Pancreatic Scarcinom A Literature Review

Allison hypothesized that “if the CTLA-4 molecular brake could be temporarily disabled, the immune system would be able to launch a more vigorous attack on cancer cells, resulting in the shrinkage of tumors. ” From this hypothesis, Allison and his colleagues set out to test the theory by delivering a synthetically developed antibody that obstructs CTLA-4 activity to mice. Wolchok did not identify a research question of hypothesis for the studies involving a second immune system-braking molecule known as PD-1, which is a molecule on the surface of many T cells that initiates self-destruction of a cell after coming in contact with cancer cells. Other than the hypothesize provided by James Allison, Wolchok does not provide other specific hypothesis or research questions that are intended to be

Pancreatic intraepithelial neoplasias (PanINs) show progressive stages of neoplastic growth that are precursors to pancreatic adenocarcinomas. The onset of Normal duct, PanIN-1A/PanIN-1B and PanIN-3 lesions are reproduced above. Figure taken from Nature Reviews Cancer 2, 897-909 (December 2002) | doi:10.1038/nrc949

The pancreas is a glandular organ that serves as two glands in one: As a hormone-producing endocrine gland that produces different important hormones, including insulin, glucagon and somoatostaina as well as serves as a digestive exocrine gland that secrets pancreatic juice which has enzymes that help break down food after it has left the stomach. pancreas is both an exocrine and endocrine cell which is arranged in clusters that is known as Langerhans. Pancreatic cancer is caused by Adenocarcinoma which is cancer of exocrine cell and this happens

Pancreatic cancer is the cancer that appears quickly and many die just as quick. Pancreatic cancer is the least known cancer to the medical world; puzzling doctors because most are not sure what diagnosis to look for. However, the risk factors include smoking, diabetes, and obesity. Studies show that pancreatic cancer has a higher percentage in the African American community due to environmental risk factors (John Hopkins Pathology, 2012).

All in all, based on retrieved information,fibrosarcomais resistant to immunotherapy and usually escape from presenting tumor antigens to T cells which play important rolein destruction of tumors(21).

The structure of a malignant tumour is not as solid as regular tissue, in terms of cellular adhesion, and it is easier for these cells to become detached from one another. The newly formed vasculature structures are tortuous,

Usually, radiation therapy is treated by neoadjuvant, adjuvant or definitive treatment with systemic therapy. Around 20% to 80 % of the patients with cancer received radiation therapy through the way of their treatment (de Gonzalez et al., 2011). In this treatment the radiation is usually given along with chemotherapy, which is recognized as chemoradiation or chemoradiotherapy. The Duke University conducts investigational study of neoadjuvant radiation therapy in 96 resectable patients. Everyday patients who received 50.4 Gy dose of radiotherapy are combined with 5-FU-based chemotherapy. After this patients were then surgically findout if there was no evidence of metastatic disease and less mortality. Overall survival (OS) and median survival was (28%:23 months) respectively (Spitz et al., 1997; White and Tyler, 2004). In 1980’s The Gastro-intestinal Tumor Study Group (GITSG) conducted randomized study in purpose of adjuvant chemoradiotherapy in resected pancreatic cancer. After R0 resection 49 patients were treated with chemorediotherapy for evaluation of adjuvant

In 1970, Gey learns that he has pancreatic cancer, and decides to volunteer as a subject in medical research and him under experimental chemo treatments that nearly killed him. Although Gey had the guts to do that I personally would not volunteer to serve as a subject in medical research, as Gey did because those treatments could have killed me like they nearly did to him. But before he died, he informed Mary that it was okay to release Henrietta's real name. It was later informed by Howard Jones that Henrietta's tumor was invasive and not an epidemic carcinoma, he realized that her cancer was "misinterpreted" and "mislabeled" (Skloot 172). Adenocarcinoma arises from glandular cells within the tissue, whereas squamous cell arises from the epithelial

Background and Rationale. Pancreatic ductal adenocarcinoma (PDAC) is highly malignant with the lowest survival of any human cancer (1). Extensive metastasis and therapeutic resistance are the two major contributors to the dismal prognosis of this malignancy (3-5). The mechanisms by which PDAC cells can successfully spread and metastasize are largely unknown, and molecular events underlying the tumor cell’s resistance to therapeutics remain to be defined (6,7). The objective of this proposal is to use a special type of cancer cell, circulating tumor cell (CTC), responsible for the poor prognosis to characterize these cells and to test therapeutics we have designed to overcome therapeutic resistance and improve patient survival.

