What Is The Effects Of Signaling Heterogeneity On Targeted Therapy

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).

In order to become cancerous a cell has many molecular changes that can occur including: tumor suppressor gene inactivation, oncogene activation, telomerase lengthening, ability to evade apoptosis, and angiogenesis (Mechanisms in Medicine, 2012). There are a few particular

Angiogenesis must be present for this occur, allowing cancer to spread to the blood, "thus the higher the density of new blood vessels within some tumors, the higher is the risk of metastasis of that tumor" (Mandal, 2014). Tumors have been documented to grow and spread without a direct blood supply and due to this physicians' are trying to discover ways to block tumor angiogenesis by investigating natural and synthetic inhibitors called "antiangiogenic agents" (National Cancer Institute, 2011). The goal is to slow the growth of cancer or prevent the disease entirely. According to the National Cancer Institute, "when vascular endothelial growth factor (VEGF) and other endothelial growth factors bind to their receptors on endothelial cells, signals within these cells are initiated that promote the growth and survival of new blood vessels" (2011, p. 1).

Mikala Egeblad used live-imaging technology to evaluate how cancer cells hijack NETs to enhance their capability to propagate. They applied a mouse model of triple-negative breast cancer - a cancer well-known to be most aggressive in human beings, and notorious for distributing and relapsing. The authors note in their paper:

II. This section will focus on the influence cancer has on the development, growth, and migration of individual cells.

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.

Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires a series of mutation during mitosis to develop, its characteristics can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells have make it hard to find a single effective treatment for cancer. The focus of research now lies

The human body is made up of millions of cells that divide continuously either for growth or replacement of worn-out cells-depending on the human stage of development. During the early stages of human development, cell division is rapid for accentuating growth while, in later years of a person’s life, cell division slows down and only takes place for replacement of worn-out or injured cells. This normal cell process is hindered by cancer cell growth. The start of cancer cell growth is manifested in the abnormal cell divisions, or rather out of control cell growth. Some of the notable difference between normal cell growth and cancer cell growth is that while normal cells die, and do not invade other tissues, cancer cell grow

We identified the affected components of most influential components in both type of perturbations. We combined all the four environmental conditions to construct the network of the most influential components with downstream targets. On these networks we mapped druggable proteins and cancer associated genes. Under inactivating perturbations, we obtained the network of PI3K, EGFR, PP2A, GRK and CaM (Figure 7A). Under activating perturbations, we obtained the network of influential components i.e. EGFR, IL1_TNFR, ERK, SHP2, RKIP, Ras, Gbg_i, Fak, Integrins, and PP2A (Figure 7B).

Neovascularization is closely involved in tumor survival, progression, and spread, - factors known to contribute significantly to the difficulties in cancer treatment. Folkman (1971) presumed that survival and proliferation of cancer depend on angiogenesis, which could be a target of cancer therapy. Similar to embryos, any tumor intending to grow bigger than 2 mm, needs functional blood vessels. According to Folkman, tumors can initially grow by capturing oxygen and nutrition via diffusion from the surrounding microenvironment, but they cannot grow beyond 2 mm without angiogenesis. The mechanisms of neovascularization in tumors are complicated and each tumor shows unique features in its vasculature, depending on tissue specificity, angiogenic

Cancer chemotherapy inhibits cancer via several potential mechanisms for example induces cell death, trap cell growth at certain stage, or induce cell differentiation.

Cancerous cells tend to mutate, grow, and divide without any particular order, and can spread unpredictably through the body via the blood stream. Most cancers start off as a single cell that undergoes an irregular mutation that alters the cells normal levels of melanin, cell membrane structure, and division speed. The cancerous cell then undergoes unprecedented division, and eventually creates a malignant abscess of tissue that overwhelms the population of healthy cells. Eventually, individual clumps of cells can break away from the parent group of cells and spread across the entire body. Although cancerous cells usually do not directly harm other cells in the body, they can block other cells ability to circulate their waste and absorb nutrients, ultimately leading to cellular starvation and death. Ever since cancer first became evident in society around 1600 B.C., humanity has striven to combat this seemingly incorrigible disease, creating procedures ranging from bloodletting to urbane chemotherapies. Although we undoubtedly improved our ability to identify and treat cancer, scientists have never had the chance to track the specific patterns it has spread in until now.

We leverage the ability of our method for modeling the magnitude of cell morphological changes to identify most significant cell morphological features in response to a compound treatment, and evaluate that its

Proteins in this pathway communicate by the addition of phosphate groups to adjacent proteins. A signaling molecule binds to the cell's surface receptor ( typically mitogen) allowing the GTPase, RAS, to exchange GDP and GTP. The tyrosine kinase EGFR, binds with EGF (epidermal growth factor), leading to phosphorylation. Docking proteins bind to SOS, then to the phosphorylated EGFR, activating SOS and removing the GDP. The GTP and Ras bind leading to activation. Proteins along this pathway can become mutated. When this occurs, the proteins are lodged in an or off position. The MAPK pathway has been discovered in cancer cells. A malfunction occurs in this pathway causing uncontrolled growth and components that inhibit this pathway, reversing the on and off effect, may be utilized as cancer

Tumor angiogenesis refers to an attribute of tumor cells residing with the capacity to elicit continuously the growth of new capillary endothelium. Tumor angiogenesis occurs by recruitment of endothelial cell precursor or by sprouting of existing capillaries as in physiologic angiogenesis. Angiogenesis (the formation of new blood vessels) is implicated in the pathogenesis of many chronic diseases including cancer. Angiogenesis in the tumor mass permits growth and invasiveness of the cancer cells as it is believed to be essential for the delivery of essential nutrients and oxygen to the tumor microenvironment. Clustered evidence suggests that angiogenesis is a critical event in the progression of solid tumors because tumor growth beyond 2 to