Tongue cancer secondary prevention: Difference between revisions
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==Overview== | ==Overview== | ||
Secondary prevention strategies following tongue cancer include monthly follow-ups for the first 12-18 months following therapy. | Secondary prevention strategies following tongue cancer include monthly follow-ups for the first 12-18 months following therapy. Drugs such as synthetic [[Retinoid|retinoids]], [[Non-steroidal anti-inflammatory drug|non-steroidal antiinflammatory drugs]], [[EGFR]] inhibition, and [[human papilloma virus]] related oropharyngeal carcinoma vaccine can be used as a secondary [[Chemoprevention|chemopreventive]] agents. | ||
==Secondary Prevention== | ==Secondary Prevention== | ||
*Postoperative patients are monitored monthly for the first 12-18 months. | *Postoperative patients are monitored monthly for the first 12-18 months. | ||
*In patients who undergo nonsurgical treatment, follow-up diagnostic imaging studies are recommended in the first 6 months. | *In patients who undergo nonsurgical treatment, follow-up diagnostic imaging studies are recommended in the first 6 months. | ||
*Beta- | *[[Beta-carotene]] and [[vitamin E]] are used as secondary [[Chemoprevention|chemopreventive]] agents.<ref name="pmid15812073">{{cite journal| author=Bairati I, Meyer F, Gélinas M, Fortin A, Nabid A, Brochet F et al.| title=A randomized trial of antioxidant vitamins to prevent second primary cancers in head and neck cancer patients. | journal=J Natl Cancer Inst | year= 2005 | volume= 97 | issue= 7 | pages= 481-8 | pmid=15812073 | doi=10.1093/jnci/dji095 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15812073 }}</ref> | ||
==== '''Synthetic retinoids''' ==== | ==== '''Synthetic retinoids''' ==== | ||
*Premalignant lesions have low levels of the nuclear retinoid | *[[Premalignant condition|Premalignant lesions]] have low levels of the nuclear [[Retinoid receptor|retinoid receptors]] which control normal growth and differentiation. Retinoid have anti[[Angiogenesis|angiogenic]] activity.<ref name="pmid10626810">{{cite journal| author=Soriano AF, Helfrich B, Chan DC, Heasley LE, Bunn PA, Chou TC| title=Synergistic effects of new chemopreventive agents and conventional cytotoxic agents against human lung cancer cell lines. | journal=Cancer Res | year= 1999 | volume= 59 | issue= 24 | pages= 6178-84 | pmid=10626810 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10626810 }}</ref> | ||
*Synthetic retinoids response rates are 59 to 92%. | *Synthetic [[retinoids]] response rates are 59 to 92%. | ||
==== Non-steroidal antiinflammatory drugs ==== | ==== Non-steroidal antiinflammatory drugs ==== | ||
*Intake | *Intake of [[nonsteroidal antiinflammatory drugs]] prevents the development of intraepithelial [[squamous cell carcinomas]] especially in the [[colon]] and [[rectum]] due to inhibition [[COX-2]] and diminished synthesis of [[prostaglandins]].<ref name="pmid9850093">{{cite journal| author=Lingen MW, Polverini PJ, Bouck NP| title=Retinoic acid and interferon alpha act synergistically as antiangiogenic and antitumor agents against human head and neck squamous cell carcinoma. | journal=Cancer Res | year= 1998 | volume= 58 | issue= 23 | pages= 5551-8 | pmid=9850093 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9850093 }}</ref> | ||
==== '''EGFR inhibition''' ==== | ==== '''EGFR inhibition''' ==== | ||
*Endothelial growth factor receptor (EGFR) is highly expressed in SCC of tongue, suggesting that EGFR inhibition may be effective in these tumors.<ref name="pmid1313356">{{cite journal| author=Klijn JG, Berns PM, Schmitz PI, Foekens JA| title=The clinical significance of epidermal growth factor receptor (EGF-R) in human breast cancer: a review on 5232 patients. | journal=Endocr Rev | year= 1992 | volume= 13 | issue= 1 | pages= 3-17 | pmid=1313356 | doi=10.1210/edrv-13-1-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1313356 }}</ref> | *[[EGFR|Endothelial growth factor receptor]] (EGFR) is highly expressed in [[Squamous cell carcinoma|SCC]] of the tongue, suggesting that [[EGFR]] inhibition may be effective in these [[tumors]].<ref name="pmid1313356">{{cite journal| author=Klijn JG, Berns PM, Schmitz PI, Foekens JA| title=The clinical significance of epidermal growth factor receptor (EGF-R) in human breast cancer: a review on 5232 patients. | journal=Endocr Rev | year= 1992 | volume= 13 | issue= 1 | pages= 3-17 | pmid=1313356 | doi=10.1210/edrv-13-1-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1313356 }}</ref> | ||
==== '''Human papilloma virus related oropharyngeal carcinoma''' | ==== '''Human papilloma virus related oropharyngeal carcinoma''' vaccine ==== | ||
