Breast Cancer Case Study

The interpretation factor Myc is an essential downstream focus of Ras-ERK flagging and numerous different pathways. It is much of the time opened up or overexpressed in malignancy; strangely, Myc can tie to promoter areas of qualities as well as upgrade transcriptional extension of polymerase II, in this manner expanding its belongings past qualities with Myc-restricting destinations in their promoters. Myc can fill in as an all inclusive intensifier of communicated qualities as opposed to simply authoritative to promoters and starting interpretation (Sever and Brugge, 2015). Development factor and cytokine flagging can impact the improvement of a few malignancy sorts. One of the key players in the improvement of tumor is Janus kinas (JAK) flag

If the APC protein were to experience a nonsense mutation, the most common mutation in regards to this specific genetic disease, the destruction complex would not perform correctly and the wnt-signaling pathway would be stimulated. Problems begin to arise when “the Wnt/Beta-catenin pathway is activated [by] a Wnt ligand [binding] to seven-pass transmembrane Frizzled receptor and its co-receptor, low-density lipoprotein related protein 6 (LRP6) or its close relative LRP5” (MacDonald, et. al 2009). Once the wnt-signaling pathway is stimulated, a Wnt-Fz-LRP6 complex forms and takes in the Dishevelled (Dvl) protein, resulting in the phosphorylation and activation of the recruitment of the axin complex, destruction complex, to the receptors. (MacDonald, et al 2009). Due to the phosphorylation within the Wnt-Fz-LRP6 complex, the axin complex is not able to phosphorylate Beta-Catenin, which leads to the excessive accumulation of the protein in the cytoplasm. Researchers witnessed the development of numerous intestinal adenomas in transgenic mice with stabilized mutant Beta-catenin, therefore the results suggest that dysregulation of Beta-catenin is a key oncogenic event that follows the loss of APC function. (Tarapore, et. al 2011). The loss of the destruction complex’s normal activities results in elevated levels of Beta-catenin and downstream effectors such as CCND1,

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].

Immunoblot analysis showed that GSK-3β knockdown caused significantly enhanced the level of β-catenin that activate the Wnt pathway, while BPA treatment decreased the level of β-catenin that enhanced due to GSK-3β knockdown group (Figure 10G-H). Furthermore, the level of downstream target genes of Wnt/β-catenin pathway such as cyclinD1 and survivin after GSK-3β knockdown enhanced but BPA treatment caused decreased their levels that enhanced due to GSK-3β knockdown (Figure

Activation of the Raf1 signaling pathway has been shown to inhibit growth in SCLC, MTC, and carcinoid cells in vitro (6, 19 ), and we showed that doxycycline-induced MEK expression also led to inhibition of cell growth in MTC cells. Taken together, these results suggest that components of the MEK signaling pathway tightly regulate the MTC phenotype. Raf-1 activation in MTC cells also leads to significant reductions in the production of tumor markers CgA and ASCL1. The findings of this study demonstrate a reduction of ASCL1 and CgA with MEK activation. At the same time, we observed similar morphological changes with both raf-1 activation and MEK activation in MTC cells, where MTC cells with either of these proteins

Oncogenes are genes that work in the opposite way of tumor suppression genes. They cause uncontrolled growth of cells and are activated when tumor suppression genes become inactive. An example of this can be found in the mutation that causes Retinoblastoma. This is a condition that is found within the eye which is caused by a malfunctioning tumor suppression gene. The tumor suppression gene that malfunctions in retinoblastoma is the RB1 gene. This malfunction causes the activation of oncogenes. This ultimately leads to cells in the retina growing uncontrollably and causing tumors and cancer to develop in the eye.

Understanding of the WNT signaling pathway in melanoma progression may be critical-studies have found canonical and noncanonical WNT signaling affect different stages of tumor progression, with canonical affecting melanoma formation and noncanonical affecting melanoma metastasis.38 There exists controversy in regards to the exact involvement of WNT signaling has on melanoma behavior. One study showed loss of nuclear beta-catenin staining was associated with aggressive melanoma behavior,39 and another study showed that elevated levels of nuclear beta-catenin was associated with reduced proliferation of melanoma cells.40 Combined these findings suggest that Wnt/beta-catenin signaling is important for melanoma cell homeostasis, and if dysregulated, can lead to transformation of melanoma

Cancer Incidence cases for New York City, 2008-2012, the annual average of new breast cancer cases is 5,544.8, of which 824.6 (15%) of those cases are reported in the county of the Bronx. The incidence rate is highest among women ranging from ages 40 - 64, who account for 453.6 (55%) of those affected. Among these groups of women, the annual average cases are higher among those 60 to 64 years of age, making up 24% of those diagnosed, followed by women in the age group of 55 to 59 who make up almost 22% of new cases among the 40 to 64 age group. The average annual cases for African American women in New York City are 1567.6, (28%) of the total average annual cases. African American women in the Bronx make up

