Journal of International Oral Health

: 2023  |  Volume : 15  |  Issue : 2  |  Page : 119--126

Expression of signaling molecules in ameloblastoma using cDNA microarray: A systematic review

Sangamithra Surendran1, Nausathkhan Ubayathulla2, Pratibha Ramani1, Monal Yuwanati1,  
1 Department of Oral and Maxillofacial Pathology, Saveetha Dental College and Hospital, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, Tamil Nadu, India
2 Department of Oral and Maxillofacial Surgery, Fujairah Specialized Dental Center and Hospitals, Fujairah, United Arab Emirates

Correspondence Address:
Dr. Pratibha Ramani
Department of Oral and Maxillofacial Pathology, Saveetha Dental College and Hospital, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai 600077, Tamil Nadu


Aim: Ameloblastoma is a benign but locally aggressive epithelial odontogenic tumor. The present review aimed to identify the most commonly expressed signaling molecule in ameloblastoma detected using cDNA microarray. Materials and Methods: It is a systematic review. In this review, articles were searched using databases—PubMed and Google Scholar and were also searched using Hand Search. All the studies which used cDNA microarray to detect the expression of signaling molecules were included. All the variants of ameloblastoma were included for the review. A total of 22 ameloblastoma cases were included in this systematic review. Out of three studies, 67% of the cases demonstrated upregulation of smoothened (SMO) and sonic hedgehog (SHH). Results: Out of three studies, 33% of the cases showed upregulation of toll-like receptor 2 (TLR2), fos proto-oncogene (FOS), Wnt family member 10a (Wnt10a), and patched and down-regulation of insulin-like growth factor 2 (IGF2). Of the 67% of the studies which described SMO and SHH, significant expression of SMO (73 times fold change) was noted. SHH expression was noted to have 0.88 times fold change. Of the 33% of the studies included, the highest average fold change was noted to be associated with FOS (14-fold change time) followed by Wnt10a (5.1-fold change times) and TLR2 (3.29-fold change times). However, downregulation of IGF2 by 0.09-fold change times was observed in 33% of the studies. Conclusion: The SMO gene from the SHH pathway was the highest expressed signaling molecule in ameloblastoma.

How to cite this article:
Surendran S, Ubayathulla N, Ramani P, Yuwanati M. Expression of signaling molecules in ameloblastoma using cDNA microarray: A systematic review.J Int Oral Health 2023;15:119-126

How to cite this URL:
Surendran S, Ubayathulla N, Ramani P, Yuwanati M. Expression of signaling molecules in ameloblastoma using cDNA microarray: A systematic review. J Int Oral Health [serial online] 2023 [cited 2023 Jun 1 ];15:119-126
Available from:

Full Text


Ameloblastoma is a rare odontogenic benign tumor, which accounts for less than 1% of head and neck tumors.[1],[2],[3],[4],[5] Despite being rare, it is the second most commonly diagnosed odontogenic tumor. Ameloblastoma mainly affects younger patients in developing countries.[6] There is not much gender predilection with males (53%) being slightly more affected than females (47%).

The conventional management is surgical resection. Even though most of the patients are cured with surgical resection, recurrences have been observed.[7],[8],[9],[10],[11] The association between recurrence rate of ameloblastoma still remains a mystery. The morbidity of the conventional management to the patient is high as a part of the jaws is removed. This often leads to loss of speech, mastication, and causes a permanent facial deformity. Furthermore, it can cause improper growth of the jaw in young patients.