*The E6 and E7 HPV viral proteins in HPV 16 are responsible for promoting cell cycle progression and viral DNA replication in differentiated normal mucosal epithelial cells. | *The [[E6 - protein|E6]] and E7 HPV viral proteins in [[Human papillomavirus|HPV]] 16 are responsible for promoting [[cell cycle]] progression and [[viral]] [[DNA replication]] in differentiated normal [[mucosal]] epithelial cells. | ||
*While E6 protein binds to p53 tumor suppressor protein and induces its degradation, the E7 protein ubiquitinates the retinoblastoma tumor suppressor protein. | *While [[E6 - protein|E6 protein]] binds to [[Tumor suppressor gene|p53 tumor suppressor protein]] and induces its degradation, the E7 protein [[Ubiquitination|ubiquitinates]] the [[retinoblastoma]] [[Tumor suppressor gene|tumor suppressor protein.]] | ||
*This process leads to driving the mucosal cells into S phase and induces cellular DNA synthesis.<ref name="pmid23953776">{{cite journal| author=Rampias T, Sasaki C, Psyrri A| title=Molecular mechanisms of HPV induced carcinogenesis in head and neck. | journal=Oral Oncol | year= 2014 | volume= 50 | issue= 5 | pages= 356-63 | pmid=23953776 | doi=10.1016/j.oraloncology.2013.07.011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23953776 }}</ref> | *This process leads to driving the [[mucosal]] cells into [[S phase]] and induces cellular [[DNA synthesis]].<ref name="pmid23953776">{{cite journal| author=Rampias T, Sasaki C, Psyrri A| title=Molecular mechanisms of HPV induced carcinogenesis in head and neck. | journal=Oral Oncol | year= 2014 | volume= 50 | issue= 5 | pages= 356-63 | pmid=23953776 | doi=10.1016/j.oraloncology.2013.07.011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23953776 }}</ref> | ||
==References== | ==References== | ||
Revision as of 00:12, 3 December 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]
Overview
Secondary prevention strategies following tongue cancer include monthly follow-ups for the first 12-18 months following therapy. Drugs such as synthetic retinoids, non-steroidal antiinflammatory drugs, EGFR inhibition, and human papilloma virus related oropharyngeal carcinoma vaccine can be used as a secondary chemopreventive agents.
Secondary Prevention
- Postoperative patients are monitored monthly for the first 12-18 months.
- In patients who undergo nonsurgical treatment, follow-up diagnostic imaging studies are recommended in the first 6 months.
- Beta-carotene and vitamin E are used as secondary chemopreventive agents.[1]
Synthetic retinoids
- Premalignant lesions have low levels of the nuclear retinoid receptors which control normal growth and differentiation. Retinoid have antiangiogenic activity.[2]
- Synthetic retinoids response rates are 59 to 92%.
Non-steroidal antiinflammatory drugs
- Intake of nonsteroidal antiinflammatory drugs prevents the development of intraepithelial squamous cell carcinomas especially in the colon and rectum due to inhibition COX-2 and diminished synthesis of prostaglandins.[3]
EGFR inhibition
- Endothelial growth factor receptor (EGFR) is highly expressed in SCC of the tongue, suggesting that EGFR inhibition may be effective in these tumors.[4]
- The E6 and E7 HPV viral proteins in HPV 16 are responsible for promoting cell cycle progression and viral DNA replication in differentiated normal mucosal epithelial cells.
- While E6 protein binds to p53 tumor suppressor protein and induces its degradation, the E7 protein ubiquitinates the retinoblastoma tumor suppressor protein.
- This process leads to driving the mucosal cells into S phase and induces cellular DNA synthesis.[5]
References
- ↑ Bairati I, Meyer F, Gélinas M, Fortin A, Nabid A, Brochet F; et al. (2005). "A randomized trial of antioxidant vitamins to prevent second primary cancers in head and neck cancer patients". J Natl Cancer Inst. 97 (7): 481–8. doi:10.1093/jnci/dji095. PMID 15812073.
- ↑ Soriano AF, Helfrich B, Chan DC, Heasley LE, Bunn PA, Chou TC (1999). "Synergistic effects of new chemopreventive agents and conventional cytotoxic agents against human lung cancer cell lines". Cancer Res. 59 (24): 6178–84. PMID 10626810.
- ↑ Lingen MW, Polverini PJ, Bouck NP (1998). "Retinoic acid and interferon alpha act synergistically as antiangiogenic and antitumor agents against human head and neck squamous cell carcinoma". Cancer Res. 58 (23): 5551–8. PMID 9850093.
- ↑ Klijn JG, Berns PM, Schmitz PI, Foekens JA (1992). "The clinical significance of epidermal growth factor receptor (EGF-R) in human breast cancer: a review on 5232 patients". Endocr Rev. 13 (1): 3–17. doi:10.1210/edrv-13-1-3. PMID 1313356.
- ↑ Rampias T, Sasaki C, Psyrri A (2014). "Molecular mechanisms of HPV induced carcinogenesis in head and neck". Oral Oncol. 50 (5): 356–63. doi:10.1016/j.oraloncology.2013.07.011. PMID 23953776.