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14 results on '"Lessans, Sherrie"'

1. Pharmacogenetic Discovery in CALGB (Alliance) 90401 and Mechanistic Validation of a VAC14 Polymorphism that Increases Risk of Docetaxel-Induced Neuropathy

Author

Hertz, Daniel L, Owzar, Kouros, Lessans, Sherrie, Wing, Claudia, Jiang, Chen, Kelly, William Kevin, Patel, Jai, Halabi, Susan, Furukawa, Yoichi, Wheeler, Heather E, Sibley, Alexander B, Lassiter, Cameron, Weisman, Lois, Watson, Dorothy, Krens, Stefanie D, Mulkey, Flora, Renn, Cynthia L, Small, Eric J, Febbo, Phillip G, Shterev, Ivo, Kroetz, Deanna L, Friedman, Paula N, Mahoney, John F, Carducci, Michael A, Kelley, Michael J, Nakamura, Yusuke, Kubo, Michiaki, Dorsey, Susan G, Dolan, M Eileen, Morris, Michael J, Ratain, Mark J, and McLeod, Howard L

Subjects
Genetics, Peripheral Neuropathy, Clinical Research, Neurosciences, Neurodegenerative, Chronic Pain, Cancer, Pain Research, Good Health and Well Being, Adult, Aged, Aged, 80 and over, Animals, Antineoplastic Combined Chemotherapy Protocols, Bevacizumab, Docetaxel, Double-Blind Method, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Intracellular Signaling Peptides and Proteins, Male, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Middle Aged, Pharmacogenomic Testing, Polymorphism, Single Nucleotide, Polyneuropathies, Prednisone, Prostatic Neoplasms, Castration-Resistant, Taxoids, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PurposeDiscovery of SNPs that predict a patient's risk of docetaxel-induced neuropathy would enable treatment individualization to maximize efficacy and avoid unnecessary toxicity. The objectives of this analysis were to discover SNPs associated with docetaxel-induced neuropathy and mechanistically validate these associations in preclinical models of drug-induced neuropathy.Experimental designA genome-wide association study was conducted in metastatic castrate-resistant prostate cancer patients treated with docetaxel, prednisone and randomized to bevacizumab or placebo on CALGB 90401. SNPs were genotyped on the Illumina HumanHap610-Quad platform followed by rigorous quality control. The inference was conducted on the cumulative dose at occurrence of grade 3+ sensory neuropathy using a cause-specific hazard model that accounted for early treatment discontinuation. Genes with SNPs significantly associated with neuropathy were knocked down in cellular and mouse models of drug-induced neuropathy.ResultsA total of 498,081 SNPs were analyzed in 623 Caucasian patients, 50 (8%) of whom experienced grade 3+ neuropathy. The 1,000 SNPs most associated with neuropathy clustered in relevant pathways including neuropathic pain and axonal guidance. An SNP in VAC14 (rs875858) surpassed genome-wide significance (P = 2.12 × 10-8, adjusted P = 5.88 × 10-7). siRNA knockdown of VAC14 in stem cell-derived peripheral neuronal cells increased docetaxel sensitivity as measured by decreased neurite processes (P = 0.0015) and branches (P < 0.0001). Prior to docetaxel treatment, VAC14 heterozygous mice had greater nociceptive sensitivity than wild-type litter mate controls (P = 0.001).ConclusionsVAC14 should be prioritized for further validation of its potential role as a predictor of docetaxel-induced neuropathy and biomarker for treatment individualization. Clin Cancer Res; 22(19); 4890-900. ©2016 AACR.

Published
2016

2. Supplementary Table 2 from Pharmacogenetic Discovery in CALGB (Alliance) 90401 and Mechanistic Validation of a VAC14 Polymorphism that Increases Risk of Docetaxel-Induced Neuropathy

Author

Hertz, Daniel L., primary, Owzar, Kouros, primary, Lessans, Sherrie, primary, Wing, Claudia, primary, Jiang, Chen, primary, Kelly, William Kevin, primary, Patel, Jai, primary, Halabi, Susan, primary, Furukawa, Yoichi, primary, Wheeler, Heather E., primary, Sibley, Alexander B., primary, Lassiter, Cameron, primary, Weisman, Lois, primary, Watson, Dorothy, primary, Krens, Stefanie D., primary, Mulkey, Flora, primary, Renn, Cynthia L., primary, Small, Eric J., primary, Febbo, Phillip G., primary, Shterev, Ivo, primary, Kroetz, Deanna L., primary, Friedman, Paula N., primary, Mahoney, John F., primary, Carducci, Michael A., primary, Kelley, Michael J., primary, Nakamura, Yusuke, primary, Kubo, Michiaki, primary, Dorsey, Susan G., primary, Dolan, M. Eileen, primary, Morris, Michael J., primary, Ratain, Mark J., primary, and McLeod, Howard L., primary

