclinical model of CIBP investigated in this thesis is suitable for testing novel analgesic interventions. This thesis identified some useful targets for the analgesic treatment of CIBP and results suggest that many different mechanisms contribute to CIBP. A point to consider is that any robust effective treatment may need to target all (or at least several) of these mechanisms.

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Bui, Lynn. "Inhibition of System Xc⁻ Reduces Cancer-Induced Bone Pain." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/321599.

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The most common cancer types have a high likelihood of metastasizing to the bone and can cause cancer-induced bone pain (CIBP). Current therapeutic options do not offer proper management and thus CIBP can severely affect a patient's quality of life. Dysregulation of the excitatory neurotransmitter, glutamate, may be involved in the complex and multifaceted mechanisms of CIBP. Because glutamatergic signaling promotes pain, a local rise in glutamate in the bone-tumor microenvironment may contribute to CIBP. Glutamate levels are regulated in part by the cystine/glutamate antiporter, system xc⁻. System xc⁻ is known to be expressed by many different cancer cell types. It functions by transporting cystine into cells and in return releasing glutamate into the extracellular space. Elevated glutamate levels driven by the upregulated expression of this antiporter may contribute to CIBP. Here we demonstrate that system xc⁻ is expressed on a spontaneously occurring murine mammary tumor cell line (66.1) and that treatment of these cells with the established inhibitor and anti-inflammatory agent, sulfasalazine, decreases glutamate secretion in a time and dose-dependent manner. Furthermore, in a novel model of breast CIBP, systemic sulfasalazine treatment not only reduces glutamate levels within the femur, but also significantly attenuates CIBP behaviors. Studies utilized 66.1 cells implanted into the femur intramedullary space of immunocompetent mice. Measurements of spontaneous and evoked pain were made 7 and 10 days post cancer cell inoculation. Systemic administration of sulfasalazine for 4 days (on days 7-10) significantly reduced spontaneous pain-related behaviors and glutamate in femur extrudate as compared to vehicle treated controls. In summary, we demonstrate that pharmacological inhibition of the system xc⁻ transporter attenuates CIBP related behaviors in mice. These data support a role for system xc⁻ in CIBP and validate it as an analgesic target. Further research is warranted to evaluate the potential repurposing of sulfasalazine as an antinociceptive agent for patients with CIBP.

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Remeniuk, Bethany Lynne. "Capturing Affective Dimensions of Cancer-Induced Bone Pain Preclinically." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/556862.

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Pain is the most feared symptom of cancer and can impact patients' lives more than the cancer itself. Despite improvements in cancer prevention and detection, pain is often the first sign of cancer, with an estimated 70-75% of advanced stage cancer patients presenting with skeletal metastases. Cancer metastasis to the bone is associated with persistent pain that increases in intensity over time. Current treatments follow the World Health Organization (WHO) analgesic ladder for cancer pain management suggesting non-steroidal anti-inflammatory drugs (NSAIDs) for mild to moderate pain and opioids for moderate to severe pain. However, estimates indicate as many as 50-80% of cancer patients worldwide receive inadequate pain management. Moreover, opioid doses required for these patients are associated with adverse side effects further diminishing quality of life. Development of improved non-opioid therapies is dependent on increased understanding of mechanisms driving cancer pain and its relief. The objective of this dissertation was to characterize a rat model of cancer-induced bone pain, to develop approaches to measure both ongoing and breakthrough pain and to investigate the contribution of underlying inflammatory mechanisms to pain, bone destruction and bone remodeling. Using female Fischer F344/NhSD rats, histocompatible MAT B III mammary adenocarcinoma cells were sealed into the intramedullary space of the right rear tibia for a time course of 13 days. Ongoing pain was characterized based on the WHO 3-step ladder for pain management utilizing novel behavioral and neurochemical assays. Morphine and peripheral nerve block were sufficient to control ongoing pain, whereas NSAID treatment failed to provide pain relief. Cancer-bearing rats selectively displayed movement-induced breakthrough pain to a background of morphine-controlled ongoing pain. Furthermore, we determined that breakthrough pain is initiated, but not maintained, by peripheral afferent input from the tumor-bearing tibia using lidocaine administration prior to or following movement. For the final part of this study, we investigated the role of transient receptor potential vanilloid 1 (TRPV1) and interleukin-6 (IL-6) blockade, as these have been shown to be important mediators in animal models CIBP. Acute blockade of TRPV1 channels by AMG9810 selectively reversed inflammatory-induced pain, but failed to control evoked or ongoing CIBP. Acute blockade of interleukin-6 signaling by TB-2-081, an IL-6 receptor antagonist, successfully reversed evoke pain responses, but like AMG9810, failed to control ongoing pain. Sustained administration of TB-2-081 reversed cancer-induced tactile hypersensitivity and tumor-induced bone remodeling of the tibia. Further in vitro analysis revealed TB-2-081 functions by inhibiting the Jak/STAT cascade on both tumor cells and osteoblasts, suggesting that blockade of IL-6 signaling can effectively modulate the bone microenvironment to reduce tumor burden and pain. Combined, our data introduce a rat model of breast cancer bone metastasis, in which the underlying mechanisms of ongoing and breakthrough CIBP can be effectively studied. From this, novel therapeutic agents can be developed and investigated to help improve quality of life in patients suffering from this disease.

