Oral Cancer Case Study

Lithium compounds have been linked to inhibition of the GSK-3 gene in vivo ‘Jia DD et al, (2013)’ The GSK-3 gene is involved in Wnt signalling pathway, where it produces a protein which phosphorylates Beta-catenin, resulting in Beta-catenin being targeted for degradation within the cell. The GSK-3 protein also phosphorylates transcription factors that regulate cellular apoptosis, downregulating the transcription factors. The resulting lowered levels of GSK-3 will result in over-expression of the Wnt signalling pathway. The Wnt signalling pathway signals for cell division within animal cells. The Wnt signalling pathway is also specifically involved in the self-renewal of neural stem cells, as it antagonises neural stem cell degradation through phosphorylating action by the GSK-3 protein. The GSK-3 protein levels affect the neural crest through suppression of B-catenin transcription, causing premature apoptosis of neural crest cells. ‘Richard S Jope et al (2003),’ ‘Roel Nusse

Background: cancer has developed mechanisms to survive and resist drugs including methotrexate, a DHFR inhibitor

For example, Connexin 43 has an effect on cell proliferation, particularly in the testes, which aid in the development of sperm cells [2]. They form a network that provides an environment to foster proper growth and development. Again, this is widely expressed in cases of tumor growth in the area.

In vitro: ICG-001 specifically inhibits T-cell factor/β-catenin transcription in a cyclicAMP responseelement binding protein binding protein (CBP)-dependent fashion. Furthermore, ICG-001 blocks selectively the β-catenin/CBP interaction without interfering with the β-catenin/p300 interaction

The methods of obtaining the cancerous epithelial samples from various areas was a clear way of observing both the level of amplification of CCND1 and the presence of cancer within those tumors or samples. The FISH technique was fitting to localize the specific DNA sequences related to the cause and effect of amplification. Epithelial tissues which contained some development of cancer cells were studied. The researchers used samples that were stored at the University Medical Center Hamburg-Eppendorf, making sure to used samples from areas distant from one another (Burandt, et. al). Taking samples from various areas helped to further see the effect of various amount of amplification of the protein and how it affected the epithelial tissues at different stages.

Cyclin D1 (CCND1) is known to be a prominent part of the cell cycle in humans by regulating the cell cycle. In this research paper, the CCND1 was examined for other things. Researchers believed that an access amount of the CCND1 was causing breast cancer, which is a wide spread problem across the country. The research consisted of 147 patients and eight different tissue cores from 4-8 tumors were taken. It was found that a high degree of homogeneity is the beginning development for breast cancer.

The research in Dr. Langenfeld’s lab focuses on the genes that regulate lung cancer. The experiment looks closely at the non-small cell lung carcinoma (NSCLC) and immortalized bronchial epithelial cells. Careful study of the carcinoma and epithelial cells has revealed that the mRNA of bone morphogenetic proteins 2 and 4 (BMP-2/4) was highly expressed in the carcinoma. Past studies have shown that BMP-2/4 have certain properties that allow them to activate the differentiation, growth, and migration of cancerous cells in the embryo. After studying these morphogens in lung carcinoma is was revealed that the BMP-2, in its mature state, is significantly more expressed in NSCLC than BMP-4 in cancerous lung tissue, but did not show much effect in normal lung tissue or benign lung tumors. The BMP-2 that was exposed in vitro to the A549 and H7249 human lung cancer lines stimulated significant migration and invasiveness. In vivo trials showed that the growth of tumors of A549 cells in nude mice was highly enhanced. Tumor growth in NSCLC was attempted to be reduced with recombinant through the exposure to noggin or the anti-BMP-2 antibody. Results showed a significant reduction in the tumor growth[1].

Nusrat Epsi, MBA is a PhD student working at the Rutgers University, School of Healthcare Professional with Dr. Antonina Mitrafanova. Prior to beginning the PhD program, Nusrat worked in the Pharmaceutical Industry. She consulted on a variety of projects which involved both qualitative and quantitative analysis to achieve strategic realignments within large pharmaceutical systems. From this work she developed an interest in drug discovery and drug structure. She is currently working on designing possible targeted cancer therapy to interfere with specific AR genes for tumor growth and progression. She also had a primary interest in the invasion of bladder cancer. She is also interested studying other Hormonal carcinogenesis. For her doctoral

