TY  - JOUR
AU  - Lazić, Andrijana
AU  - Popović, Jelena
AU  - Paunesku, Tatjana
AU  - Woloschak, Gayle E.
AU  - Stevanović, Milena
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1385
AB  - Cancer is a global health problem that is often successfully addressed by therapy, with cancer survivors increasing in numbers and living longer world around. Although new cancer treatment options are continuously explored, platinum based chemotherapy agents remain in use due to their efficiency and availability. Unfortunately, all cancer therapies affect normal tissues as well as cancer, and more than 40 specific side effects of platinum based drugs documented so far decrease the quality of life of cancer survivors. Chemotherapy-induced peripheral neuropathy is a frequent side effects of platinum-based chemotherapy agents. This cluster of complications is often so debilitating that patients occasionally have to discontinue the therapy. Sensory neurons of dorsal root ganglia are at the core of chemotherapy-induced peripheral neuropathy symptoms. In these postmitotic cells, DNA damage caused by platinum chemotherapy interferes with normal functioning. Accumulation of DNA-platinum adducts correlates with neurotoxic severity and development of sensation of pain. While biochemistry of DNA-platinum adducts is the same in all cell types, molecular mechanisms affected by DNA-platinum adducts are different in cancer cells and non-dividing cells. This review aims to raise awareness about platinum associated chemotherapy-induced peripheral neuropathy as a medical problem that has remained unexplained for decades. We emphasize the complexity of this condition both from clinical and mechanistical point of view and focus on recent findings about chemotherapy-induced peripheral neuropathy in in vitro and in vivo model systems. Finally, we summarize current perspectives about clinical approaches for chemotherapy-induced peripheral neuropathy treatment.
PB  - Wolters Kluwer Medknow Publications, Mumbai
T2  - Neural Regeneration Research
T1  - Insights into platinum-induced peripheral neuropathy-current perspective
EP  - 1630
IS  - 9
SP  - 1623
VL  - 15
DO  - 10.4103/1673-5374.276321
ER  - 

@article{
author = "Lazić, Andrijana and Popović, Jelena and Paunesku, Tatjana and Woloschak, Gayle E. and Stevanović, Milena",
year = "2020",
abstract = "Cancer is a global health problem that is often successfully addressed by therapy, with cancer survivors increasing in numbers and living longer world around. Although new cancer treatment options are continuously explored, platinum based chemotherapy agents remain in use due to their efficiency and availability. Unfortunately, all cancer therapies affect normal tissues as well as cancer, and more than 40 specific side effects of platinum based drugs documented so far decrease the quality of life of cancer survivors. Chemotherapy-induced peripheral neuropathy is a frequent side effects of platinum-based chemotherapy agents. This cluster of complications is often so debilitating that patients occasionally have to discontinue the therapy. Sensory neurons of dorsal root ganglia are at the core of chemotherapy-induced peripheral neuropathy symptoms. In these postmitotic cells, DNA damage caused by platinum chemotherapy interferes with normal functioning. Accumulation of DNA-platinum adducts correlates with neurotoxic severity and development of sensation of pain. While biochemistry of DNA-platinum adducts is the same in all cell types, molecular mechanisms affected by DNA-platinum adducts are different in cancer cells and non-dividing cells. This review aims to raise awareness about platinum associated chemotherapy-induced peripheral neuropathy as a medical problem that has remained unexplained for decades. We emphasize the complexity of this condition both from clinical and mechanistical point of view and focus on recent findings about chemotherapy-induced peripheral neuropathy in in vitro and in vivo model systems. Finally, we summarize current perspectives about clinical approaches for chemotherapy-induced peripheral neuropathy treatment.",
publisher = "Wolters Kluwer Medknow Publications, Mumbai",
journal = "Neural Regeneration Research",
title = "Insights into platinum-induced peripheral neuropathy-current perspective",
pages = "1630-1623",
number = "9",
volume = "15",
doi = "10.4103/1673-5374.276321"
}

Lazić, A., Popović, J., Paunesku, T., Woloschak, G. E.,& Stevanović, M.. (2020). Insights into platinum-induced peripheral neuropathy-current perspective. in Neural Regeneration Research
Wolters Kluwer Medknow Publications, Mumbai., 15(9), 1623-1630.
https://doi.org/10.4103/1673-5374.276321

Lazić A, Popović J, Paunesku T, Woloschak GE, Stevanović M. Insights into platinum-induced peripheral neuropathy-current perspective. in Neural Regeneration Research. 2020;15(9):1623-1630.
doi:10.4103/1673-5374.276321 .

Lazić, Andrijana, Popović, Jelena, Paunesku, Tatjana, Woloschak, Gayle E., Stevanović, Milena, "Insights into platinum-induced peripheral neuropathy-current perspective" in Neural Regeneration Research, 15, no. 9 (2020):1623-1630,
https://doi.org/10.4103/1673-5374.276321 . .