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Sukhtankar, Devki, Alec Okun, Anupama Chandramouli, Mark Nelson, Todd Vanderah, Anne Cress, Frank Porreca, and Tamara King. "Inhibition of p38-MAPK signaling pathway attenuates breast cancer induced bone pain and disease progression in a murine model of cancer-induced bone pain." BioMed Central, 2011. http://hdl.handle.net/10150/610213.

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BACKGROUND:Mechanisms driving cancer-induced bone pain are poorly understood. A central factor implicated to be a key player in the process of tumorigenesis, osteoclastogenesis and nociception is p38 MAPK. We determined the role of p38 MAPK in a mouse model of breast cancer induced bone pain in which mixed osteolytic and osteoblastic remodeling occurs.RESULTS:In cancer-treated mice, acute as well as chronic inhibition of p38 MAPK with SB203580 blocked flinching and guarding behaviors in a dose-dependent manner whereas no effect on thresholds to tactile stimuli was observed. Radiographic analyses of bones demonstrated that chronic inhibition of p38 MAPK reduced bone loss and incidence of spontaneous fracture in cancer-treated mice. Histological analysis of bones collected from mice treated with the p38 MAPK inhibitor showed complete absence of osteoblastic growth in the intramedullary space as well as significantly reduced tumor burden.CONCLUSIONS:Blockade of non-evoked pain behaviors but not hypersensitivity suggests differences in the underlying mechanisms of specific components of the pain syndrome and a possibility to individualize aspects of pain management. While it is not known whether the role of p38 MAPK signaling can be expanded to other cancers, the data suggest a need for understanding molecular mechanisms and cellular events that initiate and maintain cancer-induced bone pain for effective management for both ongoing pain as well as breakthrough pain.

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Scott, Angela C. "Cancer-induced bone pain (CIBP) : clinical characterisation and biomarker development." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/24294.