The knowledge regarding the early events which lead to the promotion of tumorigenesis in ameloblastoma still remains scarce mostly because the studies done to identify the molecular factors which initiate and cause tumorigenesis are still inconclusive. Next generation sequencing (NGS) analysis has led to the identification of high frequency B-Raf proto-oncogene V600E (BRAF V600E) and SMO L412F mutations in ameloblastoma.[7],[12],[13] Activating BRAF mutations suggests that there is involvement of a hyperactive RAS-RAF-MAPK pathway in the pathogenesis of ameloblastoma.[14],[15],[16],[17] Studies reported that the mitogen-activated protein kinase pathway and/or sonic hedgehog (SHH) signaling pathway are the most commonly seen pathways activated in ameloblastoma.[18]

In these studies, there are many ambiguous points regarding the mechanisms involving ameloblastoma. The factors that cause the formation of different histological variants in ameloblastoma are still unknown.[19],[20] The microenvironment of ameloblastoma has been found to have various mechanisms that cause the growth but the correlation between these mechanisms is still unclear.[20] These ambiguities have setback the various treatment strategies that could be employed for the management of ameloblastoma. One such method is targeted/precision medicine.

Research regarding targeted therapy for management of ameloblastoma is well received. In recent days, drugs targeting various odontogenic drugs are given to shrink the tumor to an operable size which enables the surgeon to resect the bone with least morbidity to the patient.[21],[22],[23],[24],[25],[26]

The techniques employed to identify the signaling molecules include an array of methods like RT-PCR, cDNA microarray, cDNA microarray is found to produce better results compared to the rest of the techniques when it comes to detecting signaling molecules.[26],[27],[28]

The aim of this systematic review is to find the most commonly expressed signaling molecule in ameloblastoma that can be detected using cDNA microarray. The null hypothesis for this review is that there is no commonly expressed signaling molecule in ameloblastoma that can be detected using cDNA microarray.

 Materials and Methods

This review was done in accordance with guidelines given by Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Guidelines of Systematic Review. The data collected for this review were taken till 2020. Advanced search of PubMed search engine was used using the following keywords: ((((Ameloblastoma) OR (ameloblastoma)) OR (Adamantinoma)) OR (adamantinoma)) AND ((((CDNA microarray) OR (cDNA microarray)) OR (micro array)) OR (Micro array)) AND (((Signaling molecule)) OR ((molecule expression)) OR ((protein)) OR ((proteins))) [Figure 1]. The research question to be answered by this review is “Which is the most commonly expressed signaling molecule involved in pathogenesis of ameloblastoma identified by cDNA microarray technique?” Two independent investigators were involved in the searching of the electronic databases, that is, PubMed, Google Scholar, and Hand Search.{Figure 1}

Inclusion and exclusion criteria

All the original studies that evaluated the expression of signaling molecule in ameloblastoma using cDNA microarray were included. Studies carried out on ameloblastoma tissue samples from humans were included. Studies that were published in English language were included. Review articles, animal and cell line studies, case reports, communication and letter to editors were excluded from the review. Studies that did not use cDNA microarray or provided details of expression of molecules involved in ameloblastoma were excluded. Data extraction table was made with the author name, year of publication, genes studied, methodology imparted for observing expression of signaling molecules, type of sample collection, study group, control group, results and limitations summarized in [Table 1]. Quality analysis of the articles was done using ROBINS-I tool [Table 2]. Risk of bias was evaluated. Only articles with a good quality check were included in the review.{Table 1} {Table 2}


Search results

The search identified a total of 47 articles from different databases. After removing duplicates, 44 articles titles and abstracts were screened. Out of these 44 articles, 9 were excluded based on exclusion and inclusion. 35fulltext articles were further screened for eligibility. Finally, three articles were found eligible for this review. The search strategy is described in the PRISMA flow chart [Figure 2].{Figure 2}

Search characteristics

This systematic review consisted of individual ethnicity studies. Hence this systematic review critically appraises the expression of signaling molecules in ameloblastoma using cDNA microarray using three ethnicities. Two out of three articles included were of case-control studies. One study did not use control. Only in one study, the case included tissue samples as well as ameloblastoma cell line. 17 out of 22 ameloblastomas included were from the mandible. All the studies had a major disparity between the distribution of case and control subjects. Sample collection was done either by tissue samples or tissue and cell lines. DNA extraction was done using the RT-PCR method. Multiple genes were expressed in all the variants of ameloblastoma included in the review.

