Advances in the therapy of cancer pain: from novel experimental models to evidence-based treatments

doi:10.22514/sv21.052007.4

Cited by 7 publications

(22 citation statements)

References 166 publications

(176 reference statements)

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“…56 The overall incidence of chemotherapy-induced peripheral neuropathy (CIPN) and of associated NP is high (30% to 70%). 23,57 Radiation can present with numerous clinical painful manifestations, ranging between 25 and 47%. 27,58 Following radiotherapy, the prevalence of NP in oncology units is increased, leading to sleepiness, anxiety and depression.…”

Section: 55mentioning

confidence: 99%

“…59 Diagnostic or therapeutic surgery may lead to NCP, with incidence reaching high rates (60% to 90%) in some cases, such as after surgery for breast cancer, or after thoracotomy. 23,27 Postmastectomy pain syndrome is reported in about 20% of women, 60 may be particularly troublesome and could consequently affect patients' quality of life.…”

Section: 55mentioning

confidence: 99%

“…21,22 Intractable NCP remains an important epidemiological, clinical and economical burden worldwide, posing significant societal impacts. 23 The aim of this comprehensive review is to provide the most recent knowledge regarding NCP systemic pharmacological management, focusing on evidencebased data, deriving from simple and randomized controlled trials (RCTs), consensus and expert committee reports, literature recommendations, and published guidelines. Apart from a brief reference of basic knowledge regarding terminology, definitions, epidemiology, classification, etiology, pathophysiological mechanisms and diagnosis, our scope is to present and analyze established, new or future pharmacological approaches that are or may become the mainstay in NCP treatment, mainly targeting at nociceptive inputs reduction, modulation of pain transmission to central nervous system (CNS) or alteration of pain central perception.…”

Section: Introductionmentioning

confidence: 99%

“…Symptoms may also continue for months or years after therapy discontinuation. 7,21,23,61 Oxaliplatin, a newer platinum compound, effective in advanced colon cancer, as well as in gastric, ovarian, breast and lung cancers, causes two types of neurotoxicity: an early acute reaction of dysaesthesia within hours of treatment in up to 90% of patients, and a chronic sensory neuropathy similar to that seen with cisplatin. Signs of oxaliplatin chronic neuropathy consist of proprioception alterations, which do not disappear between treatments.…”

mentioning

confidence: 99%

“…If severe, this problem can make daily activities (writing, buttoning shirts or picking up objects) extremely difficult. 7,23,61 Taxanes are indicated for the treatment of lung, breast and ovarian cancer, prolonging emissions and improving survival. Taxanes affect many sensory neurons and especially nerve fibers that conduct vibration sensation and proprioception, reducing the quality of life of cancer patients.…”

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confidence: 99%

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Pharmacological Treatment of Neuropathic Cancer Pain: A Comprehensive Review of the Current Literature

