Ameloblastic carcinoma ex ameloblastoma: report of a case–possible involvement of CpG island hypermethylation of the p16 gene in malignant transformation

2007 ◽  
Vol 103 (1) ◽  
pp. 72-76 ◽  
Author(s):  
Yoshihiro Abiko ◽  
Hiroki Nagayasu ◽  
Maiko Takeshima ◽  
Mami Yamazaki ◽  
Michiko Nishimura ◽  
...  
Keyword(s):  
Malignant Transformation ◽  
Cpg Island ◽  
Ameloblastic Carcinoma ◽  
P16 Gene

scholarly journals Frequent aberrant methylation of p16INK4a in primary rat lung tumors.

1997 ◽  
Vol 17 (3) ◽  
pp. 1366-1374 ◽  
Author(s):  
D S Swafford ◽  
S K Middleton ◽  
W A Palmisano ◽  
K J Nikula ◽  
J Tesfaigzi ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cpg Island ◽  
Homozygous Deletion ◽  
Lung Tumors ◽  
Aberrant Methylation ◽  
Rat Lung ◽  
Small Cell Lung ◽  
Gene Methylation ◽  
P16 Gene ◽  
Primary Tumors

The p16INK4a (p16) tumor suppressor gene is frequently inactivated by homozygous deletion or methylation of the 5' CpG island in cell lines derived from human non-small-cell lung cancers. However, the frequency of dysfunction in primary tumors appears to be significantly lower than that in cell lines. This discordance could result from the occurrence or selection of p16 dysfunction during cell culture. Alternatively, techniques commonly used to examine tumors for genetic and epigenetic alterations may not be sensitive enough to detect all dysfunctions within the heterogeneous cell population present in primary tumors. If p16 inactivation plays a central role in development of non-small-cell lung cancer, then the frequency of gene inactivation in primary tumors should parallel that observed in cell lines. The present investigation addressed this issue in primary rat lung tumors and corresponding derived cell lines. A further goal was to determine whether the aberrant p16 gene methylation seen in human tumors is a conserved event in this animal model. The rat p16 gene was cloned and sequenced, and the predicted amino acid sequence of its product found to be 62% homologous to the amino acid sequence of the human analog. Homozygous deletion accounted for loss of p16 expression in 8 of 20 cell lines, while methylation of the CpG island extending throughout exon 1 was observed in 9 of 20 cell lines. 2-Deoxy-5-azacytidine treatment of cell lines with aberrant methylation restored gene expression. The methylated phenotype seen in cell lines showed an absolute correlation with detection of methylation in primary tumors. Aberrant methylation was also detected in four of eight primary tumors in which the derived cell line contained a deletion in p16. These results substantiate the primary tumor as the origin for dysfunction of the p16 gene and implicate CpG island methylation as the major mechanism for inactivating this gene in the rat lung tumors examined. Furthermore, rat lung cancer appears to be an excellent model in which to investigate the mechanisms of de novo gene methylation and the role of p16 dysfunction in the progression of neoplasia.

Quantitate Detect of the Methylation of Three Hematopathy Patients’ P16 Gene

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4499-4499
Author(s):  
Bao-An Chen ◽  
Bei-ming Shou ◽  
Dong-rui Zhou ◽  
De-long Liu ◽  
Jia-hua Ding ◽  
...  
Keyword(s):  
Cpg Island ◽  
Gene Chip ◽  
The Other ◽  
P16 Gene ◽  
Precise Method ◽  
Patient Sample ◽  
Standard Curve

Abstract Objective: The changes of methylation of CpG Island are the frequent changes in epigenetic. Nowadays, there are many methods to detect the changes of methylation, but all these method are hard to quantitate precisely. In our experiment, we will establish a new precise method. Methods: Use hydrosulfite to handle the DNA, and then do PCR. The cytosine will change to thymine, if it hasn’t been methylation. On the other side, the cytosine will maintain its state if it has been methylation. Design a pair of probe, which contain one methylation probe and one un methylation probe. This pair of probe will detect three consecutive sites of CpG island in P16. Our experiment will use gene chip. Mix the the DNA of methylation and unmethylation with different ratio, then build the standard curve. Contrast the patient sample with standard curve will get the quantitate result. Results: We detected three patients, the methylation degree of the patients is 84.3%, 0%, 17.7%. Conclusion: The method we used can detect methylation degree of three consecutive sites of P16 quantitate precisely. Solve the problem of quantitate precisely.

scholarly journals Sinonasal Ameloblastic Carcinoma in a 50-Year-Old Filipino Female

2015 ◽  
Vol 30 (2) ◽  
pp. 43-46
Author(s):  
Daryl Anne A. Del Mundo
Keyword(s):  
Malignant Transformation ◽  
De Novo ◽  
English Literature ◽  
Hepatic Metastases ◽  
University Hospital ◽  
Sinus Surgery ◽  
Ameloblastic Carcinoma ◽  
Total Maxillectomy ◽  
Previous Diagnosis ◽  
Histopathologic Findings