A total of 22 ameloblastoma cases were included in this systematic review. Out of three studies, 67% of the cases demonstrated upregulation of SMO and SHH. Out of three studies, 33% of the cases showed upregulation of TLR2, FOS, Wnt10a, and patched and downregulation of IGF2 [Figure 3]. Of the 67% of the studies which described SMO and SHH, significant expression of SMO with 73 times fold change was noted. SHH expression was noted to have 0.88 times fold change. Of the 33% of the studies included, the highest fold change average was noted to be associated with FOS (14-fold change time) followed by Wnt10a (5.1-fold change times) and TLR 2 (3.29-fold change times). However, downregulation of IGF2 by 0.09-fold change times was observed in 33% of the studies [Figure 4].{Figure 3} {Figure 4}

Level of evidence

All the included articles had the expected level of evidence; hence, no further categorization was done among them [Table 3].{Table 3}


Ameloblastoma is an aggressive benign tumor of the oral cavity. In this review, the expression of various signaling molecules in ameloblastoma which were detected by cDNA microarray was analyzed. Among the various pathways found that expressed signaling molecules in ameloblastoma, the SHH pathway is found in higher frequency. In the SHH pathway, the SHH and SMO signaling molecules were most commonly expressed. These signaling molecules were found to play a major role in tumorigenesis of ameloblastoma.

In 67% of the studies, SHH shows 73 times fold increase in ameloblastoma. SHH control cell–cell interactions and cell proliferation in tissue patterning during development and SHH signal transduction are vital to embryonic development. SHH signaling molecules may play a role in epithelial-mesenchymal interaction and cell proliferation in ameloblastoma.[29] It was stated that the overexpression of upstream and downstream genes in the SHH pathway leads to the constitutive activation of this pathway in ameloblastoma and may suggest a mechanism for the development of this type of tumor.[30] SHH was also found to have anti-apoptotic properties which help in the proliferation of ameloblastoma.[31] Studies have found that there is an increased expression of SHH induced Bcl-2 in solid variant of ameloblastoma. They found out that Bcl-2 was expressed in the outer layer of ameloblastoma cells, whereas the protein was expressed in the inner stellate reticulum and squamoidcells.[32],[33] With this, it can be suggested that SHH plays an important role in the tumorigenesis and proliferation of ameloblastoma.

SMO was found to be over expressed in ameloblastoma in 67% of the studies. Missense mutation of SMO was observed more in malignant and metastasizing ameloblastoma.[34] This feature, although found in conventional ameloblastoma, was not a common finding. These missense mutations cause an increase in the rate of tumorigenesis. It alters SHH pathway and promotes tumorigenesis by affecting cell proliferation, differentiation and apoptosis. It increases the rate of cell proliferation, its differentiation.[32] These features are found more in the periphery than in the center of the tumor.[35] Thus, SMO could be one of the possible targeted therapies in treating ameloblastoma. Both SHH and SMO proteins work via the SHH pathway. This shows that the SHH pathway is one of the common routes of pathogenesis in ameloblastoma.

The second most commonly found signaling pathway is the Mitogen Activated Protein Kinase (MAPK) pathway. Within this pathway, the most commonly expressed signaling molecules were found to be IGF2, TLR2, and FOS. These signaling molecules were found to play a major role in the mechanism of development of ameloblastoma. IGF2 signaling molecule was found to enhance proliferation of ameloblastoma cell line in AMU-AM1 ameloblastoma cell line with BRAF mutation in 33% of the studies. The biological activities of IGFs include stimulation of collagen production and downregulation of collagenase synthesis in fibroblasts.[36] The increased expression of IGF could be due to the fact that IGF levels are especially high in cells that are undergoing proliferation and differentiation.[37] It is also closely related to expression of anti-apoptotic factor Bcl-2.[38] RAS-RAF-MAPK pathway promotes cell growth of ameloblastoma by mediating IGF2 signaling molecule stimulation. Thus, expression of IGF2 may suggest a mechanism for the development of ameloblastoma.

