Naked Mole-Rats

Hyaluronan (HA) is an extracellular matrix component that is secreted by fibroblasts and also works in inhibiting cell division. In a research article by Dr. Tian et al., They propose a mechanism for the cancer resistance exhibited by naked mole rats. They observed that in naked mole rats, there are greater levels of high molecular weight HA excreted from their fibroblasts. This high molecular weight HA accumulates in the tissues of the naked mole rat because the enzyme that is responsible for degrading, hyaluronan synthase 2, has decreased activity. When experiments are performed to remove HA, by the two methods, knocking down HAS2 or causing the overexpression of the enzyme Hyal2 which is responsible for the degradation of HA, the cells of

Several studies have shown the microenvironment and ECM are reservoirs of cellular and non-cellular materials, which help, modulate growth, survival, motility and invasive behaviour (LR)(Maeda et al., 2004). Hence studies on tumour epithelial cells and their niche are of current interest, as these interactions with regards to tumorigenesis have not fully been

The tumor numbers on the days 14, 21 and28were calculated in ten groups ofexperimental mice. The results designated that the tumors in the test group grew moreslowly than those in the control groups. The tumor growth wasinhibitedin immunized mice with HSP70 enriched EXOs/SEB comparing to othertest and control groups. It is also indicated that the number of tumors in PRP EXOs immunized mice were completely vanished over the time.

Al Rabey et al., (2013) analyzed that twenty male Albino rats were divided into four groups each consisted of five rats and fed the specified test diets for eight weeks. The first group (G1) is the negative group which was fed basal diet, the second group (G2) was fed 1.0% cholesterol, was the third group (G3) fed 1.0% cholesterol and 10% oats bran, and the fourth group (G4) was fed 1.0% cholesterol and 10% barley bran. Feeding rats on 1% cholesterol significantly increased serum total cholesterol, low density lipoprotein, and very low density lipoprotein and triglyceride and decreased serum high density lipoprotein. Hypercholesterolemic rats supplemented with oat bran and barley bran showed significant decrease in lipid parameters, significant increase in high density lipoprotein-cholesterol, improved antioxidant enzyme, and improved histopathology of kidney, liver, heart, and testes. Oat bran appeared more efficient than barley bran in lowering the lipid profile levels in hypercholesterolemic rats [55].

The article then looks at the role, in solid tumours, of areas of low oxygen (hypoxia) in selecting for those cells that have mutations in the p53 tumour supressing gene. A common feature inside solid tumours is hypoxia and an increase of cell death. This happens because often the rate of growth in a solid tumour outstrips the supply of oxygen to the cells. The normal reaction of a group of cells, expressing the normal p53 gene, when exposed to an hypoxic region, is an increase in the rate of apoptosis. However, in a solid tumour there are many cells with many different types of mutations. In the battle against solid tumours, some tumours resistant to treatment have cropped up. The article takes a look at the role of hypoxia possibly selecting for those cells resistant to apoptosis.

These findings are consistent with previous studies that report the effects of cytochalasin-D on fibroblasts. However, cytochalasin-D is not the only reagent that can disorganize the cortical layer of actin microfilaments. Cytochalasin-B has very similar effects on mouse fibroblasts and can disrupt organization of actin microfilaments as well (Domnina et al., 1982). This study indicates that cytochalasin-D and cytochalasin-B both alter certain characteristics of the actin cytoskeleton. Yet, cytochalasin-D can have this effect on any cell type that has actin because cytochalasin-D is altering the actin organization. Cytochalasin-D can also have clinical applications because the treatment of cells with cytochalasin-D activate the p53 protein (Rubtsova et al., 1998). This p53 protein plays a major role in the control of cell growth and in the cell’s response to various stress signals. More importantly, p53 is a gene that functions as a tumor suppressor, and if cytochalasin-D activates the p53 protein then there are possible cancer treatments that can be found. Moreover, phalloidin was used to prevent depolymerization by binding to

Another study conducted on human melanoma suggested the link between telomerase activity and cancer; it was discovered that a mutation on the promoter region of a telomere length regulating gene acts as a cancer drivers6, 7. Thus, there is a definite connection between telomeres, telomerase, and cancer.

Cancer is the uncontrolled division and growth of cells within the body. (Appendix 1) These cells are usually abnormal and are caused by mutations in genes that control the cell growth and replication. These cells damage the normal function of organs and can form tumours. Anti-cancer drugs work using number of strategies that interferes with the mitosis of the body cells, which in turn slows down the growth of the cancerous tissues. Anticancer drugs have distinct mechanisms of action which may vary in their effects on different types of cancer cells. These mechanisms of action are divided into three main categories. Anticancer drugs generally do one of the following, stop the synthesis of the pre-cursors of the DNA synthesis, damage the nucleic acid of the cell or affect the formation of the mitotic spindle. This is displayed in appendix 2. All three interfere with the division of the cells, which in turn slows down the growth of the cancerous tissue.