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Background: Cancer-induced bone pain (CIBP) is a major clinical problem and a considerable therapeutic challenge. Radiotherapy (XRT) is the gold standard treatment for CIBP, but only half of patients achieve adequate analgesia. Patients have increased morbidity, anxiety and depression and reduced performance and quality of life. Despite these issues, CIBP is a neglected area of clinical research. Animal models have increased current knowledge of the pathophysiology, but clinical research is needed to translate these findings from bench to bedside. Also lacking is a standardised, comprehensive tool to assess CIBP and clinical biomarkers to predict analgesic response to treatment. Aims: 1) To summarise current understanding of the pathophysiology, epidemiology, clinical features, assessment and management of malignant bone disease and CIBP. 2) To characterise CIBP using quantitative sensory testing as a measure of altered sensory processing. 3) To establish systematically the sensory, cognitive, affective and functional components of CIBP to develop a comprehensive assessment tool. 4) To explore whether clinical biomarkers can be developed to aid prediction of response to treatment for CIBP, in particular XRT. Results: Assessment of CIBP, characterising the multi-dimensional components, was clinically practical and acceptable to patients. Using objective measures of function, patients with CIBP were a frailer, less active population compared with healthy adults. Prior to treatment, pain was severe with relationships seen between CIBP and sensation, mood, fear avoidance, catastrophizing and function. Patients who dropped out prior to follow up were significantly less active, with higher levels of depression and fear avoidance behaviour. Sixty-nine percent of evaluable patients who completed two assessments (48% of all patients on an intention-to-treat basis), achieved an analgesic response to XRT for CIBP, as defined as an improvement of ≥ 30% in the Brief Pain Inventory worst pain score two months after treatment. All dimensions of pain, fear avoidance and catastrophizing improved significantly in responders, but not non-responders. Anxiety, depression and emotional distress fell by a greater degree in responders. No objective functional differences were seen after XRT. Clear evidence of altered sensory processing was seen at the site of CIBP with abnormalities in both mechanical and thermal parameters. XRT resulted in alterations in response to evoked stimuli in responders with a greater number of patients in whom sensation normalised after XRT compared with non-responders. Patients with a combination of altered sensation to thermal, pin prick and wind up stimuli showed the largest reduction in worst pain after XRT. Abnormal cool sensation at the site of CIBP was an independent predictor of analgesic response to treatment. Conclusion: Strong associations exist between CIBP, sensation, cognition, mood and function. Multi-dimensional assessment should be performed to improve quality of life. Translational research to provide targeted individualised treatment should be high on the research agenda. Future work should focus on thermal sensory processing as a potential clinical biomarker of response to palliative XRT for CIBP.

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Umaretiya, Puja Jagdish. "Cathepsin Inhibitor, VBY-825, Attenuates Bone Cancer Induced Pain in Mice." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/145000.

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Vardanyan, Anna. "Opioid-induced Hyperalgesia: Underlying Mechanisms and Clinical Relevance." Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/195034.

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Metastatic bone cancer causes severe pain that is primarily treated with opioids. A recently developed model of bone cancer pain was used to evaluate the effects of sustained morphine treatment. In cancer-treated mice, morphine enhanced spontaneous and evoked pain; these effects were dose-dependent and naloxone-sensitive. SP and CGRP positive DRG cells did not differ between sarcoma or control mice, but were increased following morphine in both groups. Morphine increased ATF-3 expression only in DRG cells of sarcoma mice. Morphine did not alter tumor growth in vitro or in vivo but increased sarcoma-induced bone destruction and incidence of spontaneous fracture in a dose- and naloxone-sensitive manner. Morphine increased osteoclast activity suggesting enhancement of sarcoma-induced osteolysis. Thus, morphine treatment may "add-on" additional mechanisms of pain beyond those induced by sarcoma. Despite the potential clinical significance, the exact mechanisms of opioid-induced hypersensitivity remain unknown. The vanilloid 1 receptor (TRPV1) is a molecular integrator of noxious stimuli. Sustained morphine elicited thermal and tactile hypersensitivity in WT, but not TRPV1 KO mice. Sustained morphine enhanced capsaicin-induced flinching and plasma extravasation in rats, indicating increased activity of these receptors in the periphery. Immunohistochemical studies indicate increase in TRPV1 expression in DRG and sciatic nerve, but not spinal cord, suggesting increased trafficking of TRPV1 channel to the periphery. Possible mechanisms of this enhanced expression and function of TRPV1 channels is activation of p38 MAPK. Sustained intrathecal infusion of p38 MAPK inhibitor prevents morphine-induced hypersensitivity and enhanced capsaicin-induced flinching, indicating the role of p38MAPK in the development of morphine-induced pain, possibly through sensitization of TRPV1 receptors. Acute administration of p38 MAPK inhibitor reversed morphine-induced pain suggesting the importance of p38 MAPK in the maintenance of morphine-induced hypersensitivity, likely through activation of TRPV1 channel. Sustained morphine also up-regulates NGF content in skin, which is then transported to DRG neurons where phosporilation of p38MAPK takes place. Single injection of anti-NGF peptibody blocked the development of morphine-induced hypersensitivity, enhanced capsaicin-induced flinching and plasma extravasation. Co-treatment with these compounds blocks the development of morphine-induced hyperalgesia and may optimize treatment of chronic pain states, like bone cancer pain.