TLR2 signaling molecule was found to enhance cell survival signaling in ameloblastoma in 33% of the studies. There is recent evidence which states that TLRs play a vital role in tumor survival and growth. Studies also report that TLR2 activates myeloid cells to stimulate metastasis.[39] MAP Kinase pathway is seen to upregulate TLR2 signaling molecules in ameloblastoma. TLR2 is seen to promote tumorigenesis independent of tumor inflammation, deviating from its usual course and may function proactively as it is seen to promote cell growth in ameloblastoma.[40] Enhancing cell survival and cell growth are both favorable to the tumorigenesis of ameloblastoma. Because it is found that MAP Kinase pathway upregulates TLR2 signaling molecules, it can be stated that MAPK pathway is one of the common routes in the pathogenesis of ameloblastoma.

The review identified that FOS had an eightfold increase in the expression in ameloblastoma in 33% of the studies. The FOS protein belongs to the activating protein-1 family of transcription factors and is encoded by proto-oncogene. It participates in the control of oncogenic transformation, apoptosis, cell proliferation and cell differentiation.[41] This protein is very important for the development of bone and plays as a key regulator of osteoclast-macrophage lineage determination and remodeling of bone.[42] Although many cancers display an overexpression of FOS gene in vitro,[43],[44] its role in the pathogenesis of human tumors is yet to be understood. It participates in the control of oncogenic transformation, apoptosis, cell proliferation and cell differentiation. Thus, expression of FOS may suggest a mechanism for the development of ameloblastoma.

Although not common, the WNT-beta-catenin-TCF signaling pathway is seen to be involved in ameloblastoma. Within this pathway, the WNT10A signaling molecule was found to be commonly expressed in ameloblastoma. WNT10A was found to play a role in the tumorigenesis of ameloblastoma. In 33% of the studies, WNT10A had a fivefold increase in the expression in ameloblastoma. WNT10A’s function is mostly related to developmental process including the regulation of fate of cells and its patterning during embryogenesis. It plays a key role in various carcinogenesis by the activation of WNT-beta-catenin-TCF signaling pathway. The expression of WNT10A is said to be mediated by the tumor necrosis factor-α. This factor was also found to have a high expression in ameloblastomas.[45] It is suggested to cause cytodifferentiation in ameloblastoma but further studies are needed to understand its pathogenesis.[46] Hence, WNT10A can be seen as a crucial molecule in understanding the tumorigenesis of ameloblastoma.[45]

Among the various signaling molecules seen being expressed in ameloblastoma, the molecules found in the SHH pathway and WNT-beta-catenin-TCF pathway were found to be playing a major role in tumorigenesis. Further studies can be conducted that can provide a better understanding of these two pathways and to find the presence of any correlation between them.

In this review, cDNA microarray was chosen as the technique of choice for analyzing the various signaling molecules that are expressed by ameloblastoma. The use of cDNA microarray as a technique for the quantification of genetic expression is a smart method in this growing era of high-level technological developments. Ameloblastoma, as recorded in various studies, can express various signaling molecules. Although a lot of studies have been devoted to finding the most common signaling molecule expressed in ameloblastoma, limitations in technology have restricted the studies to analyze only one or few signaling molecules at a time. CDNA microarray has overcome this limitation. CDNA microarray allows us to study thousands of genes at the same time. It also simultaneously measures the transcription level of every gene in a cell.[47] This allowed the studies to evaluate multiple signaling molecules that were expressed by ameloblastoma at the same time. This reduces the overall cost and time spent on the technical process.[48] The reviews found numerous signaling molecules that were expressed by ameloblastoma. It also found the level of expression of each signaling molecule. With the data it provided, we were able to identify the most commonly expressed signaling molecule by ameloblastoma.

