Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 + 1555 word(s) 1555 2022-01-18 07:45:25 |
2 update layout and reference -1 word(s) 1554 2022-01-20 09:48:21 |

Video Upload Options

Do you have a full video?

Confirm

Are you sure to Delete?
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Terracina, S.; Petrella, C. Alcohol and Head and Neck Cancer. Encyclopedia. Available online: https://encyclopedia.pub/entry/18546 (accessed on 29 March 2024).
Terracina S, Petrella C. Alcohol and Head and Neck Cancer. Encyclopedia. Available at: https://encyclopedia.pub/entry/18546. Accessed March 29, 2024.
Terracina, Sergio, Carla Petrella. "Alcohol and Head and Neck Cancer" Encyclopedia, https://encyclopedia.pub/entry/18546 (accessed March 29, 2024).
Terracina, S., & Petrella, C. (2022, January 20). Alcohol and Head and Neck Cancer. In Encyclopedia. https://encyclopedia.pub/entry/18546
Terracina, Sergio and Carla Petrella. "Alcohol and Head and Neck Cancer." Encyclopedia. Web. 20 January, 2022.
Alcohol and Head and Neck Cancer
Edit

As suggested from recent findings, the role of alcohol in HNC seems to be broader than that of a simple risk factor. In this entry, authors report evidence from past studies to clarify the role of alcohol consumption in head and neck cancer (HNC) onset. Moreover, we further explore the role of oral microbiota, oxidative stress and genetic expression alterations due to alcohol drinking. Although alcohol is not the exclusive risk factor for HNC carcinogenesis, it plays a major role in the etiopathogenesis of both primary tumors and their recurrences, especially by means of ethanol and its metabolic products. Alcohol modifies oral microbiota, enhances intracellular oxidative stress, expose epithelial cells to carcinogens and alters cellular genetic expressions by promoting epigenetic mutations, DNA damage, and inaccurate DNA repair related to the formation of DNA adducts. The relationship between alcohol and HNC has been well established but, unfortunately, there is no clear threshold effect of alcohol for oncogenic patients, so that prevention and monitoring with long-term markers of alcohol consumption (especially those detected in the hair) that relay information on the actual alcohol drinking habits, seem to be the most effective ways to contrast its prevalence (and complications) in HNC drinker-patients. These conclusions seem to be especially important nowadays since, despite the established association between alcohol and HNC, a concerning pattern of alcohol consumption misconducts has been found in both in the general population and HNC  survivors. Interestingly, evidence that we report on HNC etiopathogenesis suggests a key role of polyphenols and alkylating agents for patient management, especially in case of heavy chronic drinkers.

oral microbiota alcohol alkylating agents epigenetics growth factors

1. Introduction

Worldwide, head and neck cancer (HNC) accounts for more than 890,000 cases and 450,000 deaths annually [1]. Head and neck cancer is a malignancy, associated with the advanced stage at presentation and heavy outcomes (mean 5-year survival <50%), that occurs more often in the lips and oral cavity, nasopharynx, oropharynx, hypopharynx, and larynx; squamous cell carcinoma (SCC) represents the prevalent histology [2][3].
Alcohol abuse may result in significant mental [4][5][6][7][8] or physical health problems [9][10][11][12]. Furthermore, when consumed during gestation, it may induce severe damage to the newborns [13][14][15][16][17][18][19][20]. Alcohol is a well-known carcinogen compound but it is still underestimated in the general population, partially also because of the alcohol industry’s extensive misrepresentation of evidence about the alcohol-related risk of cancer [21][22]. Alcohol drinking, together with tobacco smoking, and human papillomavirus (HPV) infection (Table 1) are HNC-recognized risk factors [23][24][25][26]. Interestingly, the role of alcohol in HNC seems to be broader than that of a simple risk factor, as suggested from recent findings which highlighted how significant inverse association exists between alcohol drinking and prognosis among HNC patients [27][28]. It has been reported that, in 2012, a total of 203,511 cases of the oral cavity, oropharyngeal, hypopharyngeal, and larynx cancer were attributable to alcohol consumption (179,559 men and 23,952 women) [29]. The proportion of HNC cases attributable to alcohol is still increasing, emphasizing the importance of alcohol consumption limitation to prevent HNC. Alcohol use among HNC survivors negatively impacts patient outcomes and is an important risk factor for recurrent and second primary tumors. Despite recommendations from several cancer societies, alcohol consumption remains a common problem in this population. [30]. The estimate of the real alcohol consumption (based not only on what the patient declared during the anamnesis) would be of support in consolidating the correlation with the onset of HNC.
Table 1. Major differences between HPV + and HPV - HNSCC (mainly related to alcohol abuse and smoke). Alcohol is a major determinant of aggressive HNCs. HNSCC, head and neck squamous cell carcinomas; HPV, human papillomavirus.
  HPV + HNSCC HPV - HNSCC
Main risk factors Sexual contact, HPV type 16 and 18 Alcohol and smoking
Tumor site Oropharynx Non-oropharyngeal sites
Histopathology Basaloid, non-keratinizing, poorly differentiated Keratinizing, moderately differentiated
Main carcinogenic factor Viral protein E6 and E7 action DNA damage and inaccurate DNA repair promoted by alcohol catabolism and smoke carcinogen components action
Responsiveness to chemoradiation Better than HPV - HNSCC Worse than HPV + HNSCC
Prognosis Better than HPV - HNSCC Worse than HPV + HNSCC
Prevention HPV vaccine, condom Alcohol and smoking abstinence