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Slosky, Lauren M. "Targeting the Cystine/Glutamate Antiporter System xc⁻ in Cancer-Induced Bone Pain." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/594941.

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Many common cancers, including breast, prostate and lung cancers, have a propensity to metastasize to bone. Although these cancers go undetected in their native tissues, bone metastases often produce excruciating pain, the etiology of which is poorly understood. Cancer-induced bone pain (CIBP) is not well-controlled with existing medications, severely compromising patient quality of life. While CIBP is multifaceted, increased level of the excitatory neurotransmitter glutamate in the bone-tumor microenvironment may contribute to the pain state. Here, we demonstrate for the first time a relationship between reactive oxygen/nitrogen species, glutamate in the bone-tumor microenvironment and pain behaviors. The murine mammary adenocarcinoma cell line 66.1 is found to release glutamate via the cystine/glutamate antiporter system xc⁻. In a syngeneic model of breast CIBP in which 66.1 cells are inoculated into the femur intramedullary space, administration of sulfasalazine, an established system xc⁻ inhibitor and anti-inflammatory agent, reduces femur glutamate level and attenuates CIBP-related behaviors. Peroxynitrite, a reactive nitrogen species known to be generated in breast tumors, is shown to drive 66.1 system xc⁻ functional expression and tumor cell glutamate release. The elimination of peroxynitrite with the redox modulators FeTMPyP or SRI10 not only modulates tumor cell system xc⁻ functional expression in vitro and in vivo, significantly altering glutamate levels, but also assuages CIBP. In sum, we demonstrate that pharmacological inhibition of system xc⁻ transport attenuates CIBP-related behaviors. These data support a role for tumor-derived glutamate in CIBP and validate system xc⁻ an analgesic target in this pain state.

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Patel, S. "Neuronal mechanisms in rodent models of osteoarthritic and cancer-induced bone pain." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1348543/.

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Whilst pain serves a physiological function, chronic diseases such as osteoarthritis and cancer of the bone involve central neurones and peripheral nociceptors becoming sensitised to heighten or extend the pain experience temporally, which is detrimental to the quality of life. Mechanisms underlying central sensitization of neurones are examined in this thesis in two rodent models of pain: osteoarthritis (OA) and cancer-induced bone pain (CIBP) using pharmacology, mapping of receptive field size for lamina I neurones in OA animals and TENS. Pharmacological studies focused on NMDA and P2X3 and P2X2/3 receptors using ketamine, ifenprodil and a novel agent: AF-353. Ketamine reduced the neuronal responses to noxious stimuli in OA animals to levels observed in naïve animals. However effects were significantly stronger in CIBP animals where doses 10-fold lower produced the same effect suggesting post-synaptic NMDA receptors have a significant role in the maintenance of CIBP. Ifenprodil, which acts at NR2B subunit containing receptors, which are presynaptically located and may thus control release of neurotransmitters from the afferent terminal, more strongly inhibited electrical stimuli evoked responses in OA animals. Inhibition of natural stimuli evoked neuronal responses were similar in both models suggesting the importance of primary afferent drive in maintenance of central sensitization in OA and CIBP. AF-353 which inhibits the actions of ATP on pre-synaptically located P2X3 and P2X2/3 receptors was found to profoundly inhibit neuronal responses to noxious thermal stimuli in CIBP suggesting that thermal-stimuli induced hyperalgesia has a central component driven by the purinergic system. Finally, TENS a nonpharmacological intervention was found to have no significant effect on evoked responses of lamina V neurones in CIBP animals questioning its suitability in managing chronic pain. Differing pharmacology appears to contribute to the maintenance of central sensitization in OA and CIBP suggesting that more targeted therapy may be more clinically appropriate.

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Книги з теми "Bone cancer pain"

1963-, Davies Andrew, ed. Cancer-related bone pain. Oxford: Oxford University Press, 2007.

