Molecular Biology for Health Professions

Molecular Biology for Health Professions

Chapter 19:

Cellular junctions

Cell junctions consist of multiprotein complexes that provide contact between neighbouring cells or between a cell and the extracellular matrix. They also build up the paracellular barrier of epithelia and control paracellular transport (Keith et al., 2002). A plasma membrane is a semi-permeable membrane which controls the movement of substances in and out of the cell. Each nerve cell in the brain must be fed by blood, or the cells will quickly die of oxygen deprivation. I believe you are perhaps referring to a capillary system that sustains these cells in a way that compartmentalize them as much as possible. Cell junctions are especially abundant in epithelial tissues (Rodgers, 2004). Desmosomes bind intermediate to intermediate from one cell to another and Zonula adherents actin to actin: these both make up the anchoring junction. Desmosomes pin adjacent cells together, ensuring that cells in organs and tissues that stretch, such as skin and cardiac muscle, remain connected in an unbroken sheet (Keith et al., 2002). The epithelial cell is a protective and anchoring layer of cells in your body that is essential for stabilization and placement of organs. It is essentially your skin but lines both the outer and inner cavities of your body (Rodgers, 2004). Think of a balloon; if you press your hand into the balloon, the rubber continues from the outside to the inside, forming a cavity; this is how your lungs work, and they are lined with epithelial cells.

Chapter 20:

Hallmarks of cancer

We define seven hallmarks of cancer: selective growth and proliferative advantage, altered stress response favouring overall survival, vascularization, invasion and metastasis, metabolic rewiring, an abetting microenvironment, and immune modulation while highlighting some considerations for the future of the field (Keith et al., 2002). Cells have many different mechanisms to restrict cell division, repair DNA damage, and prevent the development of cancer. Because of this, it’s thought that cancer develops in a multi-step process, in which multiple mechanisms must fail before a critical mass is reached, and cells become cancerous (Rodgers, 2004). Specifically, most cancers arise as cells acquire a series of mutations (changes in DNA) that make them divide more quickly, escape internal and external controls on division, and avoid programmed cell death. Some people are born with a gene mutation that they inherited from their mother or father. This damaged gene puts them at higher risk for cancer than most people (Keith et al., 2002). When disease occurs because of an inherited gene mutation, it is referred to as “hereditary cancer.”

Although this is often referred to as inherited cancer, what is inherited is the abnormal gene that can lead to cancer, not the disease itself. If a healthy cell takes a second to divide and then waits a week and divides again (this is just an example, this is not accurate information), a lousy cancer cell might take a second to disconnect and then wait an hour (Rodgers, 2004). If this is the case, you will have two competent cells from one suitable cell and 168 bad ones from the cancerous cell.

Cancer-specific genes

Examples of tumour suppressor genes include BRCA1, BRCA2, and p53 or TP53. Germline mutations in BRCA1 or BRCA2 genes increase a woman’s risk of developing hereditary breast or ovarian cancers and a man’s risk of developing genetic prostate or breast cancers (Keith et al., 2002). Some faulty genes that increase the risk of cancer can be passed on from parent to child. These are called inherited cancer genes. This occurs when there is a mistake or a fault in the genes in an egg or sperm cell. Then the gene fault can be passed on to children. Cancer is unchecked cell growth. Mutations in genes can cause cancer by accelerating cell division rates or inhibiting healthy controls on the system, such as cell cycle arrest or programmed cell death (Rodgers, 2004). As a mass of cancerous cells grows, it can develop into a tumour.

References

Keith, R., Martin, R., Bruce, A., Peter, W., Julian, L. & Alexander, J. (2002). Molecular Biology of the Cell 4th Edition, Routledge, March 2002, hardcover, 1616 pages, 7.6 pounds, ISBN 0-8153-3218-1

Rodgers, M. (2004). Pandora’s Box congress. Rolling Stone 189, 37–77.