Published
2023
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3. Supplementary Figure 3: VAC14 Heterozygous Mice are Sensitive to Nociceptive Stimuli from Pharmacogenetic Discovery in CALGB (Alliance) 90401 and Mechanistic Validation of a VAC14 Polymorphism that Increases Risk of Docetaxel-Induced Neuropathy

Author

Hertz, Daniel L., primary, Owzar, Kouros, primary, Lessans, Sherrie, primary, Wing, Claudia, primary, Jiang, Chen, primary, Kelly, William Kevin, primary, Patel, Jai, primary, Halabi, Susan, primary, Furukawa, Yoichi, primary, Wheeler, Heather E., primary, Sibley, Alexander B., primary, Lassiter, Cameron, primary, Weisman, Lois, primary, Watson, Dorothy, primary, Krens, Stefanie D., primary, Mulkey, Flora, primary, Renn, Cynthia L., primary, Small, Eric J., primary, Febbo, Phillip G., primary, Shterev, Ivo, primary, Kroetz, Deanna L., primary, Friedman, Paula N., primary, Mahoney, John F., primary, Carducci, Michael A., primary, Kelley, Michael J., primary, Nakamura, Yusuke, primary, Kubo, Michiaki, primary, Dorsey, Susan G., primary, Dolan, M. Eileen, primary, Morris, Michael J., primary, Ratain, Mark J., primary, and McLeod, Howard L., primary

Published
2023
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4. Supplementary Figure 2: VAC14 Knockdown and neuronal cell sensitivity to docetaxel or paclitaxel for additional morphological phenotypes from Pharmacogenetic Discovery in CALGB (Alliance) 90401 and Mechanistic Validation of a VAC14 Polymorphism that Increases Risk of Docetaxel-Induced Neuropathy

Author

Hertz, Daniel L., primary, Owzar, Kouros, primary, Lessans, Sherrie, primary, Wing, Claudia, primary, Jiang, Chen, primary, Kelly, William Kevin, primary, Patel, Jai, primary, Halabi, Susan, primary, Furukawa, Yoichi, primary, Wheeler, Heather E., primary, Sibley, Alexander B., primary, Lassiter, Cameron, primary, Weisman, Lois, primary, Watson, Dorothy, primary, Krens, Stefanie D., primary, Mulkey, Flora, primary, Renn, Cynthia L., primary, Small, Eric J., primary, Febbo, Phillip G., primary, Shterev, Ivo, primary, Kroetz, Deanna L., primary, Friedman, Paula N., primary, Mahoney, John F., primary, Carducci, Michael A., primary, Kelley, Michael J., primary, Nakamura, Yusuke, primary, Kubo, Michiaki, primary, Dorsey, Susan G., primary, Dolan, M. Eileen, primary, Morris, Michael J., primary, Ratain, Mark J., primary, and McLeod, Howard L., primary

Published
2023
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5. Supplementary Table 3 from Pharmacogenetic Discovery in CALGB (Alliance) 90401 and Mechanistic Validation of a VAC14 Polymorphism that Increases Risk of Docetaxel-Induced Neuropathy

Author

Hertz, Daniel L., primary, Owzar, Kouros, primary, Lessans, Sherrie, primary, Wing, Claudia, primary, Jiang, Chen, primary, Kelly, William Kevin, primary, Patel, Jai, primary, Halabi, Susan, primary, Furukawa, Yoichi, primary, Wheeler, Heather E., primary, Sibley, Alexander B., primary, Lassiter, Cameron, primary, Weisman, Lois, primary, Watson, Dorothy, primary, Krens, Stefanie D., primary, Mulkey, Flora, primary, Renn, Cynthia L., primary, Small, Eric J., primary, Febbo, Phillip G., primary, Shterev, Ivo, primary, Kroetz, Deanna L., primary, Friedman, Paula N., primary, Mahoney, John F., primary, Carducci, Michael A., primary, Kelley, Michael J., primary, Nakamura, Yusuke, primary, Kubo, Michiaki, primary, Dorsey, Susan G., primary, Dolan, M. Eileen, primary, Morris, Michael J., primary, Ratain, Mark J., primary, and McLeod, Howard L., primary

Published
2023
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6. Supplementary Table 1 from Pharmacogenetic Discovery in CALGB (Alliance) 90401 and Mechanistic Validation of a VAC14 Polymorphism that Increases Risk of Docetaxel-Induced Neuropathy

