Sensorineural hearing loss in combined modality treatment of nasopharyngeal carcinoma

Chen, William; Jackson, Andrew; Budnick, Amy; Pfister, David G.; Kraus, Dennis H.; Hunt, Margie; Stambuk, Hilda E.; Levegrün, S.; Wolden, Suzanne L.

doi:10.1002/cncr.21683

Cited by 144 publications

(108 citation statements)

References 124 publications

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“…Increasing cumulative cisplatin dose (median, 400 mg/m 2 ; range, 200 to 800 mg/m 2 ) was significantly related to hearing loss at 4,6,8,10, and 12 kHz (P trends, .021 to , .001): every 100 mg/m 2 increase resulted in a 3.2-dB impairment in age-adjusted overall hearing threshold (4 to 12 kHz; P , .001). Cumulative cisplatin doses .…”

Section: Resultsmentioning

confidence: 96%

“…[4][5][6] Nonetheless, few comprehensive audiometric data exist for cisplatin-associated hearing loss in adult-onset cancer survivors. Several investigations of patients with head and neck cancer were confounded by cranial radiotherapy [7][8][9] ; limitations of other studies included small numbers, 6 concomitant vincristine, 6,10,11 and restriction of audiometric testing to just a few frequencies. 10,11 To our knowledge, only one series evaluated hearing loss in terms of cumulative cisplatin dose, 11 and none included audiometric assessments of noise-induced damage, middle ear function, or evaluation of speech processing.…”

Section: Introductionmentioning

confidence: 99%

“…10,11 To our knowledge, only one series evaluated hearing loss in terms of cumulative cisplatin dose, 11 and none included audiometric assessments of noise-induced damage, middle ear function, or evaluation of speech processing. 4,[6][7][8][9][10][11] To fill important gaps in these areas, we conducted comprehensive audiometric testing in relation to cumulative cisplatin dose in 488 men with adult-onset germ cell tumors (GCT), testing all frequencies between 0.25 and 12 kHz and evaluating audiologically defined noise-induced damage, speech processing, tinnitus, patient-reported outcomes, and middle ear function.…”

Section: Introductionmentioning

confidence: 99%

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Comprehensive Audiometric Analysis of Hearing Impairment and Tinnitus After Cisplatin-Based Chemotherapy in Survivors of Adult-Onset Cancer

Frisina

Wheeler

Fosså

et al. 2016

JCO

219

231

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Purpose Cisplatin is widely used but highly ototoxic. Effects of cumulative cisplatin dose on hearing loss have not been comprehensively evaluated in survivors of adult-onset cancer. Patients and Methods Comprehensive audiological measures were conducted on 488 North American male germ cell tumor (GCT) survivors in relation to cumulative cisplatin dose, including audiograms (0.25 to 12 kHz), tests of middle ear function, and tinnitus. American Speech-Language-Hearing Association criteria defined hearing loss severity. The geometric mean of hearing thresholds (0.25 to 12 kHz) summarized overall hearing status consistent with audiometric guidelines. Patients were sorted into quartiles of hearing thresholds of age- and sex-matched controls. Results Increasing cumulative cisplatin dose (median, 400 mg/m2; range, 200 to 800 mg/m2) was significantly related to hearing loss at 4, 6, 8, 10, and 12 kHz (P trends, .021 to < .001): every 100 mg/m2 increase resulted in a 3.2-dB impairment in age-adjusted overall hearing threshold (4 to 12 kHz; P < .001). Cumulative cisplatin doses > 300 mg/m2 were associated with greater American Speech-Language-Hearing Association–defined hearing loss severity (odds ratio, 1.59; P = .0066) and worse normative-matched quartiles (odds ratio, 1.33; P = .093) compared with smaller doses. Almost one in five (18%) patients had severe to profound hearing loss. Tinnitus (40% patients) was significantly correlated with reduced hearing at each frequency (P < .001). Noise-induced damage (10% patients) was unaffected by cisplatin dose (P = .59). Hypertension was significantly related (P = .0066) to overall hearing threshold (4 to 12 kHz) in age- and cisplatin dose–adjusted analyses. Middle ear deficits occurred in 22.3% of patients but, as expected, were not related to cytotoxic drug dosage. Conclusion Follow-up of adult-onset cancer survivors given cisplatin should include routine inquiry for hearing status and tinnitus, referral to audiologists as clinically indicated, and hypertension control. Patients should be urged to avoid noise exposure, ototoxic drugs, and other factors that further damage hearing.

