What Is Breast Cancer?

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

As the cells change, it begins to divide rapidly causing a tumor to form. The term “breast cancer” refers to a malignant tumor that has developed from cells in the breast. Breast cancer can begin in different areas of the breast, or in some cases, the tissues in between. There are many different types of breast cancer, including non-invasive, invasive, recurrent, metastatic breast cancer, as well as the intrinsic or molecular subtypes of breast cancer. Human epidermal growth factor receptor 2 (HER2) is overexpressed in around 20-30% of breast cancer tumors. It is associated with a more aggressive disease, higher recurrence rate, and increased mortality.

Breast cancer constitutes the second most prevalent cancer most common among women of the world with an estimated 1.62 million reported cases in 2012 which constitutes 25% of all cancer cases and ranks fifth among mortality due to cancer (Ferlay et al., 2015). In the United States, according to American Cancer Society an

Breast cancer is a common and potentially fatal form of cancer that affects both men and women. Different patients are given different types of treatment depending on their stage. There are also steps that people can take to not only detect, but also to prevent being affected by breast cancer. Breast cancer treatments have made great leaps forward, allowing both genders to have expectations of victory over the disease. Although breast cancer today has affected many lives among females and males, with the advancements in science and technology, it can be beaten.

When this checkpoint is passed, cdk4 and cyclin D interact. This interaction results in phosphorylation of the retinoblastoma protein, which in turn allows activation of the transcription factor E2F. Active E2F promotes expression of the cyclin E gene. Cyclin E (protein) and cdk 2 interact to

Breast cancer exists today as a vicious disease which has multiple facets for killing its host. The largest indicator of survival rate is length of time alive after diagnosis with the disease, and then whether or not the disease has metastasized to a new location in the body. For breast cancer patients, the 5-year survival rate of patients below Stage 4 is 90%. The stages below the 4 stage represent the stages where the breast cancer has not metastasized into other regions of the body. When breast cancer metastasizes into another region of the body, the 5-year survival rate of these individuals drops to 22%. The most common places of metastasis include the brain, liver, and lungs. The goal of studying cell line 231BR is that of

After decades of experience, medical research is now focusing on slowing or preventing the progression of this cancer. By learning all the biochemical pathways involved in the initiation, progression, and proliferation of cancer, scientists hope that they can find ways to change how cancer develops.

In breast cancer, the estrogen-estrogen receptor complex cause cell proliferation (Frank, 2013). Hormone therapies can target the effects of hormones in two ways: 1) by stopping the production of estrogen and testosterone, reducing their levels, and 2) by binding to the hormone receptor and blocking the hormone from binding (Frank, 2013). In breast cancer, drugs such as Lupron “prevent the ovaries from making estrogen by blocking cues from the brain that regulate the ovaries” (Frank, 2013). In prostate cancer, Lupron works the same way to prevent the testes from producing testosterone (Frank, 2013). Drugs such as tamoxifen (breast cancer) and flutamide (prostate cancer) bind to their respective hormone receptors and bloc the hormone from

Many question, “What does the Cell cycle have to do with cancer?”The cell cycle is a process in which cells develop and go on to divide.The cell cycle lies in the metaphorical heart of cancer. The cell cycle is a series of pathways by which a cell is signaled and continues to grow, the cell the replicates and divides.The process also includes different additional systems to make sure any problems that occur are corrected.If the problems are not corrected the cells fail and “commit suicide” in other words,(apoptosis).The only thing is, after apoptosis happens, cancer begins, as a result of genetic cells changing, the process then malfunctions which then causes uncontrollable cell growth.

The cell cycle of a normal cell and a cancer cell have many similarities and differences. The main similarity is that both sets of cells undergo the four phases of the cell cycle: G1, S, G2, M. There are three checkpoints within the cell cycle that tell the cell to move to the next phase or die, but cancer cancer cells do not obey the checkpoints. During the first phase, G1 phase, normal cells double in size and the number of organelles double as well. The G1 checkpoint ensures that proper doubling has occurred and allows cells to move forward to S phase. However, cancer cells that are too small or have too few organelles will not die. During the second phase, S phase, DNA replication (an identical copy of all the cell’s DNA is made)

Diverse pathological conditions, such as cancer and atherosclerosis, share a common molecular basis: deregulation of cell cycle progression . In these disease states, normally quiescent cells are induced to proliferate. Since the dysfunction of cell cycle pathways is a common thread among various conditions, regulators of these pathways would be logical targets of therapeutic agents. In order

Gene expression profiling divides breast cancer into 3 major subtypes: luminal, human epidermal growth factor receptor 2+ (HER2+), and basal like. Such classification has helped in predicting the treatment and the prognosis of each type11. Hormonal therapy and targeted therapy have replaced chemotherapy for subclasses that overexpress the corresponding receptors.

As described, chemotherapy aims to prevent or slow the growth of cancerous cells. The complex function of chemotherapy is directly related to cell division, or mitosis. To begin, the body’s immune

1. The Cell cycle consists of various phases, G 1 (growth& preparation of DNA), S (DNA synthesis), G 2 (cell preparation to divide), Mitosis (where chromosomes separate & the cell divides) and G0 (where non-dividing cells exit from the cycle). Cytotoxic therapy is the use of chemotherapy to disturb cellular growth by causing damage to the DNA and impairing cell function (Dougherty & Lister, 2011 p. 870). By affecting the growth and replication of these cells, treatments for patients diagnosed with cancer may be controlled and possibly cured.

Breast Cancer is on the fore-front of modern tumor research and scientists are continually seeking for new ways to treat and prevent cancer progression. Current treatments by hormone-dependent drugs like Tamoxifen and Raloxifene focus on estrogen receptor inhibition in mammary and endometrial cell lines. This group of drugs are known as selective-estrogen receptor modulators or SERMS, which are effective in estrogen-receptor positive (ER+) and hormone-estrogen receptor 2 positive (HER2+) breast cancers . Currently , researchers have turned their attention to retinoids – materials similar to vitamin A, which control cell proliferation and differentiation, apoptosis, and gene suppression in both normal and cancerous epithelial tissues. Specifically, fenretinide, a synthetic retinoid, is of particular interest for treating epithelial breast cancer after yielding positive results in inducing apoptosis in in vitro, in vivo, and clinical trials. Fenretinide’s exact functions in the cell for chemo-preventative use are still being discovered, such as its supposed relationship with the nuclear retinoid receptors RARɣ and RXR β, which control cell growth and apoptosis, and its effect on insulin-growth factor (IGF) receptors, which are high risk factors for breast cancer. Fenretinide has been discovered inducing cell death by other novel means through receptor-independent mechanisms . Combination therapy of fenretinide and Tamoxifen together has shown greater effect on