Author

Hertz, Daniel L., primary, Owzar, Kouros, primary, Lessans, Sherrie, primary, Wing, Claudia, primary, Jiang, Chen, primary, Kelly, William Kevin, primary, Patel, Jai, primary, Halabi, Susan, primary, Furukawa, Yoichi, primary, Wheeler, Heather E., primary, Sibley, Alexander B., primary, Lassiter, Cameron, primary, Weisman, Lois, primary, Watson, Dorothy, primary, Krens, Stefanie D., primary, Mulkey, Flora, primary, Renn, Cynthia L., primary, Small, Eric J., primary, Febbo, Phillip G., primary, Shterev, Ivo, primary, Kroetz, Deanna L., primary, Friedman, Paula N., primary, Mahoney, John F., primary, Carducci, Michael A., primary, Kelley, Michael J., primary, Nakamura, Yusuke, primary, Kubo, Michiaki, primary, Dorsey, Susan G., primary, Dolan, M. Eileen, primary, Morris, Michael J., primary, Ratain, Mark J., primary, and McLeod, Howard L., primary

Published
2023
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7. Supplementary Figure 1: Patient Disposition from Clinical Trial to Pharmacogenetic Analysis from Pharmacogenetic Discovery in CALGB (Alliance) 90401 and Mechanistic Validation of a VAC14 Polymorphism that Increases Risk of Docetaxel-Induced Neuropathy

Author

Hertz, Daniel L., primary, Owzar, Kouros, primary, Lessans, Sherrie, primary, Wing, Claudia, primary, Jiang, Chen, primary, Kelly, William Kevin, primary, Patel, Jai, primary, Halabi, Susan, primary, Furukawa, Yoichi, primary, Wheeler, Heather E., primary, Sibley, Alexander B., primary, Lassiter, Cameron, primary, Weisman, Lois, primary, Watson, Dorothy, primary, Krens, Stefanie D., primary, Mulkey, Flora, primary, Renn, Cynthia L., primary, Small, Eric J., primary, Febbo, Phillip G., primary, Shterev, Ivo, primary, Kroetz, Deanna L., primary, Friedman, Paula N., primary, Mahoney, John F., primary, Carducci, Michael A., primary, Kelley, Michael J., primary, Nakamura, Yusuke, primary, Kubo, Michiaki, primary, Dorsey, Susan G., primary, Dolan, M. Eileen, primary, Morris, Michael J., primary, Ratain, Mark J., primary, and McLeod, Howard L., primary

Published
2023
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11. Global transcriptomic profile of dorsal root ganglion and physiological correlates of cisplatin-induced peripheral neuropathy

Author

Lessans, S, Lassiter, C, Carozzi, V, Heindel, P, Semperboni, S, Oggioni, N, Chiorazzi, A, Thompson, C, Wagner, M, Holden, J, Rahn, E, David Sweatt, J, Cavaletti, G, Renn, C, Dorsey, S, Lessans, Sherrie, Lassiter, Cameron B, Carozzi, Valentina, Heindel, Patrick, Semperboni, Sara, Oggioni, Norberto, Chiorazzi, Alessia, Thompson, Carleveva, Wagner, Monica, Holden, Janean, Rahn, Elizabeth, Cavaletti, Guido, Renn, Cynthia L, Dorsey, Susan G, Lessans, S, Lassiter, C, Carozzi, V, Heindel, P, Semperboni, S, Oggioni, N, Chiorazzi, A, Thompson, C, Wagner, M, Holden, J, Rahn, E, David Sweatt, J, Cavaletti, G, Renn, C, Dorsey, S, Lessans, Sherrie, Lassiter, Cameron B, Carozzi, Valentina, Heindel, Patrick, Semperboni, Sara, Oggioni, Norberto, Chiorazzi, Alessia, Thompson, Carleveva, Wagner, Monica, Holden, Janean, Rahn, Elizabeth, Cavaletti, Guido, Renn, Cynthia L, and Dorsey, Susan G

Abstract

Background Multiple cell signaling pathways are implicated in the development, progression, and persistence of cisplatin-induced peripheral neuropathy. Although advances have been made in terms of understanding specific neurotoxic mechanisms, there are few predictive factors identified that can help inform the clinician approach to symptom prevention or management. Objective We investigate the differential sensitivity to cisplatin-induced peripheral neuropathy and examine the contribution of dorsal root ganglion (DRG) transcriptional profiles across two inbred strains of mice. Methods Cisplatin (4 mg/kg intraperitoneal or vehicle control) was administered twice a week for 4 weeks to adult female C57BL/6J and A/J mice - the C57BL/6J strain of mice characterized by a robust mechanical allodynia and the A/J with a mild largely resistant allodynia phenotype. Peripheral nerve conduction velocities (NCVs), electrophysiological evaluation of wide dynamic range (WDR) neurons, morphological examination of DRG neurons, and microarray analysis of spinal cord tissues were compared across the 4 weeks. Results The A/J strain presents with an early, mild nocifensive response to cisplatin with reduced neuronal activity in WDR neurons and small changes in cross-sectional nucleus size in DRG neurons at 4 weeks. The more nocifensive-sensitive C57BL/6J strain presents with no early changes in WDR neuron responsiveness; however, there were significant changes in DRG size. Both strains demonstrate a drop in NCV after 4 weeks of treatment, with the greatest reduction present in the A/J strain. Transcriptome data implicate neuroimmune modulation in the differential response to cisplatin in the DRGs of A/J and C57BL/6J mice. Discussion Nocifensive responses in both strains implicate involvement of small myelinated and unmyelinated fibers in neurotoxic cisplatin response, whereas reductions in NCV reflect involvement of the largest myelinated fibers in the peripheral nerves. Microarray data