2. Head and Neck Cancer and Alcohol

2.1. Diagnosis and Treatments

The HNC diagnosis usually includes laryngoscopy, imaging [Positron emission tomography/X-ray computed tomography (PET/CT) and magnetic resonance imaging (MRI)], and biopsy of the primary lesion [31][32][33][34][35]. As technology progresses, the development of non-invasive diagnostic tools in the field of head and neck oncology has been examined; the molecular analysis of tumor’s genetic features based on circulating malignance derivatives, such as circulating tumor DNA, intact circulating tumor cells (CTCs), and exosomes in patients’ blood, namely liquid biopsy, has become a concrete possible approach to improve diagnostics, treatment planning, and post-treatment surveillance in patients with the potentially curable disease [36][37][38][39].
Treatment possibilities include tumor resection (primary and/or secondary tumor), radical neck dissection, immunotherapy, radiotherapy, checkpoint inhibitors (mainly targeting the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4)), programmed cell death protein 1 (PD-1), programmed death-ligand 1 (PD-L1), and chemotherapy [40][41][42][43][44][45]. Recently, it has been showing how, in locally advanced HNSCC, the CTCs and the circulating tumor microemboli (CTM) have a significant prognostic impact on the potential role as predictors of induction chemotherapy benefit [46].
It is believed that the majority of oral cancers develop from oral potentially malignant lesions (OPMLs) [47]. Though they can be easily detected during screening, risk stratification is difficult. During screening, clinicians often find it difficult to distinguish OPMLs from benign lesions, and predicting OPMLs at risk of malignant transformation could be particularly challenging [47]. DNA aneuploidy has been known to be a marker of malignancy in a number of sites, including the oral cavity [47]. Indeed, DNA ploidy and chromatin organization of cells collected from OPMLs can identify lesions at high risk of progression several years prior [48]. This non-invasive test would enable clinicians to triage high-risk OPMLs for closer follow-up, while low-risk lesions can undergo less frequent biopsies, reducing the burden on healthcare resources [48]. Quite interestingly, in a study on individuals with Fanconi anemia (people with a 500-fold to 700-fold elevated risk, much earlier onset, and limited therapeutic options for oral SCC compared with the general population), a careful inspection of the oral cavity associated with brush biopsy-based cytology could identify visible oral lesions, either malignant or potentially malignant, that warrant treatment [49].

2.2. Alkylating Agents

Because of the mentioned key role of genetic and epigenetic alterations in HNC, treatment protocols still include the use of alkylating agents (AAs). AAs are a heterogeneous class of drugs that interfere with the cell’s DNA and inhibit cancer cells’ growth, playing a major role in HNC [50]. These genotoxic agents modify the DNA by adding binding an alkyl group to the guanine base of DNA at the number 7 nitrogen atom of the purine ring, either directly or after metabolic conversion to reactive intermediates [51][52]. These drugs produce numerous side effects targeting many organs and apparats, such as the gastrointestinal tract, bone marrow, testicles, and ovaries; furthermore, most of the alkylating agents are also carcinogenic [53][54]. AAs still play a major role in the chemotherapeutic treatment of HNC, especially cisplatin and methotrexate, in recurrent metastatic cancer, but the focus is gradually shifting to non-conventional systemic chemotherapy, especially targeted therapy and immunotherapy, which affect the tumor microenvironment and have a potentially favorable impact on HNC management [55][56][57].