TY  - JOUR
AU  - Popović, Jelena
AU  - Lazić, Andrijana
AU  - Paunesku, Tatjana
AU  - Ma, Qing
AU  - Chen, Si
AU  - Lai, Barry
AU  - Stevanović, Milena
AU  - Woloschak, Gayle E.
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1255
AB  - Chemotherapy-induced peripheral neuropathy (CIPN) is a side effect of platinum-based chemotherapy and decreases the quality of life of cancer patients. We compared neuroprotective properties of several agents using an in vitro model of terminally differentiated human cells NT2-N derived from cell line NT2/D1. Sodium azide and an active metabolite of amifostine (WR1065) increase cell viability in simultaneous treatment with cisplatin. In addition, WR1065 protects the non-dividing neurons by decreasing cisplatin caused oxidative stress and apoptosis. Accumulation of Pt in cisplatin-treated cells was heterogeneous, but the frequency and concentration of Pt in cells were lowered in the presence of WR1065 as shown by X-ray fluorescence microscopy (XFM). Transition metals accumulation accompanied Pt increase in cells; this effect was equally diminished in the presence of WR1065. To analyze possible chemical modulation of Pt-DNA bonds, we examined the platinum L-III near edge spectrum by X-ray absorption spectroscopy. The spectrum found in cisplatin-DNA samples is altered differently by the addition of either WR1065 or sodium azide. Importantly, a similar change in Pt edge spectra was noted in cells treated with cisplatin and WR1065. Therefore, amifostine should be reconsidered as a candidate for treatments that reduce or prevent CIPN.
PB  - Springer/Plenum Publishers, New York
T2  - Cellular and Molecular Neurobiology
T1  - Neuroprotective Role of Selected Antioxidant Agents in Preventing Cisplatin-Induced Damage of Human Neurons In Vitro
EP  - 636
IS  - 5
SP  - 619
VL  - 39
DO  - 10.1007/s10571-019-00667-7
ER  - 

@article{
author = "Popović, Jelena and Lazić, Andrijana and Paunesku, Tatjana and Ma, Qing and Chen, Si and Lai, Barry and Stevanović, Milena and Woloschak, Gayle E.",
year = "2019",
abstract = "Chemotherapy-induced peripheral neuropathy (CIPN) is a side effect of platinum-based chemotherapy and decreases the quality of life of cancer patients. We compared neuroprotective properties of several agents using an in vitro model of terminally differentiated human cells NT2-N derived from cell line NT2/D1. Sodium azide and an active metabolite of amifostine (WR1065) increase cell viability in simultaneous treatment with cisplatin. In addition, WR1065 protects the non-dividing neurons by decreasing cisplatin caused oxidative stress and apoptosis. Accumulation of Pt in cisplatin-treated cells was heterogeneous, but the frequency and concentration of Pt in cells were lowered in the presence of WR1065 as shown by X-ray fluorescence microscopy (XFM). Transition metals accumulation accompanied Pt increase in cells; this effect was equally diminished in the presence of WR1065. To analyze possible chemical modulation of Pt-DNA bonds, we examined the platinum L-III near edge spectrum by X-ray absorption spectroscopy. The spectrum found in cisplatin-DNA samples is altered differently by the addition of either WR1065 or sodium azide. Importantly, a similar change in Pt edge spectra was noted in cells treated with cisplatin and WR1065. Therefore, amifostine should be reconsidered as a candidate for treatments that reduce or prevent CIPN.",
publisher = "Springer/Plenum Publishers, New York",
journal = "Cellular and Molecular Neurobiology",
title = "Neuroprotective Role of Selected Antioxidant Agents in Preventing Cisplatin-Induced Damage of Human Neurons In Vitro",
pages = "636-619",
number = "5",
volume = "39",
doi = "10.1007/s10571-019-00667-7"
}

Popović, J., Lazić, A., Paunesku, T., Ma, Q., Chen, S., Lai, B., Stevanović, M.,& Woloschak, G. E.. (2019). Neuroprotective Role of Selected Antioxidant Agents in Preventing Cisplatin-Induced Damage of Human Neurons In Vitro. in Cellular and Molecular Neurobiology
Springer/Plenum Publishers, New York., 39(5), 619-636.
https://doi.org/10.1007/s10571-019-00667-7

Popović J, Lazić A, Paunesku T, Ma Q, Chen S, Lai B, Stevanović M, Woloschak GE. Neuroprotective Role of Selected Antioxidant Agents in Preventing Cisplatin-Induced Damage of Human Neurons In Vitro. in Cellular and Molecular Neurobiology. 2019;39(5):619-636.
doi:10.1007/s10571-019-00667-7 .

Popović, Jelena, Lazić, Andrijana, Paunesku, Tatjana, Ma, Qing, Chen, Si, Lai, Barry, Stevanović, Milena, Woloschak, Gayle E., "Neuroprotective Role of Selected Antioxidant Agents in Preventing Cisplatin-Induced Damage of Human Neurons In Vitro" in Cellular and Molecular Neurobiology, 39, no. 5 (2019):619-636,
https://doi.org/10.1007/s10571-019-00667-7 . .