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Genomic DNA copy number alterations from precursor oral lesions to oral squamous cell carcinoma

Salahshourifar I, Vincent-Chong VK, Kallarakkal TG, Zain RB

Oral Oncol, 2014 May;50(5):404-12.
PMID: 24613650 DOI: 10.1016/j.oraloncology.2014.02.005

Oral cancer is a multifactorial disease in which both environmental and genetic factors contribute to the aetiopathogenesis. Oral cancer is the sixth most common cancer worldwide with a higher incidence among Melanesian and South Asian countries. More than 90% of oral cancers are oral squamous cell carcinoma (OSCC). The present study aimed to determine common genomic copy number alterations (CNAs) and their frequency by including 12 studies that have been conducted on OSCCs using array comparative genomic hybridization (aCGH). In addition, we reviewed the literature dealing with CNAs that drive oral precursor lesions to the invasive tumors. Results showed a sequential accumulation of genetic changes from oral precursor lesions to invasive tumors. With the disease progression, accumulation of genetic changes increases in terms of frequency, type and size of the abnormalities, even on different regions of the same chromosome. Gains in 3q (36.5%), 5p (23%), 7p (21%), 8q (47%), 11q (45%), 20q (31%) and losses in 3p (37%), 8p (18%), 9p (10%) and 18q (11%) were the most common observations among those studies. However, losses are less frequent than gains but it appears that they might be the primary clonal events in causing oral cancer.

Matched MeSH terms: Precancerous Conditions/genetics*
Targeting the genetic landscape of oral potentially malignant disorders has the potential as a preventative strategy in oral cancer

Prime SS, Cirillo N, Cheong SC, Prime MS, Parkinson EK

Cancer Lett, 2021 10 10;518:102-114.
PMID: 34139286 DOI: 10.1016/j.canlet.2021.05.025

This study reviews the molecular landscape of oral potentially malignant disorders (OPMD). We examine the impact of tumour heterogeneity, the spectrum of driver mutations (TP53, CDKN2A, TERT, NOTCH1, AJUBA, PIK3CA, CASP8) and gene transcription on tumour progression. We comment on how some of these mutations impact cellular senescence, field cancerization and cancer stem cells. We propose that OPMD can be monitored more closely and more dynamically through the use of liquid biopsies using an appropriate biomarker of transformation. We describe new gene interactions through the use of a systems biology approach and we highlight some of the first studies to identify functional genes using CRISPR-Cas9 technology. We believe that this information has translational implications for the use of re-purposed existing drugs and/or new drug development. Further, we argue that the use of digital technology encompassing clinical and laboratory-based data will create relevant datasets for machine learning/artificial intelligence. We believe that therapeutic intervention at an early molecular premalignant stage should be an important preventative strategy to inhibit the development of oral squamous cell carcinoma and that this approach is applicable to other aerodigestive tract cancers.

Matched MeSH terms: Precancerous Conditions/genetics
Do dysplastic and adenomatous changes in large bowel hamartomas predispose to malignancy?--A report of two cases

Visvanathan R, Thambidorai CR, Myint H

Ann Acad Med Singap, 1992 Nov;21(6):830-2.
PMID: 1338270

Two patients, members of one family, with Peutz-Jeghers syndrome are described who underwent surgery for bowel obstruction. Both had multiple polyps in the gastrointestinal tract. Severe dysplasia and adenomatous change were present in two hamartomatous polyps adjacent to a stenosing colonic carcinoma in one patient and moderate dysplasia and adenomatous change were observed in two hamartomatous rectal polyps in his son. These changes support recent reports in the literature of progression towards neoplasia in these lesions.

Matched MeSH terms: Precancerous Conditions/genetics
Fulltext Prognostic Implications of DNA Repair, Ploidy and Telomerase in the Malignant Transformation Risk Assessment of Leukoplakia

Thomas G, Tr S, George S P, Somanathan T, Sarojam S, Krishnankutti N, et al.

Asian Pac J Cancer Prev, 2020 Feb 01;21(2):309-316.
PMID: 32102504 DOI: 10.31557/APJCP.2020.21.2.309

BACKGROUND: Although leukoplakia shows a higher risk for malignant transformation to oral cancer, currently there are no clinically relevant biomarker which can predict the potentially high risk leukoplakia. This study aimed to investigate the genetic alterations such as DNA ploidy, telomerase expression and DNA repair capacity as predictive markers of malignant transformation risk of leukoplakia.
METHODS: The study was initiated in September 2005 and patients were followed up to March 2014. Two hundred patients with oral leukoplakia, 100 patients with oral cancer and 100 healthy, age and sex matched adults with normal oral mucosa as controls were recruited. The DNA ploidy content was measured by high resolution flow cytometry, level of telomerase expression was identified by TRAP assay and intrinsic DNA repair capacity was measured by mutagen induced chromosome sensitivity assay of cultured peripheral blood lymphocytes. The Chi-square test or Fisher's Exact test was used for comparison of categorical variables between biomarkers. A p value less than or equal to 0.05 was considered as statistically significant. Analysis was performed with SPSS software version 16. Logistic regression was used to find the association between the dependent and three independent variables.
RESULTS: There was significant difference in the distribution of ploidy status, telomerase activity and DNA repair capacity among control, leukoplakia and oral cancer group (p<0.001). When the molecular markers were compared with histological grading of leukoplakia, both DNA ploidy analysis and telomerase activity showed statistical significance (p<0.001). Both aneuploidy and telomerase positivity was found to coincide with high-risk sites of leukoplakia and were statistically significant (p.

Matched MeSH terms: Precancerous Conditions/genetics
Fulltext Gastric precancerous lesions are associated with gene variants in Helicobacter pylori-susceptible ethnic Malays

Maran S, Lee YY, Xu S, Rajab NS, Hasan N, Syed Abdul Aziz SH, et al.

World J Gastroenterol, 2013 Jun 21;19(23):3615-22.
PMID: 23801863 DOI: 10.3748/wjg.v19.i23.3615

To identify genes associated with gastric precancerous lesions in Helicobacter pylori (H. pylori)-susceptible ethnic Malays.

Matched MeSH terms: Precancerous Conditions/genetics*