2.3. Alcohol Abuse Detection

Despite the numerous proposed biomarkers in many studies, no laboratory test is sufficiently reliable alone to support a diagnosis of alcohol use disorder (AUD) [58][59]. Sensitivity and specificity should be high for alcohol abuse biomarkers, but in reality, they mostly fluctuate considerably and depend on the involved population. Furthermore, the ideal markers should reflect an individual’s consumption of alcohol, both chronically (screening markers) and acutely (relapse markers), and, from this, the given title of “state” markers (in contrast to the “trait” markers that predict the predisposition to develop alcoholism) [60][61]. The use of long-term diagnostic tools gives crucial information on the real alcohol consumption of HNC patients so that a series of recently found useful biomarkers, which can be detected in the hair, is now in the spotlight: ethyl glucuronide (EtG), fatty acid ethyl esters (products of non-oxidative ethanol metabolism), phosphatidyl ethanol, acetaldehyde adducts to protein, and 5-hydroxytryptophol [18][62][63][64]. The main advantages of this sample material are that compounds with a relatively short lifetime in blood, but with a strong correlation to alcohol consumption, can be entrapped in the hair and are detectable for a longer time (also for years depending on the length of the hair) and at a relatively high concentration [64][65]. In particular, EtG and ethyl sulfate (EtS) are two non-oxidative ethanol metabolites (Figure 1) secreted by the liver which are mainly used as markers of alcohol intake related to incidents [66][67][68][69][70][71]. These two markers for recent alcohol intake can be detected in the blood for approximately 10 h after a small to moderate alcohol intake and up to 5 days after large and repeated alcohol intakes [67][68][69]. As the efficacy of these two tests has been demonstrated in multiple settings, it has been also suggested that EtG and EtS should be included in screening tests for injured or at-risk for alcohol abuse people (including pregnant women) to investigate the possible association between residual alcohol effects and injuries, and to verify alcohol abstinence in cases of substance-related disorders [72][73].
Figure 1. In the liver, ethanol is metabolized via oxidative and non-oxidative (less than 1%) ways. In the non-oxidative pathway, alcohol is finally processed as fatty acid ethyl ester (FAEE), phosphatidyl ethanol, ethyl glucuronide (EtG), and ethyl sulfate (EtS).

