IADR Abstract Archives

Biomarkers of progression to oral cancer in patients with dysplasia: systematic review

Objectives: Identify the biomarkers of progression to cancer in patients diagnosed with oral dysplasia.
Methods: We carried out a systematic review to carry out this investigation; the independent variables were biomarkers of progression to cancer; the dependent variables were malignant transformation to oral cancer.
Results: Studies of biomarkers of progression to cancer in premalignant lesions: Protein-type molecules. The search performed according to key words delivered 80 results, of which 67 after the title and summary review were excluded because they did not meet the eligibility criteria. Thirteen studies were obtained. Of these, 9 articles were excluded because they could not build interest groups. The articles that were selected were analyzed, recording the specific characteristics of these. The parameters are summarized in Table 1. Four studies were examined, 5 biomarkers, 4 of them are proteins that were determined using immunohistochemistry of tissues included in paraffin, the fifth biomarker refers to the degree of displeasure present in tissues with premalignant lesions and its potential for malignant transformation. Cohort sizes ranging from 34 to 141 patients were used. The most important results of the included articles are summarized in Table 2.
Conclusions: Recent research on potentially malignant lesions, such as dysplasia, leukoplakia and erythroleucoplasia, has identified potential cellular markers associated with malignant transformation and poor prognosis of patients, allowing us to use them as prognostic biomarkers. In this systematic review, we identified several potential biomarkers, such as S100A7, ALDH1A1, Prominin-1, PDPN and dysplasia, validated by quality analysis for prognostic studies of tumor markers (REMARK) (1). However, it is necessary to continue reaffirming the possible use of these cell markers, through the publication of new validated clinical studies.
Chilean Division Meeting
2018 Chilean Division Meeting (Santiago, Chile)
Santiago, Chile
2018
Viernes7_pm033
  • Figueroa Navarro, Constanza  ( Universidad de Talca , Talca , Chile )
  • Gallegos, Rocio  ( Universidad de Talca , Talca , Chile )
  • Rivera, Cesar  ( Universidad de Talca , Talca , Chile )
    • None
    Poster Session
    Viernes 7 (pm)
    Friday, 09/07/2018 , 03:30PM - 04:30PM
    Table 1
    StudyBiomarker* (gene name)ChangeDesign and methodStudy remarksCitations
    Evading growth suppressors     
    Kaur J et al., 2014Protein S100-A7
    (S100A7)    		(+)Canada
    Retrospective
    Immunohistochemistry    		S100A7 cytoplasmic overexpression serve as a useful marker for estimating the risk of oral dysplasia progressing to cancer31
    Feng JQ et al. 2013Retinal dehydrogenase 1
    (ALDH1A1)    		(+)China
    Retrospective
    Immunohistochemistry    		ALDH1 expression was significantly associated with increased risk of transformation.23
    Liu W et al. 2013Retinal dehydrogenase 1
    (ALDH1A1)
    Prominin-1 (PROM1)    		(+)China
    Retrospective
    Immunohistochemistry    		ALDH1A1 and PROM1 are correlated with malignant transformation in patients with premalignant oral leukoplakia.39
    Activating invasion and metastasis     
    de Vicente JC et al., 2013Podoplanin
    (PDPN)    		(+)Spain.
    Retrospective
    Immunohistochemistry    		Could be a valuable biomarker for risk assessment of malignant transformation in patients with oral leukoplakia along with histological assessment37
    Histopathologic features     
    Kaur J et al., 2014Dysplasia (grade)(+)Canada
    Retrospective
    Histopathology    		Degree of dysplasia emerged as an independent factor for identifying high-risk dysplasia.31
    Liu W et al. 2013Dysplasia (grade)(+)China
    Retrospective
    Histopathology    		Grade of dysplasia were significantly associated with increased risk of malignant transformation.39
    Studies are grouped according to the hallmarks of cancer and histopathologic analysis. *UniProt name. HGNC gene name between parentheses. (+) Up-regulated/overexpressed. Citations according to Google Scholar (June, 2018).
    Table 2
    StudyBiomarkerClinical diagnosisNCases vs. reference (events/group)HRCIp-value
    Evading growth suppressors       
    Kaur J et al., 2014S100A7Oral lesions with dysplasia110Overexpression (32/70) vs. low (7/40)2.40.9-8.40.041
    Feng JQ et al. 2013ALDH1A1Oral erythroplakia34Positive (14/19) vs. negative (3/15)8.9**1.7-47.40.011
    Liu W et al. 2013ALDH1A1
    PROM1    		Oral leukoplakia141
    141    		Positive (26/54) vs. negative (11/76)
    Positive (19/32) vs. negative (18/109)    		4.2
    2.9    		2.0-8.9
    1.5-5.6    		<0.001
    0.002
    Activating invasion and metastasis       
    de Vicente JC et al., 2013PDPNOral leukoplakia58Score 2–3 (11/22) vs. 0–1 (2/36)8.71.8-41.60.007
    Histopathologic features       
    Kaur J et al., 2014Dysplasia
    Dysplasia
    		Oral lesions with dysplasia97
    71    		Moderate (18/39) vs. mild (12/58)
    Severe (9/13) vs. mild (12/58)    		2.5
    5.4    		1.6-10.8
    2.6-23.2    		0.013
    <0.001
    Liu W et al. 2013Dysplasia
    		Oral leukoplakia141High (13/32) vs low-grade (24/109)2.41.2-4.80.018
    Articles are grouped according to the hallmarks of cancer. For biomarkers, HGNC recommended names were used. N, number of subjects in the contrast. *Malignant transformation (dysplasia to oral cancer). HR, hazard ratio. **Odds ratio (multiple logistic regression). ). Diagnosis, risk, confidence interval and p-values are reported as they originally appear in selected articles.