Chemotherapy-induced peripheral neuropathy in the adult

Saad, Mehdi; Tafani, C.; Psimaras, Dimitri; Ricard, Damien

doi:10.1097/cco.0000000000000139

Cited by 18 publications

(12 citation statements)

References 49 publications

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“…ROS modulation of K+ channel activity has already been reported[41] and CO plays multiple roles in nociception[47]. Moreover, it has been proposed that oxidative stress promotes the development of acquired forms of neuropathy, like diabetic neuropathy[48, 49] and chemotherapy-induced neuropathy[50, 51]. …”

Section: Discussionmentioning

confidence: 99%

Mutations in the Heme Exporter FLVCR1 Cause Sensory Neurodegeneration with Loss of Pain Perception

et al. 2016

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Pain is necessary to alert us to actual or potential tissue damage. Specialized nerve cells in the body periphery, so called nociceptors, are fundamental to mediate pain perception and humans without pain perception are at permanent risk for injuries, burns and mutilations. Pain insensitivity can be caused by sensory neurodegeneration which is a hallmark of hereditary sensory and autonomic neuropathies (HSANs). Although mutations in several genes were previously associated with sensory neurodegeneration, the etiology of many cases remains unknown. Using next generation sequencing in patients with congenital loss of pain perception, we here identify bi-allelic mutations in the FLVCR1 (Feline Leukemia Virus subgroup C Receptor 1) gene, which encodes a broadly expressed heme exporter. Different FLVCR1 isoforms control the size of the cytosolic heme pool required to sustain metabolic activity of different cell types. Mutations in FLVCR1 have previously been linked to vision impairment and posterior column ataxia in humans, but not to HSAN. Using fibroblasts and lymphoblastoid cell lines from patients with sensory neurodegeneration, we here show that the FLVCR1-mutations reduce heme export activity, enhance oxidative stress and increase sensitivity to programmed cell death. Our data link heme metabolism to sensory neuron maintenance and suggest that intracellular heme overload causes early-onset degeneration of pain-sensing neurons in humans.

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Section: Discussionmentioning

confidence: 99%

Mutations in the Heme Exporter FLVCR1 Cause Sensory Neurodegeneration with Loss of Pain Perception

et al. 2016

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“…Demographics, Health, and Clinical History Self-report prevalence of chronic medical conditions was obtained by the Charlson comorbidity index, 19 physical activity levels with the Community Healthy Activities Model Program for Seniors questionnaire, 3 and cancer history and demographics with an in-house questionnaire.…”

Section: Assessment Of Cipn Symptomsmentioning

confidence: 99%

“…2 Falls share overlapping causes with functional declines and are another significant concern for cancer survivors. The risk of falls increases after a cancer diagnosis when compared with prediagnosis fall rates, 3 and fall rate in cancer survivors can be twice that of cancer-free peers 4 or communitydwelling older adults. 5 A persistent cancer treatment-related symptom that may influence physical function, fall risk, and quality of life (QOL) is chemotherapy-induced peripheral neuropathy (CIPN).…”

Section: Introductionmentioning

confidence: 99%

Falls, Functioning, and Disability Among Women With Persistent Symptoms of Chemotherapy-Induced Peripheral Neuropathy

Winters-Stone

Horak

Jacobs

et al. 2017

JCO

271

211

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Chemotherapy-induced peripheral neuropathy (CIPN) may persist after treatment ends and may lead to functional decline and falls. This study compared objective and self-report measures of physical function, gait patterns, and falls between women cancer survivors with and without symptoms of CIPN to identify targets for functional rehabilitation. MethodsA secondary data analysis of 512 women cancer survivors (age, 62 6 6 years; time since diagnosis, 5.8 6 4.1 years) categorized and compared women self-reporting symptoms of CIPN (CIPN+) with asymptomatic women (CIPN2) on the following: maximal leg strength, timed chair stand, physical function battery, gait characteristics (speed; step number, rate, and length; base of support), selfreport physical function and disability, and falls in the past year. ResultsAfter an average of 6 years after treatment, 47% of women still reported symptoms of CIPN. CIPN+ had significantly worse self-report and objectively measured function than did CIPN2, with the exception of maximal leg strength and base of support during a usual walk. Gait was slower among CIPN+, with those women taking significantly more, but slower and shorter, steps than did CIPN2 (all P , .05). CIPN+ reported significantly more disability and 1.8 times the risk of falls compared with CIPN2 (P , .0001). Increasing symptom severity was linearly associated with worsening function, increasing disability, and higher fall risk (all P , .05). ConclusionThis work makes a significant contribution toward understanding the functional impact of CIPN symptoms on cancer survivors. Remarkably, 47% of women in our sample had CIPN symptoms many years after treatment, together with worse function, greater disability, and more falls. CIPN must be assessed earlier in the clinical pathway, and strategies to limit symptom progression and to improve function must be included in clinical and survivorship care plans.J Clin Oncol 35.

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“…The search for anticancer drugs from natural sources has mobilized several research fields. New chemotherapeutic drugs are needed, in particular to attenuate the many harmful side effects observed with current common‐use chemotherapeutics (Aluise et al, ; Nematbakhsh et al, ; Saad et al, ). While plants and terrestrial microorganisms have been in the limelight of Natural Products Research for several decades, the marine environment is one of the current hotspots for the bio‐prospection of new bioactive molecules (Montaser and Luesch, ).…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic activity of Secondary Metabolites from Marine‐derived Fungus Neosartorya siamensis in Human Cancer Cells

Prata‐Sena

Ramos

Buttachon

et al. 2016

Phytotherapy Research

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Compounds isolated from the marine sea fan-derived fungus Neosartorya siamensis (KUFA 0017), namely, 2,4-dihydroxy-3-methylacetophenon (1), chevalone C (2), nortryptoquivaline (4), tryptoquivaline H (6), tryptoquivaline F (7), fiscalin A (8), epi-fiscalin A (9), epi-neofiscalin A (11) and epi-fiscalin C (13) were tested for anti-proliferative activity by MTT assay, DNA damage induction by comet assay, and induction of cell death by nuclear condensation assay on colon HCT116, liver HepG2 and melanoma A375 cancer cell lines. Compounds 2, 4, 8, 9, 11 and 13 presented IC values ranging from 24 to 153 μM in the selected cell lines. Cell death was induced in HCT116 by compounds 2, 4 and 8. In HepG2, compounds 4, 8, 9 and 11 were able to induce significant cell death. This induction of cell death is possibly not related to genotoxicity because none of the compounds induced significant DNA damage. These results suggest that selected compounds present an interesting anti-proliferative activity and cell death induction, consequently showing potential (specifically epi-fiscalin C) as future leads for chemotherapeutic agents. Further studies on mechanisms of action should ensue. Copyright © 2016 John Wiley & Sons, Ltd.

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Chemotherapy-induced peripheral neuropathy in the adult

Cited by 18 publications

References 49 publications

Mutations in the Heme Exporter FLVCR1 Cause Sensory Neurodegeneration with Loss of Pain Perception

Mutations in the Heme Exporter FLVCR1 Cause Sensory Neurodegeneration with Loss of Pain Perception

Falls, Functioning, and Disability Among Women With Persistent Symptoms of Chemotherapy-Induced Peripheral Neuropathy

Cytotoxic activity of Secondary Metabolites from Marine‐derived Fungus Neosartorya siamensis in Human Cancer Cells

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