References

  1. Sung, H.; Ferlay, J.; Siegel, R.L.; Laversanne, M.; Soerjomataram, I.; Jemal, A.; Bray, F. Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries. CA Cancer J. Clin. 2021, 71, 209–249.
  2. Kawakita, D.; Matsuo, K. Alcohol and head and neck cancer. Cancer Metastasis Rev. 2017, 36, 425–434.
  3. De França, G.M.; da Silva, W.R.; Medeiros, C.K.S.; Júnior, J.F.; Santos, E.D.M.; Galvão, H.C. Five-year survival and prognostic factors for oropharyngeal squamous cell carcinoma: Retrospective cohort of a cancer center. Oral Maxillofac. Surg. 2021, 1–9.
  4. Ledda, R.; Battagliese, G.; Attilia, F.; Rotondo, C.; Pisciotta, F.; Gencarelli, S.; Greco, A.; Fiore, M.; Ceccanti, M.; Attilia, M.L. Drop-out, relapse and abstinence in a cohort of alcoholic people under detoxification. Physiol. Behav. 2019, 198, 67–75.
  5. Ceccanti, M.; Hamilton, D.; Coriale, G.; Carito, V.; Aloe, L.; Chaldakov, G.; Romeo, M.; Iannitelli, A.; Fiore, M. Spatial learning in men undergoing alcohol detoxification. Physiol. Behav. 2015, 149, 324–330.
  6. Ceccanti, M.; Coriale, G.; Hamilton, D.A.; Carito, V.; Coccurello, R.; Scalese, B.; Ciafrè, S.; Codazzo, C.; Messina, M.P.; Chaldakov, G.N.; et al. Virtual Morris task responses in individuals in an abstinence phase from alcohol. Can. J. Physiol. Pharmacol. 2018, 96, 128–136.
  7. Coriale, G.; Battagliese, G.; Pisciotta, F.; Attilia, M.L.; Porrari, R.; De Rosa, F.; Vitali, M.; Carito, V.; Messina, M.P.; Greco, A.; et al. Behavioral responses in people affected by alcohol use disorder and psychiatric comorbidity: Correlations with addiction severity. Ann. Dell’Istituto Super. Sanita 2019, 55, 131–142.
  8. Coriale, G.; Gencarelli, S.; Battagliese, G.; Delfino, D.; Fiorentino, D.; Petrella, C.; Greco, A.; Ralli, M.; Attilia, M.L.; Messina, M.P.; et al. Physiological Responses to Induced Stress in Individuals Affected by Alcohol Use Disorder with Dual Diagnosis and Alexithymia. Clin. Ter. 2020, 171, e120–e129.
  9. Ceci, F.M.; Ceccanti, M.; Petrella, C.; Vitali, M.; Messina, M.P.; Chaldakov, G.N.; Greco, A.; Ralli, M.; Lucarelli, M.; Angeloni, A.; et al. Alcohol Drinking, Apolipoprotein Polymorphisms and the Risk of Cardiovascular Diseases. Curr. Neurovascular Res. 2021, 18, 150–161.
  10. Ceccanti, M.; Inghilleri, M.; Attilia, M.L.; Raccah, R.; Fiore, M.; Zangen, A. Deep TMS on alcoholics: Effects on cortisolemia and dopamine pathway modulation. A pilot study. Can. J. Physiol. Pharmacol. 2015, 93, 283–290.
  11. Ceccanti, M.; Sasso, G.F.; Nocente, R.; Balducci, G.; Prastaro, A.; Ticchi, C.; Bertazzoni, G.; Santini, P.; Attilia, M.L. Hypertension in early alcohol withdrawal in chronic alcoholics. Alcohol Alcohol. 2005, 41, 5–10.
  12. Ceccanti, M.; Attili, A.; Balducci, G.; Attilia, F.; Giacomelli, S.; Rotondo, C.; Sasso, G.F.; Xirouchakis, E.; Attilia, M.L. Acute alcoholic hepatitis. J. Clin. Gastroenterol. 2006, 40, 833–841.
  13. Fiore, M.; Petrella, C.; Coriale, G.; Rosso, P.; Fico, E.; Ralli, M.; Greco, A.; De Vincentiis, M.; Minni, A.; Polimeni, A.; et al. Markers of Neuroinflammation in the Serum of Prepubertal Children with Fetal Alcohol Spectrum Disorders. CNS Neurol. Disord. Drug Targets 2021, 20, 1.
  14. Terracina, S.; Ferraguti, G.; Tarani, L.; Messina, M.P.; Lucarelli, M.; Vitali, M.; De Persis, S.; Greco, A.; Minni, A.; Polimeni, A.; et al. Transgenerational Abnormalities Induced by Paternal Preconceptual Alcohol Drinking. Findings from Humans and Animal Models. Curr. Neuropharmacol. 2021, 19, 1.