et al. 2011

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Neuropathic cancer pain (NCP), commonly encountered in clinical practice, may be cancer-related, namely resulting from nervous system tumor invasion, surgical nerve damage during tumor removal, radiation-induced nerve damage and chemotherapy-related neuropathy, or may be of benign origin, unrelated to cancer. A neuropathic component is evident in about 1/3 of cancer pain cases.Although from a pathophysiological perspective NCP may differ from chronic neuropathic pain (NP), such as noncancer-related pain, clinical practice, and limited publications have shown that these two pain entities may share some treatment modalities. For example, co-analgesics have been well integrated into cancer pain-management strategies and are often used as First-Line options for the treatment of NCP. These drugs, including antidepressants and anticonvulsants, are recommended by evidence-based guidelines, whereas, others such as lidocaine patch 5%, are supported by randomized, controlled, clinical data and are included in guidelines for restricted conditions treatment. The vast majority of these drugs have already been proven useful in the management of benign NP syndromes. Treatment decisions for patients with NP can be difficult. The intrinsic difficulties in performing randomized controlled trials in cancer pain have traditionally justified the acceptance of drugs already known to be effective in benign NP for the management of malignant NP, despite the lack of relevant high quality data. Interest in NCP mechanisms and pharmacotherapy has increased, resulting in significant mechanism-based treatment advances for the future. In this comprehensive review, we present the latest knowledge regarding NCP pharmacological management. n INTRODUCTIONFollowing EFIC's (European Federation of IASP Chapters) declaration in 2001, pain is not a symptom but a disease in its own right, necessitating appropriate treatment. The word pain usually refers to a discrete sensory experience, triggered by an identifiable set of ''painful'' stimuli, acting on a unique or stable ''pain'' pathway and eliciting an invariant sensation. However, pain, and particularly neuropathic pain (NP) can also exist as a diverse group of complex phenomena of unpleasant and distressing nature. NP encloses numerous complicated neurobiologic constituents and reflects potentially dynamic mechanisms, interacting at multiple neuraxial sites. 1Modern neurobiological techniques have led to tremendous progress in the exploration of pain pathogenetic mechanisms. [2][3][4] Research indicates that pain can be produced in multiple ways, at different locations, co-existing between and across various pathological conditions. 5,6 Novel therapeutic targets have been discovered and are used by the pharmaceutical industry for the construction of highly specific molecules, acting as potential innovative analgesics. Recent targets' application, specific to precise NP mechanisms, will very soon enable treatment to be focused at particular mechanisms, introducing a mechanism-based therap...

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Section: 55mentioning

confidence: 99%

Section: 55mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

mentioning

confidence: 99%

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Pharmacological Treatment of Neuropathic Cancer Pain: A Comprehensive Review of the Current Literature

et al. 2011

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Multifunctional compounds: Smart molecules for multifactorial diseases

Bansal

Silakari

2014

European Journal of Medicinal Chemistry

189

120

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Morphine efficacy is altered in conditional HIV-1 Tat transgenic mice

Fitting

Scoggins

et al. 2012

European Journal of Pharmacology

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Opiate abuse reportedly can exaggerate complications of human immunodeficiency virus type-1 (HIV-1) infection in the central nervous system (CNS), while opiate drugs are often indicated in the treatment of HIV-1-related neuropathic pain. Despite this quandary, few studies have assessed the relationship between the duration or extent of HIV-1 infection and the intrinsic neurobehavioral responsiveness to opioids. To address this problem, doxycycline (DOX)-inducible HIV-Tat1-86 transgenic mice were used as a model for HIV-1-associated neurocognitive disorders, which permitted the regulation of Tat exposure and duration. The effects of continuous Tat induction on the activity of morphine were examined at weekly intervals using standard behavioral assays for nociception and motor function. In the spinal cord, Tat mRNA levels did not increase until the second and third weeks following induction, which corresponded to a significant loss of morphine antinociception as assessed in the tail-flick test. Alternatively, in the striatum, sustained increases in Tat mRNA expression during the second week of induction coincided with significant decreases in rotarod performance and interactions with morphine. Importantly, the behavioral effects of morphine differed depending on the timing and location of Tat expression; with increases in Tat transcript levels in the spinal cord and striatum corresponding to significant alterations in morphine-dependent nociception and rotarod performance, respectively. Assuming Tat levels contribute to the clinical manifestations of HIV-1, the results suggest that regional differences in viral load and opioid phenotype might influence the nature and degree that opiate responsiveness is altered in HIV-1 infected individuals.

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Advances in the therapy of cancer pain: from novel experimental models to evidence-based treatments

Cited by 7 publications

References 166 publications

Pharmacological Treatment of Neuropathic Cancer Pain: A Comprehensive Review of the Current Literature

Pharmacological Treatment of Neuropathic Cancer Pain: A Comprehensive Review of the Current Literature

Multifunctional compounds: Smart molecules for multifactorial diseases

Morphine efficacy is altered in conditional HIV-1 Tat transgenic mice

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