Published
2019

12. The Role for Epigenetic Modifications in Pain and Analgesia Response

Author

Lessans, Sherrie and Dorsey, Susan G.

Subjects
Article Subject
Abstract

Pain remains a poorly understood and managed symptom. A limited mechanistic understanding of interindividual differences in pain and analgesia response shapes current approaches to assessment and treatment. Opportunities exist to improve pain care through increased understanding of how dynamic epigenomic remodeling shapes injury, illness, pain, and treatment response. Tightly regulated alterations of the DNA-histone chromatin complex enable cells to control transcription, replication, gene expression, and protein production. Pathological alterations to chromatin shape the ability of the cell to respond to physiologic and environmental cues leading to disease and reduced treatment effectiveness. This review provides an overview of critical epigenetic processes shaping pathology and pain, highlights current research support for the role of epigenomic modification in the development of chronic pain, and summarizes the therapeutic potential to alter epigenetic processes to improve health outcomes.

Published
2013
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14. [Mechanism of electroacupuncture on "Zusanli (ST 36)" for chemotherapy-induced peripheral neuropathy].

Author

Sui M, Lessans S, Yan T, Cao D, Lao L, and Dorsey SG

Subjects
Animals, Antineoplastic Agents administration & dosage, Humans, Interleukin-1beta genetics, Interleukin-1beta metabolism, Male, Mice, Mice, Inbred C57BL, Peripheral Nervous System Diseases etiology, Peripheral Nervous System Diseases genetics, Peripheral Nervous System Diseases metabolism, Tumor Necrosis Factor-alpha genetics, Tumor Necrosis Factor-alpha metabolism, Acupuncture Points, Antineoplastic Agents adverse effects, Electroacupuncture, Neoplasms drug therapy, Peripheral Nervous System Diseases therapy
Abstract

Objective: To observe the effects and duration of electroacupuncture on the mechanical pain threshold induced by paclitaxel and explore its analgesic mechanism., Methods: Sixty-four C57BL/6J male mice were randomly divided into 4 groups, a normal+sham EA group, a normal+EA group, a medicine+sham EA(Med+ sham EA) group, a medicine + EA (Med + EA) group, 16 cases in each group. The model of chemotherapy-induced peripheral neuropathy was established with paclitaxel intraperitoneal injection on the 1st, 3rd, 5th, 7th day in the Med + sham EA group and the Med + EA group. EA of 30 min was used on bilateral "Zusanli (ST 36)" on the 9th, 11th, 13th, 16th, 18th, 20th, 23rd, 25th, 27th, 30th day in the EA groups, 2 Hz/100 Hz and 1~ 1.5 mA. Acupuncture was applied on the same acupoint at the same times in the sham EA groups. Mechanical pain thresholds were tested by VonFrey before and after model establishment, namely on the 8th, 14th; 21st and, 28th day. The heart blood of 8 mice was drawn quickly to collect serum in every group on the 31st day, and the contents of tumor necrosis factor α (TNF-α), interleukin-1α (IL-1α), interleukin-1β (IL-1β) in proinflammatory cytokine were examined by ELISA. Mechanical pain thresholds were tested by VonFrey for the rest 8 mice of each group until there was no apparent difference in the two paclitaxel groups once a week,namely on the 35th, 42nd, 49th day., Results: The pain thresholds of each group were not statistically different before model establishment (P > 0.05). After model establishment (on the 8th day), thresholds of the paclitaxel groups were lower than those of the normal groups (all P < 0.05). After EA, the mechanical pain thresholds of the Med + EA group were higher than those of the Med + sham EA group at all the time points, and there was statistical difference on the 14th, 21st and 28th day (all P < 0.05). The analgesic effect was lasting to the 49th day. The contents of TNF-α, IL-1α, IL-1β of the Med + EA group were decreased than those of the Med+sham EA group in different degree, with statistical significance of IL-1α (P < 0.05)., Conclusion: EA can effectively treat paclitaxel-induced peripheral neuropathy,and the analgesic mechanism is probably related to decreasing the proinflammatory cytokine.

Published
2016

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