Furthermore, Hedgehog Signalling Pathway in the malignant tumor cells plays a key role in aggravating the disease. Activation of Hedgehog Pathway leads to metastasis through various mechanisms like increase in protein expression, angiogenesis etc. Hedgehog signalling begins in the stroma cells. Stroma cells are dense supporting tissue, it consists of fibroblasts, pancreatic stellate cells (PSCs) and extracellular matrix proteins, collagens I and III and fibronectin. It influences the biological properties of the tumor. It has been proven in previous in-vivo studies that the PSC’s promoted tumor growth and metastasis through cell proliferation, migration, invasion and colony formation in dose-dependent manner. Hedgehog Signalling remains inactive

This year, an estimate of 53,070 adults, have been or will be diagnosed with pancreatic cancer. (27,670 men and 25,400 women). Pancreatic cancer is the ninth most common cancer in women. Pancreatic cancer should have the most attention because doctors still don’t know how to diagnose this type of cancer yet. The main problem is cost-effective screening tests that easily and reliably find early-stages of pancreatic cancer in people, sometimes show no symptoms.Often “times it is” not found until later stages when the cancer can no longer be surgically removed and has spread from the pancreas to other parts of the body. ("Pancreatic Cancer: Statistics", 2017)

Association of cancer cells with TAMs throughout the tumour significantly increases their motility, this gets further amplified when cancer cells are found in close proximity to perivascular TAMs. Moreover, cancer cells were observed to invade blood vessels only where perivascular TAMs were located.

Considerable research has been done over the past few years focused mainly on identifying molecular events in pancreatic carcinogenesis, and the correlation with clinic pathological status (Sarkar, 2007). With that being said there has been many discoveries along the lines of symptom recognition to the point that like symptoms can be evaluated simplified. Within all that it was discovered that there were multiple subsets of genes that undergo changes genetically. The activation of oncogenes and the inactivation of tumor suppressor genes are partly

The afore mentioned intricate network of interactions during EMT leads to many important changes in the phenotype and behavior of the cells. Epithelial cells undergo prominent morphological changes including the loss of cell-cell adhesion and the loss of apical-basal polarity. The cobblestone-like monolayer of epithelial cells with an apical-basal polarity is converted to dispersed, spindle-shaped mesenchymal cells with migratory protrusions. In addition to these morphological changes, cells undergoing EMT loose the expression of E-cadherin and other epithelial differentiation markers and gain the expression of mesenchymal markers such as vimentin, N-cadherin and fibronectin. These changes lead to the acquisition of migratory and invasive properties which enable the cells to migrate and invade through the ECM and the adjacent stroma (Boyer and Thiery, 1993). Thus, during cancer progression the EMT confers all the traits to the carcinoma cells which are required to overcome natural tissue barriers on their way to metastasis formation. These gained traits go hand in hand with a reduced proliferative potential of the mesenchymal-like tumor cells (Vega et al., 2004).

Colorectal cancer is still a critical issue and threatening society’s health (36,37). Tumors have developed different mechanisms for deceiving, counteracting, and onslaught the immune defense (38). Tumor cells secret different soluble factors, cytokines, chemokines (16,38,39), and exosomes (40) that recruit different heterogeneous supporting inflammatory cells such as B-cells, T-cells, mast cells, fibroblasts, myofibroblasts, mononuclear cells (MNCs), macrophages and MDSCs in the TME. The TME infiltrate with the recruited different cells by secreted factors from tumors (39,41). These recruited cells secrets various soluble factors, such as tumor-promoting, inhibitory, inflammatory (e.g., IL-6, IL-12b, TNF-α, IFN-ɣ),