Effects Of Breast Cancer Development

Cancer, medically called ‘tumorigenesis’ (Thaker, Lutgendorf, & Sood, 2007, p.430) occurs when cells in the body orient themselves for malignant growth. Such cells show ‘self-sufficiency in growth signals’, are ‘insensitive to anti-growth signals’ and have ‘limitless replicative potential’ (Thaker, Lutgendorf, & Sood, 2007, p.430). Once a particular set of cells become malignant, the malignancy can spread to other set of cells in different organs due to ‘crosstalk’ between the affected cells and their surrounding ‘tissues’ and ‘micro-environments’(Thaker, Lutgendorf, & Sood, 2007, p.430).

As suggested by Seagull et al. (1980), while the rate of cytoplasmic streaming does not vary with the size of the motile particle (organelle, cargo molecule, etc.) or the size of the cell itself, larger cells with increased surface area may absorb these mechanism-inhibitory substances more readily and may therefore have slower rates of cytoplasmic streaming as less F-actin is available to the myosin complex at any one time.

Dr Jennifer Chan, the head of this tumor research, is an Associate Professor & Neuropathologist in the Department of Pathology & Laboratory Medicine, Oncology, and Clinical Neuroscience in the University of Calgary. Besides her work on education, she is also directing a tumorigenesis research team at the University of Calgary, and a tumor banking program which supports pediatric cancer research. Nonetheless, she is also a member of both the Southern Alberta Cancer Research Institute and the Experimental and Applied Therapeutics Program (ExpAT).

The purpose of this research was to determine the mechanisms in naked mole-rats that restricts cell proliferation and tumor formation. Contact inhibition is a mechanism observed where cell proliferation stops when two cells come in contact with one another. This process is caused by elevated levels of p27 cyclin-dependent kinase inhibitor which stops cells in the G1 phase from dividing. The cylcin-dependent kinase inhibitor p16 is also thought to regulate contact inhibition but its levels do not change in mice or human samples. Tumor-suppressor genes Rb and p53 are present in high concentration during contact inhibition to help control cell proliferation and apoptosis respectively. It was hypothesized that the naked mole-rats' cancer resistivity

Breast Cancer is a type of cancer where in the breast cells growth are uncontrolled. To enhance our understanding of breast cancer, knowing how any cancer can develop is crucial. Cancer develops as a result of the alteration of the genes, or abnormal changes in the genes accountable for managing the growth of the cells and maintaining their health. In each nucleus, the genes operates as the “control room.” The cells in our bodies replace themselves through a process called cell growth in which the

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.

Breast cancer is a disease in which certain cells in the breast become abnormal and multiply uncontrollably to form a tumor. Breast cancer is the second most commonly diagnosed cancer in women. (Only skin cancer is more common.) About one in eight women in the United States will develop invasive breast cancer in her lifetime. Researchers estimate that more than 230,000 new cases of invasive breast cancer will be diagnosed in U.S. women in 2015. Cancers occur when a buildup of mutations in critical genes—those that control cell growth and division or repair damaged DNA—allow cells to grow and divide uncontrollably to form a tumor. Breast cancer can be caused by inherited genetic factors. These genetic

Breast Cancer is made up of glands also known as lubes. In a women breast the small tubes (lobules) carry milk to the nipples (ducts) . Breast cancer begins in the cells that are in the in the ducts. It can also start in other cells of the breast tissues. There is a pathway in the breast called lymph. Lymph causes the cancer to spread throughout the breast. The vessels that carry clear fluid instead of blood connect lymph.

Breast cancer is an uncontrollable division of cells within the breast tissue that affects about 12% of women in their lifetime. Cancer can be caused by sporadic mutations influenced by environment or by genetic disposition. Several genes play a role in cell division: Oncogenes are responsible for directing mitosis, and tumor suppression genes prevent the expression of genes involved in cell division. Mutations that occur in either gene can lead to carcinogenic tumor growth and immortal cell lines.