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Edward, Chow, and Merrick Joav 1950-, eds. Advanced cancer: Pain and quality of life. Hauppauge, N.Y: Nova Science, 2010.

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Brennfleck, Shannon Joyce, ed. Pain sourcebook: Basic consumer health information about acute and chronic pain, including nerve pain, bone pain, muscle pain, cancer pain, and disorders characterized by pain, such as arthritis, temporomandibular muscle and joint (tmj) disorder, carpal tunnel syndrome, headaches, heartburn, sciatica, and shingles, and facts about diagnostic tests and treatment options for pain, including over-the-counter and prescription drugs, physical rehabilitation, injection and infusion therapies, implantable technologies, and complementary medicine; along with tips for living with pain, a glossary of related terms, and a directory of additional resources. 3rd ed. Detroit: Omnigraphics, 2008.

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Davies, Andrew, ed. Cancer-related Bone Pain. Oxford University Press, 2007. http://dx.doi.org/10.1093/med/9780199215737.001.0001.

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Colvin, Lesley A., and Marie Fallon. Cancer-induced bone pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0132.

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Bone is the third most common site of metastatic disease, after liver and lung, with approximately 75% of these patients suffering from related pain. Cancer-induced bone pain (CIBP) is a major clinical problem, with limited options for predictable, rapid, and effective treatment for some of the elements without unacceptable adverse effects. Our understanding of how current therapy acts is based mainly on studies in non-cancer pain syndromes, which are likely to be quite different, not only in clinical presentation, but also in terms of pathophysiology. It can be difficult to study the specific neurobiological changes associated with CIBP, although development of laboratory models of isolated bone metastases has allowed more specific study of pain mechanisms in this syndrome. In order to evaluate our current therapies properly and direct the development of new therapies logically, it is important to understand the underlying mechanisms of CIBP. This chapter discusses pain processing and the mechanisms and management of CIBP.

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Cancer-Related Bone Pain. Oxford University Press, Incorporated, 2014.

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Davies, Andrew. Cancer-Related Bone Pain. Oxford University Press, Incorporated, 2007.

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Doré-Savard, Louis, Nicolas Beaudet, and Philippe Sarret. Mechanisms of bone cancer pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0037.

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The landmark paper discussed in this chapter focuses on pain arising from malignancy of the bone, which, whether primary or originating from a distant site, is the cause for a majority of cancer pain syndromes. Bone is an innervated organ that can relay nociceptive signals triggered by nerve damage, acidosis, inflammation, and hypoxia. The understanding of the physiopathology of skeletal pain has leaped significantly forwards over the last 15 years. The development of animal models that allowed for the visualization of bone microenvironment modifications by the tumour played an important role in recent advances. One of the most significant discoveries was the contribution of local nerve growth factor (NGF) to nerve remodelling in the bone periosteum presented by Mantyh and colleagues in 2010. NGF remains one the most promising treatment avenues for malignant bone pain, and peripheral innervation has become a therapeutic target in several skeletal pathologies.

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Davies, Andrew. Cancer-related Bone Pain (Oxford Pain Management Library S.). Oxford University Press, USA, 2007.

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Chow, Edward. Advanced Cancer: Pain and Quality of Life. Nova Science Publishers, Incorporated, 2021.

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Частини книг з теми "Bone cancer pain"

Hamamoto, Darryl T., and Donald A. Simone. "Cancer Pain Model, Bone Cancer Pain Model." In Encyclopedia of Pain, 414–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_547.

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O'Donnell, Patrick W., and Denis R. Clohisy. "Bone Cancer and Pain." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 720–27. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch87.

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O’Donnell, Patrick W., Nancy M. Luger, and Denis R. Clohisy. "Bone Pain Associated with Cancer Metastasis." In Bone and Cancer, 167–79. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84882-019-7_11.

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Baciuchka-Palmaro, M., J. L. Mouysset, and D. Spiegel. "Therapeutic Approaches to Bone Cancer Pain." In Bone Metastases, 147–55. London: Springer London, 2002. http://dx.doi.org/10.1007/978-1-4471-3251-6_14.