  15. Ceccanti, M.; Coccurello, R.; Carito, V.; Ciafrè, S.; Ferraguti, G.; Giacovazzo, G.; Mancinelli, R.; Tirassa, P.; Chaldakov, G.N.; Pascale, E.; et al. Paternal alcohol exposure in mice alters brain NGF and BDNF and increases ethanol-elicited preference in male offspring. Addict. Biol. 2016, 21, 776–787.
  16. Ferraguti, G.; Codazzo, C.; Petrella, C.; Coccurello, R.; Ceccanti, M.; Fiore, M. Brainstem expression of SLC6A4, HTR2C, NGF, BDNF, TRKANGF, TRKBBDNF and P75NTR following paternal alcohol exposure in the male mouse. Biomed. Rev. 2020, 31, 75–89.
  17. Carito, V.; Ceccanti, M.; Ferraguti, G.; Coccurello, R.; Ciafrè, S.; Tirassa, P.; Fiore, M. NGF and BDNF Alterations by Prenatal Alcohol Exposure. Curr. Neuropharmacol. 2019, 17, 308–317.
  18. Ferraguti, G.; Merlino, L.; Battagliese, G.; Piccioni, M.G.; Barbaro, G.; Carito, V.; Messina, M.P.; Scalese, B.; Coriale, G.; Fiore, M.; et al. Fetus morphology changes by second-trimester ultrasound in pregnant women drinking alcohol. Addict. Biol. 2020, 25, e12724.
  19. Coriale, G.; Fiorentino, D.; Di Lauro, F.; Marchitelli, R.; Scalese, B.; Fiore, M.; Maviglia, M.; Ceccanti, M. Fetal Alcohol Spectrum Disorder (FASD): Neurobehavioral profile, indications for diagnosis and treatment. Riv Psichiatr. 2013, 48, 359–369.
  20. Fetal alcohol spectrum disorders awareness in health professionals: Implications for psychiatry. Riv. Psichiatr. 2020, 55, 79–89.
  21. Kiviniemi, M.T.; Orom, H.; Hay, J.L.; Waters, E.A. Limitations in American adults’ awareness of and beliefs about alcohol as a risk factor for cancer. Prev. Med. Rep. 2021, 23, 101433.
  22. Petticrew, M.; Hessari, N.M.; Knai, C.; Weiderpass, E. How alcohol industry organisations mislead the public about alcohol and cancer. Drug Alcohol Rev. 2018, 37, 293–303.
  23. Maso, L.D.; Torelli, N.; Biancotto, E.; Di Maso, M.; Gini, A.; Franchin, G.; Levi, F.; La Vecchia, C.; Serraino, D.; Polesel, J. Combined effect of tobacco smoking and alcohol drinking in the risk of head and neck cancers: A re-analysis of case–control studies using bi-dimensional spline models. Eur. J. Epidemiol. 2016, 31, 385–393.
  24. Hashibe, M.; Brennan, P.; Benhamou, S.; Castellsagué, X.; Chen, C.; Curado, M.P.; Dal Maso, L.; Daudt, A.W.; Fabianova, E.; Wünsch-Filho, V.; et al. Alcohol Drinking in Never Users of Tobacco, Cigarette Smoking in Never Drinkers, and the Risk of Head and Neck Cancer: Pooled Analysis in the International Head and Neck Cancer Epidemiology Consortium. J. Natl. Cancer Inst. 2007, 99, 777–789.
  25. Applebaum, K.M.; Furniss, C.S.; Zeka, A.; Posner, M.R.; Smith, J.F.; Bryan, J.; Eisen, E.A.; Peters, E.S.; McClean, M.D.; Kelsey, K.T. Lack of Association of Alcohol and Tobacco with HPV16-Associated Head and Neck Cancer. J. Natl. Cancer Inst. 2007, 99, 1801–1810.
  26. Gillison, M.L.; Chaturvedi, A.K.; Anderson, W.F.; Fakhry, C. Epidemiology of Human Papillomavirus–Positive Head and Neck Squamous Cell Carcinoma. J. Clin. Oncol. 2015, 33, 3235–3242.
  27. Sawabe, M.; Ito, H.; Oze, I.; Hosono, S.; Kawakita, D.; Tanaka, H.; Hasegawa, Y.; Murakami, S.; Matsuo, K. Heterogeneous impact of alcohol consumption according to treatment method on survival in head and neck cancer: A prospective study. Cancer Sci. 2016, 108, 91–100.
  28. Kawakita, D.; Oze, I.; Hosono, S.; Ito, H.; Watanabe, M.; Yatabe, Y.; Hasegawa, Y.; Murakami, S.; Tanaka, H.; Matsuo, K. Prognostic Value of Drinking Status and Aldehyde Dehydrogenase 2 Polymorphism in Patients with Head and Neck Squamous Cell Carcinoma. J. Epidemiol. 2016, 26, 292–299.