(2000) reported that 90% of IBC tumours displayed an over expression of RhoC GTPase, an oncogene that contributes to the invasive nature of IBC. Rho protein activation causes the actin-myosin contractile filaments and focal adhesion complexes to assemble, leading to the formation of lamellipodia. Lamellipodia form at the edge of cells and drive cell migration and motility, furthering metastasis in IBC (Machesky 2008).

As medicine is growing in our times, researcher are looking for a new medicine to fight female breast cancer. Many people talk about the topic of breast cancer, but do they truly know what it is? In which case, I would be happy to inform you about breast cancer. Breast cancer is a disease in which tissue cells from the breast starts growing in an abnormal and uncontrollable way. These cells usually form a malignant tumor inside the breast and it is often felt as a lump or seen in an mammogram. There are different types of cancer such as: ductal carcinoma, lobular carcinoma, and inflammatory breast cancer. Researchers are looking for new ways that might lower the risk of obtaining breast cancer especially in cases where it is hereditary.

Today, breast cancer can no longer be seen as one disease but rather a group of diseases. Histological appearance is not the only criteria to classify breast cancer. Biologists and doctors nowadays look at the expression of receptors and gene that promote the growth of cancerous cells to define

This ability of malign cancer to make their way across basement membrane and into blood vessels is what makes cancer so fatal and impossible to be cure by surgery alone. The result of metastasis and invasion in normal tissue by cancer cells are often seen as one of the distinctive features of malignancy (Ruoslahti 1996). Even though the ability of invasion and metastasis are one of the hallmarks for cancer, these abilities are not unique to cancer cells as it can also occur during the early development stage of the embryo, in healthy organisms and in many noncancerous diseases (Mareel & Leroy 2003). It does not matter whenever the organism has developed benign or malign cancer, all cancer cells have the ability to disturb the normal cell cycle and threaten the survival of the organism.

Background: The issue of breast cancer affecting many individuals is a growing one. At the present time period it is now found that one in every eight women will be told they have breast cancer (“National Breast Cancer Foundation”, 2012). Therefore there is a significant amount of research going into this area. In addition, to the large amount of women and smaller amount of men who will be potentially diagnosed with breast cancer has become a global burden because those with metastatic cancer will eventually have cancer cells travel to other parts of their body (“National Breast Cancer Foundation”, 2012). MCF-7 cells are commonly used to study the mechanism of action and how the tumor works for human breast cancer (Osborn, Trent& Hobbs, n.d.). These types of cells are the most common in laboratories for cancer research. According to C. Osborn MCF-7 cells are used because they typically “demonstrate similar morphology”, however the chromosomal structures can be different. Thus leading to varied results. In addition, Osborn states that MCF-7 cell lines will usually have estrogen receptors, and progesterone receptors. The amounts of estrogen and progesterone receptors can affect the proliferation of the cells. (Osborn, Trent, & Hobbs, n.d.). Therefore, the experiment will be using cells taken from a sixty nine year old patient with metastatic cancer.

The ability of cancerous cells to migrate from their primary site and invade a secondary site is a hallmark of malignant progression. The invasive potential of a tumor hinges on the rigidity of its epithelial microenvironment in vivo, or the stiffness of the matrix on which the cells are grown in vitro. The serine/threonine protein kinase Cα (PKCα) promotes cell movement and contributes to tumor invasion, partially due to its activity on two newly discovered substrates, CEP4 and α6-tubulin. We set out to characterize the role of these PKCα substrates in the invasive phenotype of an aggressive metastatic mammary carcinoma cell line LM2-4175. We hypothesized that phosphorylation-resistant mutants of CEP4 and α6-tubulin would decrease the invasive phenotype. To test this, we transiently transfected LM2-4175 cells with either wild type or phosphorylation-resistant CEP4 or α6-tubulin and studied their migratory efficiency in transwells fitted with matrices of differing stiffness. In parallel, cells were treated with a PKC activator. As predicted, migration was potentiated by stiffer matrices under all conditions, with the exception of cells transfected with phosphorylation resistant CEP4 and α6-tubulin where the invasion in the softer matrix was greater. Furthering our understanding of the individual contributions of substrates of PKCα holds clinical promise, as it will permit the development of novel targeted therapeutics to curb cell migration and metastasis.