PTEN Essay

However, the majority of known anti-cancer drugs target normal cells as well. Methotrexate, formerly known as amethopterin, is an antimetabolite used in the treatment of some forms of cancer (Shacter and Law, 1956). It inhibits the function of dihydrofolate reductase (DHFR) by tightly binding to the enzyme. Following this slow interaction between methotrexate and DHFR, an enzyme-NADPH-inhibitor complex is formed (Stone et al., 1984). Therein, DHFR is rendered unable to catalyze the NADPH-dependent reduction of dihydrofolate to tetrahydrofolate (Anderson, 2017). Tetrahydrofolate is an important methyl group shuttle in the de novo synthesis of purine and pyrimidine nucleotides and some amino acids (Barbara and Hiroshi, 2002). Therefore, eliminating it from cells is a good therapeutic strategy against cancer cells, as it would limit the de novo synthesis of purines and pyrimidines (Lane and Fan, 2015). Inhibiting the function of DHFR by its competitive inhibitor methotrexate is one such good therapeutic strategy, as it would disable DHFR from converting dihydrofolate into tetrahydrofolate. However, some types of cancer cells had acquired some forms of resistance against methotrexate (Hans et al., 2011). Equally important, methotrexate should be administered in well established low doses, because it affects

In 2007, PPCPs such as diclofenac, iopamidol, musks and carbamazepine were identified as future emerging priority candidates. Ibuprofen, clofibric acid, triclosan, phthalates and bisphenol A are proposed additions to this list [45].

In this heavily pretreated patient population, pemetrexed, a 2nd generation antifolate agent produced an objective response of 26% (4/15) in patients with thymoma. 2 complete responses and 2 partial responses were documented, whereas there was only one partial response in patients with thymic carcinoma. The response rate of 9% in patients with thymic carcinoma suggests that pemetrexed is not active in this more aggressive phenotype. This is the first study to prospectively demonstrate the clinical activity of pemetrexed in thymic malignancies and solidifies the role of pemetrexed in the second line, and beyond in advanced thymoma. Prior to this, a Phase I trial of pemetrexed conducted in Japan demonstrated a partial response in one patient

Seidlin reported on the success of radioactive iodine (I-131) in treating a patient with advanced thyroid cancer. Later, the use of I-131 was expanded to applications such as thyroid gland imaging, hyperthyroidism treatment and quantification of thyroid function. By the 1950s, the clinical use of nuclear medicine had become widespread as researchers increased their understanding of detecting radioactivity and using radionuclides to monitor biochemical processes.” (Dr. Ananya Mandal, MD) With this information, we know that nuclear medicine is successful with multiple cases of diseases. Our technology today has improved on how treatments can be done. Nuclear medicine has improved from the time being. If treating a disease with nuclear medicine back then had been successful, imagine all of the success stories of everyone today who has had the chance of using nuclear medicine. Nowadays, the science and technology has developed so much that it is easy to cure any type of disease when proper guidance is given. If the technology is used properly, the side effects can be reversed. Today, we can easily figure out a way to reverse the effects of what we did to ourselves with all of the equipment, tools, and technology that people

A radioactive scan may be done to see whether the entire thyroid gland is overactive. In this scan, radioactive iodine is administered to the patient which then may demonstrate diffuse enlargement and increased uptake of radioiodine. The extent of this uptake helps determine the dose of radioactive iodine necessary for treatment. Ultrasound may also be utilized to help determine the size and location of the affected thyroid gland, which can then be paired with the radioactive

Well, fucoidan has been found to also have a role in this. It stops a tumor cell from being able to anchor to any surface in the body and without being able to anchor, there is no growing it can do. These are just some of the ways in which this compound is amazing, but science is still working out what else it can do and how it can be worked into treatments.

At this time, it is not clear how much diagnostic radiation is contributing to the increase in thyroid cancer cases. It is possible that the increase in the diagnosis of thyroid cancer can be attributed to a greater rate of detection by use of ultrasonography and fine needle aspiration3. The thyroid tissue itself is among the tissues that are less sensitive to radiation, however, thyroid cancer is still such a concern because the thyroid is so superficial in the body1 (77). “Even doses as small as 50–100 mGy have been associated with an increased risk of thyroid malignancy in children, with a

The doctor can tell more about these if it is required .Medullary thyroid cancer is the third most common type of thyroid cancer. The common medullary thyroid cancer symptoms and treatments as well as medullary thyroid cancer diagnosis and prognosis can be discussed. Characteristics of Medullary Thyroid Cancer: Occurs in 4 clinical settings associated with other endocrine tumors, it is more common in females than males, Regional metastases which spread to neck lymph nodes occurs early in the disease, Spread to distant organs (metastasis) which occurs late and can be to the liver, bone, brain, and adrenal medulla, it is not related with radiation exposure, and mostly originates in the upper central lobe of the thyroid, Poor prognostic factors include mean older than 50 years old, distant spread (metastases), and due to MEN II-B syndrome seen in patients with other endocrine tumors, other residual disease or recurrence can be detected by measuring calcitonin. Medullary carcinoma of the thyroid (MTC) is a distinct thyroid carcinoma that originates in the Para follicular C cells of the thyroid gland. These C cells produce