Peutz-Jeghers syndrome is a genetic disease in which benign tumors develop in the gastrointestinal tract. CDH1 is an abbreviation for Caherin 1 and is a tumor suppressor gene that enables the attachment and organization of cells to form tissues. A mutation in this gene can increase the risk of developing cancer because it can allow a cancer cell to break off and form breast cancer. All these genes proper expression play a large role in prohibiting the growth of tumors. In most cases it is not simply the presence of a mutated form of BRCA1 or BRCA2 that causes the development of breast cancer but a combination of mutated forms of these genes as well. Thus, it is incredibly imperative to not only analyze BRCA1 or BRCA2 but also STK11, CDH1, PALB2, CHEK2, P53 and PTEN as their presence can multiply the chances of an individual developing breast cancer. The ultimate transmission of breast cancer “interest genes” is not solely based on BRCA1 and BRCA2, but more accurately and often it is the presence of a mutated form of either of those previously listed and the presence of a mutated form of one of many of the tumor suppressors or localizers.

Oral cancer is a general term for oral malignant tumor which mostly occurs in the squamous cell, as known as mucosal mutate. In clinical practice, oral cancer include the gums, tongue, soft palate cancer, carcinoma of the mandible, floor of the mouth cancer, oropharyngeal cancer, salivary gland cancer, lip cancer, maxillary sinus cancer, and some cancer occurs in the facial skin and mucous membranes. Oral cancer is one of the more common head and neck malignant tumor.

Several decades of cancer research have identified thousands of mutation causing carcinogens, genetic mutations in DNA repair systems and mutations that cause dysregulation in critical signal pathways involved in cell cycle progression, cell growth and programmed cell death. Human cancers cannot be classified as a single disease because they are each unique on the molecular level. Often the same documented cancer type can inflict two patients with similar symptoms, but the required treatment for each patient will be different because the molecular mechanisms causing the symptoms must be treated differently. This is the primary reason why there is no “cure for cancer” because we may have one word to describe all cancers; it is a classification of many diseases. (The question is irrational and misinformed. If cancer were one disease with an underlying fundamental mutation or pathogen that could be isolated, then we would have found the cure by now.) Each type of cancer is inherently unique containing a minimum of 5 to 6 mutations that comprise the genotype, which could result in similar phenotypes. However, they have similar properties for which they are classified, called “hallmarks of cancer”. The “hallmarks of cancer” include persistent signaling for cell proliferation, circumventing growth/tumor suppressors, evading cell death, promoting endless replication, activating angiogenesis, and triggering metastasis and invasive properties (Hanahan and Weinberg 2011). The constant

3.11.1 β catenin expression : Membranous and cytoplasmic expression of β catenin were assessed in 110 primary OSCC using histopathological examination and immunostaining. EGFR expression and Cyclin D1 staining were also reported. Association between β catenin, clinicopathological features, molecular markers and between EGR and cyclin D1 in OSCC revealed reduced membranous expression of β catenin that was significantly correlated with nodal metastasis and invasive growth pattern. Abnormal β catenin expression with no gene mutation of β catenin has been said to cause tumor progression (Odajima et al, 2005). β catenin expression in tongue carcinoma and its correlation with tumour metastasis have been studied. OSCC of the tongue has been

Cancer is a growing health problem around the world. According to a report by the World Health Organization (WHO), there are more than 10 million cases of cancer per year worldwide and the disease causes over six million deaths a year (Jemal et al., 2009). By 2020, it is projected that there will be approximately 15 million new cancer cases and 10 million cancer deaths per year (Petersen, 2008). Oral cancer is one of the most frequently occurring cancers worldwide. It is the world’s 11th most common human neoplasm and account for 3% of all newly diagnosed cancer cases with estimated 400,000 new cases annually (Parkin et al., 2005). Oral cancer mortality has risen and is among the largest recorded for any common neoplasm (Vecchia, 2004). Consequently, oral cancer incidence in Malaysia has been increasing with an increasing number of

For metastatic outgrowth extravasation of tumor cells and secondary seeding are important. In secondary organs fibronectin expression is upregulated by primary tumors via resident fibroblasts, which serves as a docking site for VEGFR1+ hematopoietic progenitor cell (HPC) clusters and secondary seeding. During metastasis of breast cancer to lung, interaction of VCAM-1+ cancer cells with VLA-4-expressing macrophages, activates PI3K/Akt signaling in tumor cells, protecting them from caspase-induced apoptosis. Bone metastasis is also facilitated by interaction of VCAM1 with different integrin partner, α4β1, in osteoclasts. Thus, we can conclude that disruption of adhesion signaling between stromal cells and tumor cells can

Although molecular and histological features of the tumor play an increasingly important role in the prognostication of OSCC,