TTF-1 ( Nkx2-1), a homeodomain-containing nuclear transcription factor has been a marker in the diagnosis of lung adenocarcinomas and in differentiating them from tumors of other origin.(1) Nkx2-1 is known for its transcriptional activity in the developing lung, thyroid and forebrain. Altered expression of TTF-1 resulting from mutations, polymorphisms and/or epigenetic modifications can predispose an individual to developmental disorders including thyroid dygenesis and thyroid cancer.(2) Mutations of the TTF-1 gene that induce haploinsufficiency may endow a negative effect on the wild-type gene.(3) Nkx2.1 is essentially involved with morphogenesis in the lung by modulating epithelial-mesenchymal interaction. Mouse models with functional

Fermt1 has been studied widely with the focus on its function in keratinocytes. Herz et al., in

In about a third of primary ovarian tumour, EEF1A2 is raised in copy number, and whilst EEF1A2 mRNA is not measurable in normal ovarian epithelium, the rate of EEF1A2 mRNA is increased in a third of ovarian tumours. It appears here that EEF1A2 is an important ovarian cancer oncogene (Lee, 2003). Moreover, when the eEF1A2 expression is induced in human ovarian cell line, the eEF1A2 expressing cell line is more tumorigenic; this proves that eEF1A2 promotes malignancy in ovarian cells (Anand et al., 2002). EEF1A2 is also an oncogene in lung adenocarcinoma (Li et al., 2006). And in a high proportion of pancreatic carcinoma, eEF1A2 is up-regulated while it is just a little bit expressed in normal pancreas (Cao et al., 2009). EEF1A2 over-expression seems to enhance cell growth, proliferation, motility, survival and invasion of pancreatic cancer cells (Cao et al., 2009). In two third of breast cancer, EEF1A2 is over-expressed, which indicates that eEF1A2 might be an oncoprotein (Tomlinson et al., 2005). But interestingly, it has been shown that eEF1A2 also augurs

Pulmonary carcinoma, also known as Lung Cancer, in among the most prevalent and thermal kinds of cancers in the world. A network around Matriptase including it 's inhibitor HAI-1, HAI-2 and it 's downstream substrate prostasin play a significant role in both the epithelia construction in normal epithelial cells and tumor development and progression in cancer cells. My research focuses on the expression of matriptase, HAI-1, HAI-2 and prostasin in lung cancer cell line NCI-H209, NCI-H292 and NCI-H1944 by means of Western blot and Inmunoflurescense. Antibodies M23, M19 and DC16 are used to recognize matriptase, HAI-1 and HAI-2, respectively and antibidies YL89, YL11 and YL10 are used to recognize prostasin in both experiment. All the 4 proteins in the network are detected to express in all cells line used in research and they express both on cells menbrane and inside cells in NCI-H1944. Both HAI-1 and HAI-2 can act as inhibitors to both matriptase and prostasin while HAI-1 is the predominant inhibitor. This network should be very essential to the oncogenesis and metastasis of lung cancer cells.

agreement with other studies [11, 22, 23]. This result supports the hypothesis proposed by Sakaki et al. (2010) that upregulation of galectin-1 may be an early event in cancer development and carcinogenesis [8]. Zuniga et al (2001) have found an association between resistance to treatment of RCC and high expression of galectin- 1 in these tumors. They have related that to the effect of galectin- 1 in the immune T cell response. Higher levels of galectin-1 have been shown to induce T-cell apoptosis, thereby providing a potential immune escape mechanism [24].

is clearly implicated in the TGF-β1, Notch, Fringe, and selectin functions or signalling [8, 9].

β-catenin is a proto-oncogene and it is encoded by CTNNB1 gene. It forms a component of the E-cadherin – catenin unit which plays essential roles in the cell differentiation and maintenance of the normal tissue architecture. Also, it involves in the signal transduction, the canonical WNT signalling pathways (β-catenin dependent WNT signalling pathways). The activated canonical WNT signalling pathways increase the level of β-catenin in the cytoplasm, causing translocation of β-catenin into the nucleus. This raises the level of β-catenin in the nucleus, leading to the initiation of the transcriptional activation through the LEF/Tcf pathway. The process involves in the canonical WNT signalling pathways is important in cell proliferation. The deactivated canonical WNT signalling pathways will casue β-catenin to undergo ubiquitination and proteosomal degradation through the β-TrCP/Skp pathway. These processes happen under normal circumstances of functional β-catenin.