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O’Donnell, Patrick W., and Denis R. Clohisy. "Biology of Bone Cancer Pain." In Metastatic Bone Disease, 37–44. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-5662-9_3.

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Tarumi, Yoko. "Bone Cancer Pain and Skeletal Complications." In Textbook of Palliative Medicine and Supportive Care, 313–22. 3rd ed. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9780429275524-33.

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Mantyh, Patrick W., and Stephen P. Hunt. "Mechanisms That Generate and Maintain Bone Cancer Pain." In Osteoarthritic Joint Pain, 221–40. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470867639.ch15.

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Fakata, Keri L., and Arthur G. Lipman. "Adjuvant Analgesics in Management of Cancer-Related Bone Pain." In Encyclopedia of Pain, 68–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_105.

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Lam, Marnix G. E. H., John M. H. de Klerk, and Peter P. van Rijk. "186Re-HEDP for Metastatic Bone Pain in Breast Cancer Patients." In Breast Cancer, 257–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-36781-9_20.

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Caraceni, Augusto, Ernesto Zecca, Fabio Formaglio, and Francesca Ricchini. "Bone Metastases from Prostate Cancer: From Symptom Control to Pain Palliation." In Bone Metastases from Prostate Cancer, 251–70. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42327-2_19.

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Тези доповідей конференцій з теми "Bone cancer pain"

Geneviève, R., M. Lemire, K. Belleville, N. Beaudet, J. Martinez, and S. Philippe. "Abstract P1-03-08: Targeting Neurotensinergic Receptors for Bone Cancer Pain Relief." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p1-03-08.

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Balenko, Matthew D., Eric Seidlitz, and Gurmit Singh. "Abstract 3687: Analgesic effects of capsazepine on a mouse model of bone cancer pain." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3687.

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Park, Keon Uk, Mi Hwa Heo, Jin Young Kim, Ilseon Hwang, and Hun Mo Ryoo. "Abstract 4189: Analgesic effect of quetiapine on the cancer induced bone pain animal model." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4189.

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Maxwell, CL, AS Guinigundo, L. Vanni, PK Morrow, M. Reiner, A. Shih, Z. Klippel, and E. Blanchard. "Abstract P5-09-13: The effect of bone pain–specific education vs general chemotherapy side-effect education on reported bone pain in patients (pts) with breast cancer receiving chemotherapy and pegfilgrastim." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p5-09-13.

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Jimenez-Andrade, Juan Miguel, Aaron P. Bloom, Magdalena J. Kaczmarska, Elizabeth A. Burton, Jiazhong Zhang, Paul S. Lin, Brian L. West, and Patrick W. Mantyh. "Abstract A246: Blockade of CSF-1R/CSF-1 signaling by PLX3397 attenuates prostate cancer cell growth in bone, prostate cancer-induced skeletal pain, and pathological bone remodeling." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a246.

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Schwartzberg, L., M. Mo, R. Harms, and C. Vogel. "Reported Bone Pain in Patients with Breast Cancer Receiving Taxane-Based Chemotherapy in Clinical Trials of Pegfilgrastim." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-1117.

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Fernandes, Donald J., Mariappan Senthiappan Athiyamaan, Sandesh Rao, Sharaschandra Shankar, and Abhishek Krishna. "Comparison of Various Radiotherapy Dose Fractionation Schedules in Palliation of Bone Metastasis." In Annual Conference of Indian Society of Medical and Paediatric Oncology (ISMPO). Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1735374.

