Impact of Smoking on Outcomes of HPV-related Oropharyngeal Cancer Treated with Primary Radiation or Surgery

Vawda, N.; Banerjee, Robyn; Debenham, Brock

doi:10.1016/j.ijrobp.2018.11.046

Cited by 47 publications

(46 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many studies show that differences in survival outcomes can be attributed to demographic differences such as race/ethnicity, age, and gender 31‐33 or risk factors such as increased comorbid disease 34,35 and smoking 36,37 . Our study, however, was unable to detect significant differences in LRDFS outcomes based on race/ethnicity, age, gender, smoking, or comorbid disease.…”

Section: Discussioncontrasting

confidence: 74%

Evaluation of lymph node ratio and lymph node yield as prognosticators of locoregional recurrence in p16‐associated oropharyngeal squamous cell carcinoma

et al. 2020

View full text Add to dashboard Cite

Background The prognostic value of lymph node yield (LNY) and lymph node ratio (LNR), or the ratio of number of metastatic LNs to total number dissected, has not been well established in p16‐associated oropharyngeal squamous cell carcinoma (OPSCC). Methods This retrospective cohort study evaluated locoregional disease‐free survival (LRDFS) in 82 patients with p16+ OPSCC who underwent neck dissection at a single institution from 2009 to 2017. LNR and LNY cutoffs were estimated using time‐dependent receiver operator characteristic (ROC) curves. Prognostic significance of these cutoffs was compared with Eighth Edition AJCC Nodal Staging. Results An increased LNR ≥ 0.129 was associated with worse 2‐year LRDFS (66.9% vs 96.8%, P = .005). LNY was not significantly associated with LRDFS (P = .304). An LNR‐based risk model was a better prognosticator than Eighth Edition AJCC Nodal Staging (Harrell's C, 0.9065 vs 0.7668). Conclusions LNR has good prognostic utility in predicting LRDFS in p16+ OPSCC, but further evaluation of this measure is warranted.

show abstract

Section: Discussioncontrasting

confidence: 74%

Evaluation of lymph node ratio and lymph node yield as prognosticators of locoregional recurrence in p16‐associated oropharyngeal squamous cell carcinoma

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Notably, previous work has demonstrated that active smoking at diagnosis is an adverse prognostic factor in this population 13,14 . The current study extends our previous work by Xiao et al 14 and complements the work by Vawda et al 13 by analyzing time from smoking cessation as a continuous variable, using nonlinear regression, and applying the RPA methodology.…”

Section: Discussionsupporting

confidence: 72%

Rethinking the 10‐pack‐year rule for favorable human papillomavirus–associated oropharynx carcinoma: A multi‐institution analysis

Broughman

Xiong

Moeller

et al. 2020

Cancer

View full text Add to dashboard Cite

BACKGROUND: De-intensified treatment strategies for early human papillomavirus-positive (HPV+) oropharynx cancer (OPC) rely on selecting patients with an excellent prognosis. The criterion for enrollment in current de-intensification trials is ≤10 pack-years. More nuance to the pack-year criteria may expand enrollment, improve patient outcomes, and prevent overtreatment. It was hypothesized that patients with more than 10 pack-years may experience favorable outcomes if smoking cessation has been achieved. METHODS: From an institutional review board-approved database, patients with HPV+ oropharyngeal squamous carcinoma treated definitively with radiation with or without chemotherapy were retrospectively identified. Patients with a history of smoking who were eligible for national de-intensification trials were included (cT1-2N1-2b or T3N0-2b [American Joint Committee on Cancer, seventh edition]). Cox regression with penalized smoothing splines was used to evaluate nonlinear effects of cessation. Recursive partitioning analysis (RPA) was used to objectively search for relationships between the 2 colinear variables (pack-years and time since cessation). RESULTS: Among 330 patients meeting the inclusion criteria, 130 (40%) were never smokers, 139 (42%) were former smokers, and 61 (18%) were current smokers. With standard therapy, all former smokers achieved a progression-free survival (PFS) rate higher than 91%, regardless of pack-year exposure. Nonlinear Cox regression demonstrated that more recent cessation was associated with significantly worse PFS even among those with ≤20 pack-years. RPA demonstrated that only current smokers experienced a 2-year PFS rate lower than 91%; former smokers, regardless of pack-years, experienced a 2-year PFS rate higher than 91%. CONCLUSIONS: The 10-pack-year rule may not apply to all early HPV+ OPCs, particularly for former smokers. Future randomized de-intensification trials should consider a broader and more nuanced approach until the predictive role of smoking status is established. Cancer 2020;126:2784-2790.