  29. Praud, D.; Rota, M.; Rehm, J.; Shield, K.; Zatoński, W.; Hashibe, M.; La Vecchia, C.; Boffetta, P. Cancer incidence and mortality attributable to alcohol consumption. Int. J. Cancer 2016, 138, 1380–1387.
  30. Teckie, S.; Wotman, M.; Marziliano, A.; Orner, D.; Yi, J.; Mulvany, C.; Ghaly, M.; Parashar, B.; Diefenbach, M.A. Patterns of alcohol use among early head and neck cancer survivors: A cross-sectional survey study using the alcohol use disorders identification test (AUDIT). Oral Oncol. 2021, 119, 105328.
  31. Koo, K.; Harris, R.; Wiesenfeld, D.; Iseli, T.A. A role for panendoscopy? Second primary tumour in early stage squamous cell carcinoma of the oral tongue. J. Laryngol. Otol. 2015, 129, S27–S31.
  32. Metzger, K.; Horn, D.; Pfeiffer, T.; Moratin, J.; Kansy, K.; Ristow, O.; Engel, M.; Hoffmann, J.; Freier, K.; Schaible, A.; et al. Is panendoscopy a necessary staging procedure in patients with lacking risk factors and oral squamous cell carcinoma? J. Cranio-Maxillofac. Surg. 2019, 47, 1968–1972.
  33. Koerdt, S.; Raguse, J.-D.; Neumann, F.; Beck-Broichsitter, B.; Kreutzer, K.; Neumann, K.; Heiland, M.; Doll, C. Value of Panendoscopy in the Identification of Synchronous Malignancies in Patients Suffering from Oral Squamous Cell Carcinoma Without Clinical Signs of a Second Primary Tumor. Anticancer. Res. 2021, 41, 2039–2044.
  34. Dittberner, A.; Ziadat, R.; Hoffmann, F.; Pertzborn, D.; Gassler, N.; Guntinas-Lichius, O. Fluorescein-Guided Panendoscopy for Head and Neck Cancer Using Handheld Probe-Based Confocal Laser Endomicroscopy: A Pilot Study. Front. Oncol. 2021, 11, 2186.
  35. Sheppard, S.C.; Borner, U.; Wartenberg, M.; Giger, R.; Nisa, L. Diagnostic use of fine-needle aspiration cytology and core-needle biopsy in head and neck sarcomas. Head Neck 2021, 43, 1939–1948.
  36. Schmidt, H.; Kulasinghe, A.; Kenny, L.; Punyadeera, C. The development of a liquid biopsy for head and neck cancers. Oral Oncol. 2016, 61, 8–11.
  37. Economopoulou, P.; Kotsantis, I.; Kyrodimos, E.; Lianidou, E.; Psyrri, A. Liquid biopsy: An emerging prognostic and predictive tool in Head and Neck Squamous Cell Carcinoma (HNSCC). Focus on Circulating Tumor Cells (CTCs). Oral Oncol. 2017, 74, 83–89.
  38. Payne, K.; Spruce, R.; Beggs, A.; Sharma, N.; Kong, A.; Martin, T.; Parmar, S.; Praveen, P.; Nankivell, P.; Mehanna, H. Circulating tumor DNA as a biomarker and liquid biopsy in head and neck squamous cell carcinoma. Head Neck 2018, 40, 1598–1604.
  39. Marcus, C.; Sheikhbahaei, S.; Shivamurthy, V.K.N.; Avey, G.; Subramaniam, R.M. PET Imaging for Head and Neck Cancers. Radiol. Clin. N. Am. 2021, 59, 773–788.
  40. Gogna, S.; Kashyap, S.; Gupta, N. Neck Cancer Resection and Dissection; StatPearls Publishing: Treasure Island, FL, USA, 2021.
  41. Pharaon, R.R.; Xing, Y.; Agulnik, M.; Villaflor, V.M. The Role of Immunotherapy to Overcome Resistance in Viral-Associated Head and Neck Cancer. Front. Oncol. 2021, 11, 649963.
  42. Cripps, C.; Winquist, E.; Devries, M.C.; Stys–Norman, D.; Gilbert, R.; the Head and Neck Cancer Disease Site Group. Epidermal Growth Factor Receptor Targeted Therapy in Stages III and IV Head and Neck Cancer. Curr. Oncol. 2010, 17, 37–48.
  43. Kaidar-Person, O.; Gil, Z.; Billan, S. Precision medicine in head and neck cancer. Drug Resist. Updat. 2018, 40, 13–16.
  44. Choi, J.S.; Sansoni, E.R.; Lovin, B.D.; Lindquist, N.R.; Phan, J.; Mayo, L.L.; Ferrarotto, R.; Su, S. Abscopal Effect Following Immunotherapy and Combined Stereotactic Body Radiation Therapy in Recurrent Metastatic Head and Neck Squamous Cell Carcinoma: A Report of Two Cases and Literature Review. Ann. Otol. Rhinol. Laryngol. 2019, 129, 517–522.