Report on quality of evidence looked up on

Two out of three studies included in this review were case-control studies. One article did not use control in their study. The level of evidence of these articles included in this review is of high quality. SMO gene from the SHH pathway was the highest expressed signaling molecule in ameloblastoma. However, further studies are required to consider the level of these expressions in other ethnicities.


The present systematic review considers only the published data for results. The unpublished raw data of the studies have not been included for interpretation. Due to the heterogeneous nature of the various genes assessed in this review, pooling of data was not possible. The sample distribution between the case and control was uneven. However, low sample size is a major limitation.

Future scope

Studies with increased sample size, standardization of study design, methodology, and method of evaluation are needed to assess the expression of signaling molecules in ameloblastoma.


After critically appraising the studies, this review concluded that the SMO gene from the SHH pathway was the highest expressed signaling molecule in ameloblastoma.


We would like to acknowledge all the authors who have contributed their efforts for this systematic review.

Financial support and sponsorship


Conflict of interest

The authors declare no conflict of interest.

Authors contributions

Not applicable.

Ethical policy and Institutional Review board statement

Not applicable.

Patient declaration of consent

Not applicable.

Data availability statement

Not applicable.


1Barnes L Surgical Pathology of the Head and Neck. Boca Raton, Florida: CRC Press; 2019.
2Gorlin RJ, Chaudhry AP, Pindborg JJ Odontogenic tumors. Classification, histopathology, and clinical behavior in man and domesticated animals. Cancer 1961;14:73-101.
3Pindborg JJ, Kramer IRH, Torloni H Histological Typing of Odontogenic Tumours. Jaw Cysts, and Allied Lesions.. Cancer, Geneva, Switzerland; 1971.
4Lucas RB, Cawson RA, Speight PM, Binnie WH Lucas’s Pathology of Tumors of the Oral Tissues. London, United KIngdom: Churchill Livingstone; 1998.
5Reichart P, Philipsen HP Odontogenic Tumors and Allied Lesions. New Maldon, United Kingdom: Quintessence Publishing Company; 2004.
6Sahoo T, Bhuyan S, Bhuyan R, Das P Recurrence of plexiform ameloblastoma as acanthomatous ameloblastoma: A rare case report. Contemp Clin Dent 2019;10:178.
7El-Naggar AK, Chan JKC, Grandis JR, Slootweg PJ WHO Classification of Head and Neck Tumours. IARC Who Classification of Tumours. Lyon, France: IARC Publications; 2017.
8Odukoya O, Effiom OA Clinicopathological study of 100 Nigerian cases of ameloblastoma. Niger Postgrad Med J 2008;15:1-5.
9Rizzitelli A, Smoll NR, Chae MP, Rozen WM, Hunter-Smith DJ Incidence and overall survival of malignant ameloblastoma. PLoS ONE 2015;10:e0117789.
10Brad W, Neville DDS, Douglas D, Damm DDS, Allen DDSC, Angela C, et al. Oral and Maxillofacial Pathology. Amsterdams, Netherlands: Elsevier Health Sciences; 2015.
11Hendra FN, Van Cann EM, Helder MN, Ruslin M, de Visscher JG, Forouzanfar T, et al. Global incidence and profile of ameloblastoma: A systematic review and meta-analysis. Oral Dis 2020;26:12-21.
12Fletcher CDM Diagnostic Histopathology of Tumors E-Book. Amsterdams, Netherlands: Elsevier Health Sciences; 2019.