show abstract

“…This observation must be considered in the inclusion criteria for future dose de-escalation studies in early stage HPV+ OPSCC. In agreement with these results, a recent study by Vawda et al 36 has demonstrated that higher intensity of smoking exposure was associated with poorer outcomes in a cohort of exclusively HPV+ oropharyngeal cancer patients treated with primary radiation or surgery. The study, however, lacked the comparison with an HPV-cohort.…”

Section: Discussionsupporting

confidence: 71%

Tobacco exposure as a major modifier of oncologic outcomes in Human PapillomaVirus (HPV) associated oropharyngeal squamous cell carcinoma

Elhalawani

Elgohari

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: The incidence of oropharyngeal squamous cell carcinoma (OPSCC) in the US is rapidly increasing, driven largely by the epidemic of human papillomavirus (HPV)-mediated OPSCC. Although survival for patients with HPV mediated OPSCC (HPV+ OPSCC) is generally better than that of patients with non-viral HPV+ OPSCC, the improvement is not uniform. We hypothesized that tobacco exposure remains a critical modifier of survival for HPV+ OPSCC patients. Methods: We conducted a retrospective analysis of 611 OPSCC patients with concordant p16 and HPV testing treated at a single institute (2002-2013). Survival analysis was performed using Kaplan-Meier analysis and Cox regression. Recursive partitioning analysis (RPA) was used to define tobacco exposure associated with survival (p<0.05). Results: Tobacco exposure impacted overall survival (OS) for HPV+ patients on univariate and multivariate analysis (p=0.002, p=0.003 respectively). RPA identified 30 pack-years (PY) as a threshold at which survival became significantly worse in HPV+ patients. OS and disease-free survival (DFS) for HPV+ >30 PY patients didn’t differ significantly from HPV- group (p= 0.72, p= 0.27, respectively). HPV+ >30 PY patients had substantially lower 5-year OS when compared to their ≤30 PYs counterparts: 78.4% vs 91.6%; p= 0.03, 76% vs 88.3%; p= 0.07, and 52.3% vs 74%; p= 0.05, for stages I, II, and III (AJCC 8 th Edition Manual), respectively. Conclusions: Tobacco exposure can eliminate the survival benefit associated with HPV+ status in OPSCC patients. Until this effect can be clearly quantified using prospective datasets, de-escalation of treatment for HPV+OPSCC smokers should be avoided.

show abstract

Impact of Smoking on Outcomes of HPV-related Oropharyngeal Cancer Treated with Primary Radiation or Surgery

Cited by 47 publications

References 25 publications

Evaluation of lymph node ratio and lymph node yield as prognosticators of locoregional recurrence in p16‐associated oropharyngeal squamous cell carcinoma

Evaluation of lymph node ratio and lymph node yield as prognosticators of locoregional recurrence in p16‐associated oropharyngeal squamous cell carcinoma

Rethinking the 10‐pack‐year rule for favorable human papillomavirus–associated oropharynx carcinoma: A multi‐institution analysis

Tobacco exposure as a major modifier of oncologic outcomes in Human PapillomaVirus (HPV) associated oropharyngeal squamous cell carcinoma

Contact Info

Product

Resources

About