Surgery is done to remove as much of the cancer as possible. The bigger the lump, the more of the thyroid gland must be removed. Frequently, the entire gland is taken out. After the surgery, most patients should receive radioactive iodine, which is usually taken by mouth. This substance kills any remaining thyroid tissue. It also helps make medical images clearer, so doctors can see if there is any additional cancer. If surgery is not an option, external radiation therapy can be useful. After surgery or radioactive iodine, the patient will need to take medication hormone that the thyroid would normally

Radioiodine Scintigraphy plays an important role in diagnosing and staging thyroid cancer. This journal article by Anca M. Avram explains the role SPECT/CT is now playing in association with radioiodine imaging and therapy in nuclear medicine. This article explains the different ways SPECT/CT is being used, its advantages, disadvantages and limitations. The author Avram adds her conclusions on if SPECT/CT advantages outweigh its disadvantages.

Within the 2H88 complex II protein, an inhibitor was also discovery when they were analyzing the structure of it. The malate like intermediate, TEO, mentioned before was found to be an inactive suicide inhibitor. During normal functions, without the presence of TEO, FAD functions normally by grabs the hydrogen from Succinate and form FADH2. However, when TEO is present such inhibitor serves as a negative feedback (Shen, J.T.et. al. 2006). When too much Ubiquinone were produced, and not enough electrons are transferred fast enough to form ubiquinol, the excessive Ubiquinone can oxidize TEO to oxaloacetate (OAA) . OAA then inhibits succinate oxidation. TEO binds to FAD functions to inhibit in the form of Oxaloacetate the flavin protein

Medullary thyroid carcinoma: This type of thyroid cancer occurs in about 4% of the population, develops from the C cells of the thyroid gland1. The most concerning aspect of this cancer is the fact that by the time it is diagnosed, it has spread to lymph nodes, lungs, liver, or the bones1. Medullary thyroid cancers (MTC) cause the patient’s body to release too much calcitonin and a protein called carcinoembryonic antigen (CEA) into the blood1. MTC also does not absorb radioactive iodine that would be helpful in its treatment and to see if it had metastasized. The prognosis is much worse for this type of cancer than the previously discussed differentiated types. The two types of MTC are Sporadic MTC, which only impacts one thyroid lobe through a somatic mutation and is not inherited, and Familial MTC, which is an inherited cancer that is caused by a germ-line mutation1. In addition, these patients usually have cancer in several areas of both

Iodine therapy is another option for treatment and “is used in coordination with thyroidectomy to completely ablate the thyroid gland and to postoperatively eradicate possible residual cancer” (Nguyen, et al., 2015). Iodine 131 has had a significant part in the treatment and of thyroid cancer since the mid 1940’s (Nguyen, et al., 2015). Iodine 131 works “by entering the thyroid cells via the sodium iodide transporters and emitting short-wavelength beta rays, causing acute cell death” (Nguyen, et al., 2015). The use of Iodine 131 is done in two ways. “When administered the first time after surgery, it is referred to as ablation, whereas subsequent administrations for residual disease are referred to as treatment” (Nguyen, et al., 2015). Iodine

The thyroid is a butterfly-shaped nodule found in the neck just under the Adam's apple. This organ is the largest in the endocrine system, a system of glands responsible for releasing the hormones such as triiodothyronine (T3) and thyroxine (T4) that control necessary body functions. Thyroid cancer is characterized by malignant growth resulting from the division of abnormal thyroid cells. The disease isn't very common in the United States — 95% of reported nodule growths turn out to be benign and not cancerous. In addition, most thyroid cancers are very treatable. However, the disease shows very few symptoms so it takes a bit of time to diagnose.

Promising Agent: Our promising agent is a rational drug because we know the target and are designing a drug to target that specific protein. The protein we are targeting is the Sirtuin 1 protein. This drug works on a molecular level by decreasing the amount of protein SIRT1 found in kidney epithelial cells. SIRT1 has been found to prevent cystic epithelial apoptosis, meaning it prevents cells from dying that cause the formation of cysts in the kidneys. By inhibiting SIRT1, apoptosis will be activated and increased, and cystic cells will die, which will slow the growth of existing cysts, and prevent the growth of new cysts in the kidneys, and possibly the liver, and other organs this disease can sometimes affect.