13International Academy of Pathology, International Agency for Research on Cancer, World Health Organization. Pathology and Genetics of Skin Tumours. Lyon, France: IARC Publications; 2006.
14Rodríguez-Vázquez M, Muñiz-Lino MA, Shibayama M, Cruz-Tapia RO, Portilla-Robertson J, Ortiz-García JZ, et al. Overexpression and extra-mitochondrial localization of the chaperonin Hsp60 in ameloblastoma. J Oral Biosci 2021;63:271-7.
15Capella DL, Embaló B, Vieira DSC, Gondak RO, Rivero ERC Differentiated immunohistochemical expression of osteoclastogenic markers in radicular cyst, odontogenic keratocyst, and ameloblastoma. Appl Immunohistochem Mol Morphol 2021;29: 352-8.
16do Amaral-Silva GK, Pereira TDSF, Rocha AC, Mariz BALA, Prado-Ribeiro AC, Fonseca FP, et al. DNA methylation status of MutS genes in ameloblastoma. Oral Dis 2021;28:1901-6.
17Varshney A, Aggarwal S, Gill SK, Aggarwal A, Jaiswal Y, Sharma J Comparison of calretinin expression in dentigerous cysts and ameloblastoma: An immunohistochemical study. Natl J MaxillofacSurg 2020;11:224-30.
18Ganjre AP, Sarode G, Sarode S Molecular characterization of metastasizing ameloblastoma: A comprehensive review. J Cancer Res Ther 2019;15:455-62.
19Fuchigami T, Suzuki H, Yoshimura T, Kibe T, Chairani E, Kiyono T, et al. Ameloblastoma cell lines derived from different subtypes demonstrate distinct developmental patterns in a novel animal experimental model. J Appl Oral Sci 2020;28:e20190558.
20Fuchigami T, Ono Y, Kishida S, Nakamura N Molecular biological findings of ameloblastoma. Jpn Dent Sci Rev 2021;57:27-32.
21Zhukov N, Mareeva Y, Konovalov D, Druy A, Grachev N, Litvinov D Potentially curative targeted therapy for undifferentiated high-grade sarcoma developing after malignant transformation of a BRAF V600E–mutated ameloblastic fibroma. JCO Precis Oncol 2019;3:1-6.
22Brunet M, Khalifa E, Italiano A Enabling precision medicine for rare head and neck tumors: The example of BRAF/MEK targeting in patients with metastatic ameloblastoma. Front Oncol 2019;9:1204.
23Kaye FJ, Ivey AM, Drane WE, Mendenhall WM, Allan RW Clinical and radiographic response with combined BRAF-targeted therapy in stage 4 ameloblastoma. J Natl Cancer Inst 2015;107:378.
24Broudic-Guibert M, Blay JY, Vazquez L, Evrard A, Karanian M, Taïeb S, et al. Persistent response to vemurafenib in metastatic ameloblastoma with BRAF mutation: A case report. J Med Case Rep 2019;13:245.
25Pircher M, Winder T, Trojan A Response to vemurafenib in metastatic triple-negative breast cancer harbouring a BRAF V600E mutation: A case report and electronically captured patient. Case Rep Oncol 2021;14:616-21.
26Maleka A, Åström G, Byström P, Ullenhag GJ A case report of a patient with metastatic ocular melanoma who experienced a response to treatment with the BRAF inhibitor vemurafenib. BMC Cancer 2016;16.
27Lee HJ, Wark AW, Corn RM Microarray methods for protein biomarker detection. Analyst 2008;133:975-83.
28Juanes-Velasco P, Carabias-Sanchez J, Garcia-Valiente R, Fernandez-García J, Gongora R, Gonzalez-Gonzalez M, et al. Microarrays as platform for multiplex assays in biomarker and drug discovery. In: Rapid Test—Advances in Design, Format and Diagnostic Applications. Intechopen: 2018.
29Thanvi DG, Jaipur M Joint preservation & management of ameloblastoma—A case report. J Med Sci Clin Res 2019;7:322-7.