  45. Hui, C.; Chau, B.; Gan, G.; Stokes, W.; Karam, S.D.; Amini, A. Overcoming Resistance to Immunotherapy in Head and Neck Cancer Using Radiation: A Review. Front. Oncol. 2021, 11, 2619.
  46. De Oliveira, T.B.; Braun, A.C.; Nicolau, U.R.; Abdallah, E.A.; Alves, V.D.S.; de Jesus, V.H.F.; Calsavara, V.F.; Kowaslki, L.P.; Chinen, L.T.D. Prognostic impact and potential predictive role of baseline circulating tumor cells in locally advanced head and neck squamous cell carcinoma. Oral Oncol. 2021, 121, 105480.
  47. Datta, M.; Laronde, D.; Palcic, B.; Guillaud, M. The role of DNA image cytometry in screening oral potentially malignant lesions using brushings: A systematic review. Oral Oncol. 2019, 96, 51–59.
  48. Datta, M.; Laronde, D.M.; Rosin, M.P.; Zhang, L.; Chan, B.; Guillaud, M. Predicting Progression of Low-Grade Oral Dysplasia Using Brushing-Based DNA Ploidy and Chromatin Organization Analysis. Cancer Prev. Res. 2021, 14, 1111–1118.
  49. Velleuer, E.; Dietrich, R.; Pomjanski, N.; de Santana Almeida Araujo, I.K.; Silva de Araujo, B.E.; Sroka, I.; Biesterfeld, S.; Bocking, A.; Schramm, M. Diagnostic accuracy of brush biopsy–based cytology for the early detection of oral cancer and precursors in Fanconi anemia. Cancer Cytopathol. 2020, 128, 403–413.
  50. Vogel, E.W.; Nivard, M.J. The subtlety of alkylating agents in reactions with biological macromolecules. Mutat. Res. Mol. Mech. Mutagen. 1994, 305, 13–32.
  51. Burtness, B.; Bourhis, J.P.; Vermorken, J.B.; Harrington, K.J.; Cohen, E.E.W. Afatinib versus placebo as adjuvant therapy after chemoradiation in a double-blind, phase III study (LUX-Head & Neck 2) in patients with primary unresected, clinically intermediate-to-high-risk head and neck cancer: Study protocol for a randomized controlled trial. Trials 2014, 15, 469.
  52. Zech, H.B.; Moeckelmann, N.; Böttcher, A.; Muenscher, A.; Binder, M.; Vettorazzi, E.; Bokemeyer, C.; Schafhausen, P.; Betz, C.S.; Busch, C.-J. Phase III study of nivolumab alone or combined with ipilimumab as immunotherapy versus standard of care in resectable head and neck squamous cell carcinoma. Futur. Oncol. 2020, 16, 3035–3043.
  53. Irshad, R.; Haider, G.; Hashmi, M.; Hassan, A. Efficacy of Gefitinib and Methorexate in Patients with Advanced Stage and Recurrent Head and Neck Cancer. Cureus 2021, 13, e15451.
  54. Vermorken, J.B.; Mesia, R.; Rivera, F.; Remenar, E.; Kawecki, A.; Rottey, S.; Erfan, J.; Zabolotnyy, D.; Kienzer, H.-R.; Cupissol, D.; et al. Platinum-Based Chemotherapy plus Cetuximab in Head and Neck Cancer. N. Engl. J. Med. 2008, 359, 1116–1127.
  55. Specenier, P.; Vermorken, J.B. Optimizing treatments for recurrent or metastatic head and neck squamous cell carcinoma. Expert Rev. Anticancer Ther. 2018, 18, 901–915.
  56. Patil, V.M.; Noronha, V.; Joshi, A.; Abhyankar, A.; Menon, N.; Dhumal, S.; Prabhash, K. Beyond conventional chemotherapy, targeted therapy and immunotherapy in squamous cell cancer of the oral cavity. Oral Oncol. 2020, 105, 104673.
  57. Lau, A.; Yang, W.; Li, K.-Y.; Su, Y.-X. Systemic Therapy in Recurrent or Metastatic Head and Neck Squamous Cell Carcinoma- A Systematic Review and Meta-Analysis. Crit. Rev. Oncol. 2020, 153, 102984.
  58. Musshoff, F. Chromatographic methods for the determination of markers of chronic and acute alcohol consumption. J. Chromatogr. B 2002, 781, 457–480.
  59. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Alcohol consumption and ethyl carbamate. IARC Monogr. Eval. Carcinog. Risks Hum. 2010, 96, 3–1383.
