C4564 Unit 2 Lab Report
SRT1720 Description: EC50: 0.16 μM SRT1720 is a selective activator of SIRT1. Previous in vitro and in vivo studies using various cancer cell models show the role of SIRT1 either as an oncogene or a tumour suppressor gene. The oncogenic potential of SIRT1 is exemplified by studies indicating that blockade of SIRT1, like other HDACs, triggers growth arrest and apoptosis in breast, colon and lung cancers.
In the late 1940s, scientific research began taking off as innovative technologies and diseases were being created and discovered. One important field of study during the time was cancer. Like many types of new research, there were a few problems getting the ball on the roll. One problem scientists faced was obtaining cancerous cells that would stay long enough to study. One scientist struggled with this until a particularly unique strand of cells came along.
In the Phase 1 study, 17 patients with all sorts of solid tumors were treated for up to 7 days with a dose of 110 mg/kg of AS1411 per day. The results were that there was no “severe toxicity” to the patient seen at levels that would cause them to recover. AS1411 has only a small amount of toxicity because it can leave the blood very quickly; it has a half-life of only 20 minutes or less. Clinical trials are now evaluating AS1411 to be used to treat
CYTARABINE Cytarabine (arabinofuranosyl cytidine or ara-C) is a chemotherapeutic antimetabolic agent, used to treat cancers of white blood cells like acute myeloid leukemia and non-Hodgkin lymphoma. Its chemical name is 1β-arabinofuranosylcytosine. It kills cancer cells by interfering with synthesis of DNA, when the cell is in S-phase of the cell cycle. It is also called cytosine arabinoside implying that it combines arabinose sugar with cytosine base. Usually, cytosine pairs with deoxyribose to form deoxycytidine (a DNA component).
Forces and Newton II Elias Ghantous PHYS 151 – Section NQ Thursday 10:10am Hasbrouck Lab Room 214 October 13, 2017 Abstract In this experiment, I studied how forces cause an object to accelerate. I also studied the relationship between force vectors, mass and acceleration. Gathering of data took place through the use of a force table and a PAScar track system.
Retinoblastoma gene The unphosphorylated retinoblastoma protein binds and represses transcription factors from the E2F family which are responsible for transcribing genes required for DNA replication and cell division. The cells remain in the G1 phase and are prevented from passing the G1 checkpoint and moving on to the S phase as shown in figure 1. The retinoblastoma protein is phosphorylated by cyclin-dependent kinases (CDKs) and cyclins and forms a complex with them. This causes E2F to unbind and activate genes responsible for cell division and cells finally move into the S phase. The pRb protein remains phosphorylated up until the cell reaches the M phase.
Therefore, the involvement of ribosomal protein mutations in tumor formation via a p53 degradative mechanism is a prominent possibility. A study was conducted in this regard to identify the link between p53 and ribosomal
RT kills cancer cells by damaging their DNA, it can in two ways: The first one with damage DNA directly, the second with free radicals. After that, these cells cannot divide and die.
Cancer is easily one of the leading causes of death worldwide. Everyone knows that when detected early, cancer can be treated with the right equipment and resources. One method of treatment is via the use of alcohol. Indeed, the use of alcohol in cancer treatment is not unfamiliar. The treatment, known as ethanol ablation, uses ethanol – a type of alcohol – to destroy crucial proteins and fatally empties the cancer cell.
It is essential for cells to be small, as compact structure is crucial to the function, acquiring nutrients in and expelling waste out by diffusion utilizing free energy. Before a cell undergoes division, cells are in interphase, where they spend the majority of their time as they must progress through multiple checkpoints including G1 and G2. The G1 checkpoint assesses the size of the cell, and demand for division, as well as DNA formation. Retinoblastoma protein (Rb), p53 and p21 are tumor suppressors that function to stop the cell cycle during the G1 checkpoint. P53 identifies damaged DNA, if the DNA cannot be salvaged p53 triggers the cell to go into G0, or causes cell death, by blasting apart the cell membrane, referred to as cell apoptosis.
The past twenty years have host to some of the biggest advances in biomedical sciences. However there are few that are more significant and important of these three advances; the development of gene therapy and its first successful use worldwide clinically, the use of monoclonal antibodies in order to treat cancer, and the sequencing of the human genome. There is also a problem in the world at the moment with antibiotic resistance in harmful bacteria and the challenge has been set to find new antibiotics in order to combat these bacteria. In the next decade, significant steps will be made towards this advance.
Non-Hodgkin's lymphoma refers to a large group of lymphatic cancers that is made up of approximately 90% of all diagnosed lymphomas.4 All lymphomas are defined as cancerous growth of lymphocytes, also called white blood cells. It is the body's primary defense against infection and disease. These lymphocytes, which is also known as white blood cells mutate and grows abnormally crowding out those healthy cells which lead to forming tumors. 4 There are many different types of non-Hodgkin lymphomas [NHLs], that is classified by the varied types of affected cells and the rate of abnormal growth.
Your cancer cells absorb the radioactive substance more than normal cells. This means they receive a higher Quantity of radiation, causing them to die! There are a lot of different types of radioisotope treatments depending on what type of cancer you have!
A colorimeteric cleavage assay that helps in assessing cell survival and proliferation, also it can aid in quantifying macrophage-mediating cytotoxicity. MTT assay is a highly sensitive and reproductive method, it doesn’t require presence of radioactive compounds, easy to perform and quantify and it’s a rapid method.(Ferrari et al., 1990) A study was conducted on doxorubicin (DOX) and doxorubicin poly(N-isopropylacylamide-co-acrylic aid) (PNA) conjugates to assess their cytotoxicity
The biological effects of low levels of radiation have been investigated and debated for more than a century. The risk of cancer induced by radiation is the primary consideration of biological effects associated with diagnostic radiography procedures Ionising radiation has the potential to disrupt the structure of organic molecules in cells (Tubiana et al., 1990). Little question exists that intermediate and high doses of ionising radiation produce deleterious consequences in humans, including, but not exclusively, cancer (Pollycove & Feinendegen, 1999; Dickson et al., 2005). It is universally accepted that there is no safe level of radiation and even a single low dose exposure carries an associated risk and this risk increases with the dose received (Berrington de Gonzales and Darby, 2004).
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