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Section: Resultsmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Comprehensive Audiometric Analysis of Hearing Impairment and Tinnitus After Cisplatin-Based Chemotherapy in Survivors of Adult-Onset Cancer

Frisina

Wheeler

Fosså

et al. 2016

JCO

219

231

View full text Add to dashboard Cite

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“…one is sensory perception of sound, where 9 of 15 up-regulated genes are targeted by underexpressed mirnAs. Hearing impairment is frequently associated with nasopharyngeal carcinoma, nonetheless, whether the high frequency hearing loss is the cause or the effect of npc is still unclear (37)(38)(39). It is conjectured that the up-regulation of genes involved in sound perception is a mechanism of compensation for the impairment of hearing ability.…”

Section: Identification Of Pathways Enriched With Targets Of Differenmentioning

confidence: 99%

microRNA expression profiling of nasopharyngeal carcinoma

Chen

Fu³

et al. 2011

Oncol Rep

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Abstract. nasopharyngeal carcinoma (npc) is posing a serious health problem worldwide. the association between its pathogenesis and micrornAs (mirnA) has not been elucidated. In this study, miRNA expression profiling was performed to screen the mirnA expression changes in 8 npc tissues and 4 normal nasopharyngeal tissues. thirtyfour miRNAs were identified to be differentially expressed; of these, one mirnA (miR-18a) was overexpressed and 33 mirnAs (miR-34b, miR-34c, let-7 family, etc.) were underexpressed in npc tissues compared to the normal samples. Validation was performed by real-time quantitative pcr for two altered mirnAs (miR-34b and let-7g) and one nondifferentially expressed mirnA (miR-30c). Unsupervised hierarchical clustering analysis showed that the aberrant mirnAs were correlated with the clinical stage of npc patients. In addition to several biological pathways that are well characterised in npc and which were significantly targeted by the underexpressed mirnAs, two novel pathways, nervous system development and sensory perception of sound, were identified to be strongly associated with NPC development. Furthermore, a c-Myc centered mirnA regulatory network was inferred in npc. our study reveals that aberrantly expressed mirnAs play important roles in npc tumorigenesis and may serve as potential targets for novel therapeutic strategies in the future. IntroductionMicroRNAs (miRNAs) are a newly identified class of short (about 19-22 nt), endogenous, non-coding, single-stranded rnA molecules, which are conserved in sequence between distantly related organisms. More and more evidence has proved mirnAs play important roles in diverse biological functions, including development, differentiation, proliferation and apoptosis (1,2). MirnAs regulate protein expression by binding to the 3' untranslated regions (3' Utr) of messenger rnAs (mrnAs) and suppressing translation or inducing degradation or deadenylation with varying degrees of sequence complementarity (3). In humans, strong links between cancer and mirnA deregulation have been suggested by recent studies. The relevance of miRNAs to cancer was first reported in 2002 when calin et al observed that miR-15a and miR-16-1 were down-regulated or even deleted in the majority of chronic lymphocytic leukemia patients (4). they also found that many known mirnAs are located in the regions of human chromosomes with high frequencies of copy number alterations in cancers (4). so far, distinct mirnA profiles have been reported and the potential role of mirnAs in various human haematological and solid cancers have been indicated by many studies. lu et al used mirnA expressions to classify human cancers associated with the developmental lineage and differentiation state (5). Johnson et al reported that the down-regulation of let-7 is a significant cause of lung cancer tumorigenesis (6). this body of evidence indicates that the aberrations of mirnA expression in cancer are strongly correlated with tumor carcinogenesis and progression.nasopharyngeal carcinoma (npc) is ...

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“…Thus limiting the dose delivered to the cochlea seems critical. For conventionally fractionated RT or IMRT to minimize the risk for SNHL, the mean dose to the cochlea was suggested to be limited to 45 Gy (Pan et al, 2005;Chen et al, 2006), or more conservatively 40 Gy (Fleury and Lapeyre, 2010). In case of association with other causes of toxicity (such as age, low baseline value, association to cisplatin), this dose should be as low as possible (Fleury and Lapeyre, 2010).…”

Section: Radiation Dose Limitationmentioning

confidence: 99%