  60. Sharpe, P.C. Biochemical detection and monitoring of alcohol abuse and abstinence. Ann. Clin. Biochem. Int. J. Lab. Med. 2001, 38, 652–664.
  61. Laposata, M. Assessment of Ethanol Intake: Current Tests and New Assays on the Horizon. Am. J. Clin. Pathol. 1999, 112, 443–450.
  62. Ferraguti, G.; Ciolli, P.; Carito, V.; Battagliese, G.; Mancinelli, R.; Ciafrè, S.; Tirassa, P.; Ciccarelli, R.; Cipriani, A.; Messina, M.P.; et al. Ethylglucuronide in the urine as a marker of alcohol consumption during pregnancy: Comparison with four alcohol screening questionnaires. Toxicol. Lett. 2017, 275, 49–56.
  63. Pragst, F.; Yegles, M. Determination of Fatty Acid Ethyl Esters (FAEE) and Ethyl Glucuronide (EtG) in Hair: A Promising Way for Retrospective Detection of Alcohol Abuse During Pregnancy? Ther. Drug Monit. 2008, 30, 255–263.
  64. Yegles, M.; Labarthe, A.; Auwärter, V.; Hartwig, S.; Vater, H.; Wennig, R.; Pragst, F. Comparison of ethyl glucuronide and fatty acid ethyl ester concentrations in hair of alcoholics, social drinkers and teetotallers. Forensic Sci. Int. 2004, 145, 167–173.
  65. Wurst, F.M.; Alexson, S.; Wolfersdorf, M.; Bechtel, G.; Forster, S.; Alling, C.; Aradóttir, S.; Jachau, K.; Huber, P.; Allen, J.P.; et al. Concentration of fatty acid ethyl esters in hair of alcoholics: Comparison to other biological state markers and self reported-ethanol intake. Alcohol Alcohol. 2004, 39, 33–38.
  66. Ceci, F.M.; Fiore, M.; Agostinelli, E.; Tahara, T.; Greco, A.; Ralli, M.; Polimeni, A.; Lucarelli, M.; Colletti, R.; Angeloni, A.; et al. Urinary ethyl glucuronide for the assessment of alcohol consumption during pregnancy: Comparison between biochemical data and screening questionnaires. Curr. Med. Chem. 2021, 28, 1.
  67. Budhwani, H.; Dinaj, V.; Jacques-Tiura, A.J.; Pennar, A.L.; Naar, S. Feasibility of Ethyl Glucuronide Nail Testing Biomarker for Alcohol Use Among Youth Living with HIV. J. Adolesc. Health 2021, 69, 346–348.
  68. Cappelle, D.; Neels, H.; De Keukeleire, S.; Fransen, E.; Dom, G.; Vermassen, A.; Covaci, A.; Crunelle, C.L.; van Nuijs, A.L. Ethyl glucuronide in keratinous matrices as biomarker of alcohol use: A correlation study between hair and nails. Forensic Sci. Int. 2017, 279, 187–191.
  69. Fosen, J.T.; Morini, L.; Sempio, C.; Giarratana, N.; Enger, A.; Mørland, J.; Høiseth, G. Ethyl Glucuronide Elimination Kinetics in Fingernails and Comparison to Levels in Hair. Alcohol Alcohol. 2017, 52, 580–586.
  70. Bogstrand, S.T.; Høiseth, G.; Rossow, I.; Normann, P.T.; Ekeberg, Ø. Prevalence of Ethyl Glucuronide and Ethyl Sulphate Among Patients Injured When Driving or at Work. Alcohol Alcohol. 2014, 50, 68–73.
  71. Dengiz, H.; Daglioglu, N.; Goren, I.E. Assessment of recent alcohol consumption by detecting ethyl glucuronide and ethyl sulphate level among traffic accident patients. Traffic Inj. Prev. 2020, 21, 371–374.
  72. Skipper, G.E.; Weinmann, W.; Thierauf, A.; Schaefer, P.; Wiesbeck, G.; Allen, J.P.; Miller, M.; Wurst, F.M. Ethyl glucuronide: A biomarker to identify alcohol use by health professionals recovering from substance use disorders. Alcohol Alcohol. 2004, 39, 445–449.
  73. Liu, H.; Dai, M.; Guan, H.; Gao, X.; Zhou, Y.; Sun, X.; Zhou, J.; Hu, X.; Li, X.; Song, Y.; et al. Preoperative Prognostic Nutritional Index Value is Related to Postoperative Delirium in Elderly Patients After Noncardiac Surgery: A Retrospective Cohort Study. Health Policy 2021, 14, 1–8.
More
Information
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : ,
View Times: 545
Revisions: 2 times (View History)
Update Date: 20 Jan 2022
1000/1000