Objective: To report the possible malignant transformation of primary sinonasal ameloblastoma into sinonasal ameloblastic carcinoma. Methods: Design: Case Report Setting: Tertiary Public University Hospital Patient: One (1) Result: A 50-year-old woman with a previous diagnosis of sinonasal ameloblastoma reported recurrence of symptoms of right-sided nasal obstruction and epistaxis two years after endoscopic sinus surgery. Clinical examination, CT scans, and subsequent total maxillectomy with orbital exenteration revealed a left intranasal mass with maxillary, ethmoid, and orbital floor extension and pulmonary and hepatic metastases.  Histopathologic findings of palisading columnar epithelium with reverse polarity with malignant features were consistent with ameloblastic carcinoma. Despite subsequent cycles of chemotherapy, the patient died two years after surgery. To the best of our knowledge, there have been no published reports of a primary sinonasal ameloblastoma with malignant transformation in the English literature. Conclusion: Ameloblastic carcinoma is a rare neoplasm which may arise de novo or from malignant transformation of an ameloblastoma. Because ameloblastoma is commonly encountered in our setting, clinicians should be aware of this possibility and closely follow their patients accordingly. Keywords: sinonasal, maxillary, ameloblastic carcinoma, malignant transformation

scholarly journals EPCO-02. MOLECULAR CHARACTERIZATION OF TWO NOVEL MPNST SUBGROUPS IDENTIFIES THERAPEUTIC OPPORTUNITIES

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii69-ii69
Author(s):  
Suganth Suppiah ◽  
Sheila Mansouri ◽  
Yasin Mamatjan ◽  
Jeff Liu ◽  
Vikas Patil ◽  
...  
Keyword(s):  
Malignant Transformation ◽  
Cellular Proliferation ◽  
Cpg Island ◽  
Therapeutic Option ◽  
In Vivo Models ◽  
Peripheral Nerve Sheath Tumors ◽  
Shh Pathway ◽  
Pathway Activation

Abstract Malignant peripheral nerve sheath tumors (MPNSTs) are highly aggressive Schwann-cell derived sarcomas. These tumors are resistant to all current therapies, with exception to gross total surgical resection, and unresectable or metastatic tumors are considered incurable. Our understanding of the molecular alterations driving malignant transformation is limited, and to date, targeted therapies have proven ineffective. In this study, we leverage multi-platform genomic and epigenomic profiling of human MPNSTs and neurofibromas to identify targetable molecular pathways that lead to malignant transformation. Unsupervised consensus hierarchical clustering of the top 20K most variable methylated probes yielded seven stable and robust subgroups that are clinically relevant. The high-grade MPNSTs formed two distinct methylation-based clusters (MPNST-G1 and MPNST-G2). MPNST-G1 had worse prognosis compared to MPNST-G2 (0.6 years versus 1.4 years, p < 0.05). PTCH1 loss or SMO gain was prevalent in MPNST-G1 compared to MPNST-G2 (75% vs 12.5%, p < 0.05). In addition, MPNST-G1 harbored PTCH1 CpG island promoter hypermethylation in (87.5% vs 12.5%, p < 0.001). Transcriptome profiling recapitulated the two distinct MPNST subgroups. We next demonstrated that that RB1 signaling pathways are aberrant in both MPNST-G1 and MPNST-G2. However, SHH pathway activation is observed in MPNST-G1, while WNT/CCND1/ ß-catenin pathway activation is observed in MPNST-G2. Network-based drug-disease proximity analysis identified SMO inhibitors as a potential FDA approved drug as a potential targeted therapy. To determine if SHH pathway activation is sufficient for malignant transformation, we knocked out PTCH1 in immortalized neurofibroma cells lines. In 3 different cell lines with PTCH1 knockout, we observed induction of a malignant phenotype, with increased cellular proliferation and invasion. Most importantly, in-vitro and in-vivo models confirm that targeting the SHH pathway, with sonidegib, was effective in inhibiting tumor growth proving SMO inhibition to be a novel therapeutic option in these lethal cancers.