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Abstract Introduction Bone metastasis is a common manifestation of malignancy. Bone metastases causes various morbidities and affect the quality of life. External beam radiotherapy is the mainstay of treatment of uncomplicated painful bone metastases. Different radiotherapy fractionation schedules are in practice for palliation of painful bone metastases. Objectives This study was aimed to compare and report the outcomes of various fractionation schedules of radiation therapy (RT) in terms of pain relief and quality of life in patients with painful bone metastases. Materials and Methods Eighty patients were randomized into four treatment arms with different RT fractionation schedules, namely, 8 Gy in 1 fraction, 20 Gy in 5 fractions, 24 Gy in 6 fractions, and 30 Gy in 10 fractions. Patients were assessed for pain by visual analog scale (VAS), performance status and quality of life before initiating the treatment, on the day of completion of treatment, and 1 week, 1 month, and 3 months of treatment completion. Results Majority of the metastases constituted from breast followed by lung cancer. Of these, 27.5% had metastases to the thoracic vertebra, 26.25% to the lumbar vertebra, 22.5% to the pelvis, 8.75% to the sternum, 6.25% each to cervical vertebra and femur, and 1.25% each to humerus and ribs. The mean VAS score prior to start of RT was 5.31, 5.21, 5.54, and 4.87 in arms A, B, C, and D, respectively. At the end of treatment, the scores were 3.0, 3.29, 2.77, and 2.47, respectively. At the end of 3 months, the scores were 1.54, 0.57, 0.54, and 0.60, respectively. The pain reduction was significant in all the four arms (p < 0.05). Also, 25% of the patients’ arm A had complete pain relief, whereas 45% of patients in arms B, C, and D had complete pain relief. In arm A, the performance status failed to improve at 3 months when compared with 1-week post-RT but the improvement was significant in the remaining three arms. There was improvement in the quality of life in all the arms, both in terms of function and symptoms. The mean score of symptomatic quality of life based on the EORTC BM22 module prior to start of RT was 38.14, 34.91, 28.85, and 29.17 in arms A, B, C, and D, respectively. There was a significant drop to 9.29, 6.55, 5.13, and 6.11 at 1-month posttreatment in the four arms, respectively. The outcomes in terms of functional quality of life showed a similar trend. Conclusion This study demonstrated that pain reduction by various RT fractionation schedules were similar, and no statistically significant difference was noted. Performance status and quality of life improved in all the four treatment arms post-RT.

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Sakurai, T., T. Sakurai, T. Sakurai, T. Umemura, E. Jinta, T. Suzuma, P. Williams, et al. "Inhibition of Calcitonin Gene-Related Peptide and Insulin-Like Growth Factor: A Potential New Therapeutic Strategy To Reduce Bone Pain in Bone Metastases of Breast Cancer." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-1110.

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Schmidt, M., J. Seraphin, B. Luhn, and U. Soeling. "Major issues in the treatment of metastatic bone disease: renal safety and maintained bone pain effectiveness of ibandronate in breast cancer patients in clinical practice; interim results of a non interventional study in Germany." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-1159.

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Kosugi, T., M. Kubo, A. Ishikawa, and T. Yumiba. "ESRA19-0527 The effect of ganglion impar block on cancer pain caused by pubic bone metastasis: report of 4 cases." In Abstracts of the European Society of Regional Anesthesia, September 11–14, 2019. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/rapm-2019-esraabs2019.377.

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Звіти організацій з теми "Bone cancer pain"

Shrivastava, S. C., and J. Lister-James. Tin-117m DTPA, A Radiopharmaceutical for the Treatment of Cancer-Related Bone Pain. Office of Scientific and Technical Information (OSTI), August 1999. http://dx.doi.org/10.2172/770452.

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Mohapatra, Durga P., Andrew Shepherd, and Lipin Loo. Therapeutic Targeting of TRPV1 for the Treatment of Chronic Pain Associated with Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada612310.

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Mohapatra, Durga P., Betty Diamond, Lipin Loo, and Andrew Shepherd. Therapeutic Targeting of TRPV1 for the Treatment of Chronic Pain Associated with Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566497.

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Li, Lekun, Yujie Liu, Xiaofeng Ren, Kai Qu, and Xiaona Liu. Effectiveness of advanced nursing care (ANC) on bone cancer pain, psychological disorders and quality of life in patients with primary bone cancers: protocol for a PRISMA-compliant meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0037.

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Wang, Fei, Guihua Lai, Fang Zhou, Shujun Lei, Zhuojun Wu, Qing Deng, and Jianxiong Cao. Efficacy and Safety of External Application of Traditional Chinese Medicine Combined with Oral Opioids for Cancer-induced Bone Pain: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0004.

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