Animals: Our team will inject 6-week-old female SCID mice with HER2-positive SK-BR-3 or HER2-negative MDA-MB-231. The left flank of each animal will be injected subcutaneously with 5×106 cancer cells mixed with Matrigel Matrix. We will monitor tumor growth at 3-day intervals by measuring the length and the width of the tumor with a caliper as well as calculating the tumor volume on the basis of the following formula: V = 0.5ab2, using the longest (a) and shortest (b) diameters of the tumor. When the tumor volume reaches approximately 100 mm3, we will randomly assign the mice to the experimental groups as detailed below.

We examined the viability of the cells in response to the chemotherapeutic as a function of the matrix stiffness (Figure 2C). We observed that as the cells underwent apoptosis they detached from the substrates. Consequently, we collected the media before (Day 7) and after (Day 10) the chemotherapy to quantify the number of cells in suspension. As depicted on Figure 2C, the PC cells cultured on softer substrates experience larger increase in dead cells resulting from the chemotherapy compared to the PC cells growing on stiffer substrates. As Figure 2A shows, both Gemcitabine concentrations lead to a change in cell morphology and a higher decrease in cell area on the softer PC tumors (3kPa and 8kPa) compared to the stiffer PC tumors (25kPa and control group).

This indicate the TNA may result in modification of the cellular protein lead to clustering or aggregation and this could explain the variations in the cells shape and spreading behaviours that we observed earlier. Our preliminary result suggested the interaction of the TNA surfaces with bound cells may induce structural and cellular changes could be due to the surface roughness, chemistry and wettability that may count as the cell interaction factors. Therefore, we would like to suggest further detail study of genomic and proteomic test that can help us to explain this phenomenon. We would also like to screen several oncogene and tumor suppressor gene expression in order to study the potential carcinogenesis effect of this material.

A cancerous cell must adapt to various biological, chemical pathways, and modify it to impose its malignant behavior in human’s cell. The authors, Douglas Hanahan and Robert A. Weinberg points out six significant variations in cell physiology that leads to the composition of most of these cancerous cell. The cell’s autonomy in growth signals, insensivity to growth-inhibitory signals, circumvent apoptosis, endless replication, angiogenesis sustainability, as well as neighboring tissue invasion along with metastasis are main acquired capabilities of cancer cells. The article’s significance depends on its simplicity to convey information by providing concise methods as to how the cancer cell acquires the capabilities to turn normal human cells into cancerous one.

The p53 (protein having a molecular weight of 53 (kilodaltons) is a hereditary gene concerned with Li-Fraumeni Syndrome, a condition that involves development of independent tumor within the body tissue. The tumor protein accounts on all general human genes. P53 protein is believed to be among the unifying factor in cancer disease. Its activity alters the formation of tumors by compressing them. The activities may at times result to uncontrolled cell divisions creating risks for DNA genes. When the suppression activities are disabled, a person experiencing gene mutation is prone to cancer disease. P53 mutations within the body tissue enhance the tumor formation by modifying the molecular networks and increasing the mutagenic effects. Its protein bind stimulates the formation of p21, which in turn associates with the cell division stimulating protein (cdk2). The process of cell division is thereby stopped as the p21 composited with the cdk2 cannot facilitate the next stage of cell division. This creates a path way for the division and formation of tumors as the p21 proteins are inadequate. Thus, p21 is regarded as a component for terminating tumor formation.

     Abstract: Cancer has been known and feared since antiquity, but its imperative danger could only be realized until fairly recently. Indeed as knowledge of the disease grew in the nineteenth and twentieth centuries, fear increased when people became more aware that most cancers had no available cure. Cancer is a disease in which abnormal cells reproduce without control, destroy healthy tissue, and eventually cause deterioration to the body. This paper is a discussion on how cancer develops and spreads, some of the various types of cancer, and the causes of the disease.

Protein p53 is regarded as the “genome guardian”, since it controls the cell cycle, avoiding abnormal growth finding in cancerous diseases [34,37]. Positive immunoexpresion of p53 is considered abnormal, due to its short-life to be detected in samples. The detection of this tumour-suppressor gene indicates mutation and loss of function, facilitating cancer formation. Mutation of p53 can occur by different processes and, especially in skin cancers, UV radiation is considered the most important associated mutagenic factor of skin cells. In addition, some viral infections, can also play a role in carcinogenesis due to viral binding on this gene [34,37]. UV radiation initiates tumorigenesis by inducing mutations in the p53 tumor suppressor gene [34,37,71,72]. As UV exposition increases mutation rates of this genomic guardian, [34,37] it was expected that OSCC would have a high prevalence of p53 immunoexpression. The association between OSCC in cattle and p53 mutations were previously studied. In one study, p53 were positive