Hypermethylation of promoter 5′CpG island of p16 gene in glioma tissue and plasma

2008 ◽  
Vol 7 (4) ◽  
pp. 241-244
Author(s):  
Chengdong Wang ◽  
Lili Wu ◽  
Lixue Guan ◽  
Daokui Wang ◽  
Yuting Wang ◽  
...  
Keyword(s):  
Cpg Island ◽  
Glioma Tissue ◽  
P16 Gene

Aberrant Protein Expression and Promoter Methylation of p16 Gene Are Correlated With Malignant Transformation of Salivary Pleomorphic Adenoma

2011 ◽  
Vol 135 (7) ◽  
pp. 882-889
Author(s):  
Yu-Hua Hu ◽  
Chun-Ye Zhang ◽  
Zhen Tian ◽  
Li-Zhen Wang ◽  
Jiang Li
Keyword(s):  
Protein Expression ◽  
Pleomorphic Adenoma ◽  
Malignant Transformation ◽  
Promoter Methylation ◽  
Intracellular Localization ◽  
Carcinoma Ex Pleomorphic Adenoma ◽  
P16 Gene ◽  
P16 Protein ◽  
Polymerase Chain ◽  
Lower Expression

Abstract Context.—The significance of promoter methylation of the p16 gene and intracellular localization of p16 protein in the carcinogenesis of salivary carcinoma ex pleomorphic adenoma (Ca-ex-PA) is not clear. The correlation of the promoter methylation of the p16 gene and the expression and localization of p16 protein in Ca-ex-PA need to be further clarified. Objective.—To investigate the p16 protein expression and promoter methylation of p16 gene in Ca-ex-PA and their roles in the malignant transformation of pleomorphic adenoma to Ca-ex-PA. Design.—The p16 protein expression and promoter methylation of the p16 gene were determined in both benign and malignant components of 50 primary salivary Ca-ex-PA tissues by immunohistochemistry and methylation-specific polymerase chain reaction. Expression of p16 protein and promoter methylation of the p16 gene between the benign and the malignant components was compared statistically. Results.—The tumor cells in the malignant components showed significantly higher p16 protein expression in the cytoplasm and lower expression in the nuclei than those in the benign components. Promoter methylation frequency of the p16 gene in the malignant components (36%) was significantly higher than that in the benign components (16%). There were no correlations between p16 protein expression and promoter methylation of the p16 gene in either benign or malignant components. Conclusions.—Overexpression of p16 protein in the cytoplasm and decreased expression of p16 protein in the nucleus may play important roles in the evolution of pleomorphic adenoma to Ca-ex-PA. Promoter methylation of the p16 gene may be correlated with the malignant transformation of pleomorphic adenoma.

Ameloblastic carcinoma of the maxilla

1995 ◽  
Vol 109 (10) ◽  
pp. 1019-1022 ◽  
Author(s):  
Christopher M. Lolachi ◽  
Shashi K. Madan ◽  
John R. Jacobs
Keyword(s):  
Malignant Transformation ◽  
Current Literature ◽  
English Literature ◽  
Primary Tumour ◽  
Metastatic Potential ◽  
Histological Classification ◽  
Ameloblastic Carcinoma ◽  
Histological Appearance ◽  
Odontogenic Carcinoma ◽  
Unusual Lesion

AbstractAmeloblastic carcinoma is an unusual tumour. There have been a total of 34 cases of ameloblastic carcinoma in the English literature to date. Of these only 11 cases have occurred in the maxilla. The authors report the 12th such case. The histological classification for odontogenic carcinoma has been debated for many years and recently revised, thus differentiating between malignant ameloblastoma and ameloblastic carcinoma. The authors review the current literature regarding diagnosis and treatment of this unusual lesion, and support the use of the term malignant ameloblastoma for the tumours that metastasize in spite of their benign histological appearance, whereas, the ameloblastic carcinoma is referred to as the primary tumour with malignant transformation, regardless of its metastatic potential.

Application of Transmission Electron Microscope and Scanning Electron Microscope in experimental tumor studies

1990 ◽  
Vol 48 (3) ◽  
pp. 306-307
Author(s):  
Gao Fengming
Keyword(s):  
Electron Microscope ◽  
Scanning Electron Microscope ◽  
Malignant Transformation ◽  
Transmission Electron Microscope ◽  
Experimental Tumor ◽  
Transmission Electron ◽  
Embryo Cells ◽  
Tumor Studies ◽  
Scanning Electron

Transmission electron microscope(TEM) and scanning electron microscope(SEM) were widely used in experimental tumor studies. They are useful for evaluation of cellular transformation in vitro, classification of histological types of tumors and treating effect of tumors. We have obtained some results as follows:1. Studies on the malignant transformation of mammalian cells in vitro. Syrian golden hamster embryo cells(SGHEC) were transformed in vitro by ThO2 and/or ore dust. In a few days after dust added into medium, some dust crystals were phagocytized. Two weeks later, malignant transformation took place. These cells were of different size, nuclear pleomorphism, numerous ribosomes, increasing of microvilli on cell surface with various length and thickness, and blebs and ruffles(Figs. 1,2). Myelomonocytic leukemic transformation of mouse embryo cells(MEC) was induced in vitro by 3H-TdR. Transformed cells were become round from fusiform. The number of mitochondria and endoplasmic reticulum was reduced, ribosomes and nucleoli increased, shape of nuclei irregular, microvilli increased, and blebs and ruffles appeared(Fig. 3).

Sign in / Sign up

Export Citation Format

Share Document