30Gurgel CAS, Buim MEC, Carvalho KC, Sales CBS, Reis MG, de Souza RO, et al. Transcriptional profiles of SHH pathway genes in keratocysticodontogenic tumor and ameloblastoma. J Oral Pathol Med 2014;43:619-26.
31Vered M, Peleg O, Taicher S, Buchner A The immunoprofile of odontogenic keratocyst (keratocystic odontogenic tumor) that includes expression of PTCH, SMO, GLI-1 and bcl-2 is similar to ameloblastoma but different from odontogenic cysts. J Oral Pathol Med 2009;38:597-604.
32Mishra P, Panda A, Bandyopadhyay A, Kumar H, Mohiddin G Sonic hedgehog signalling pathway and ameloblastoma—A review. J Clin Diagn Res 2015;9:ZE10-3.
33Kumamoto H, Ooya K Immunohistochemical analysis of bcl-2 family proteins in benign and malignant ameloblastomas. J Oral Pathol Med 1999;28:343-9.
34Kumamoto H, Takahashi N, Ooya K K-Ras gene status and expression of Ras/mitogen-activated protein kinase (MAPK) signaling molecules in ameloblastomas. J Oral Pathol Med 2004;33:360-7.
35Sweeney RT, McClary AC, Myers BR, Biscocho J, Neahring L, Kwei KA, et al. Identification of recurrent SMO and BRAF mutations in ameloblastomas. Nat Genet 2014;46:722-5.
36Froesch ER, Hussain M IGFs: Function and clinical importance 5 therapeutic potential of rhIGF-I in diabetes and conditions of insulin resistance. J Intern Med 1993;234:561-70.
37Stromberg T, Ekman S, Girnita L, Lennartsson J, Hellman U, Carlson K, et al. Targeting the insulin-like growth factor-I receptor (IGF-IR) in multiple myeloma cells using selective IGF-IR tyrosine kinase inhibitors. Blood 2004;104:639.
38Schillaci R, Galeano A, Becu-Villalobos D, Spinelli O, Sapia S, Bezares RF Autocrine/paracrine involvement of insulin-like growth factor-I and its receptor in chronic lymphocytic leukaemia. Br J Haematol 2005;130:58-66.
39Braunstein MJ, Kucharczyk J, Adams S Targeting toll-like receptors for cancer therapy. Target Oncol 2018;13:583-98.
40Kondo S, Ota A, Ono T, Karnan S, Wahiduzzaman M, Hyodo T, et al. Discovery of novel molecular characteristics and cellular biological properties in ameloblastoma. Cancer Med 2020;9: 2904-17.
41Heikinheimo K, Jee KJ, Aalto Y, Happonen R-P, Leivo I, et al Gene expression profiling of ameloblastoma and human tooth germ by means of a cDNA microarray. J Dent Res 2002;81:525-30.
42Kano J, Sugimoto T, Kanatani M, Kaji H, Yamaguchi T, Fukase M, et al. Involvement ofc-fos gene in the regulation of osteoblast proliferation and osteoclast differentiation by parathyroid hormone and parathyroid hormone-related protein. J Bone Miner Metab 1994;12:S39-43.
43Gamberi G, Benassi MS, Bohling T, Ragazzini P, Molendini L, Sollazzo MR, et al. C-myc and c-fos in human osteosarcoma: Prognostic value of mRNA and protein expression. Oncology (Huntingt) 1998;55:556-63.
44Yakabi K, Iwabuchi H, Nakamura T, Endo K, Fukunaga Y, Kumaki I, et al. Neural expression of fos protein in the brain after intravenous injection of gastrin. Gastroenterology 2001;120: A159.
45DeVilliers P, Suggs C, Simmons D, Murrah V, Wright JT Microgenomics of ameloblastoma. J Dent Res 2011;90:463-9.
46Molinolo AA, Amornphimoltham P, Squarize CH, Castilho RM, Patel V, Gutkind JS Dysregulated molecular networks in head and neck carcinogenesis. Oral Oncol 2009;45:324-34.
47Trevino V, Falciani F, Barrera-Saldaña HA DNA microarrays: A powerful genomic tool for biomedical and clinical research. Mol Med 2007;13:527-41.
48Govindarajan R, Duraiyan J, Kaliyappan K, Palanisamy M Microarray and its applications. J Pharm BioalliedSci 2012;4: S310-2.