PHC320H1 Lecture : Targeted cancer therapies

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azuresquirrel208

11 Apr 2012

School

UTSG

Department

Pharmaceutical Chemistry

Course

PHC320H1

Professor

Giaever

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Document Summary

Cells in multicellular organisms continuously signal each other and the environment. In cancer, there is a loss of balance in signaling. Problem: humans go through a large number of cell divisions in lifespan, each division possible mutation. One normal cell type multiply uncontrollably chaos (tumor) Traditional cancer chemotherapy: major medical advance of 20th century, adjuvant chemotherapy (chemotherapy along with removal of tumor) for breast, In certain cancers, chemotherapy is curative colon, and lung cancer increases survival benefit: narrow therapeutic index, side effects: alopecia, gi symptoms, myelosuppression (decrease in immune cells, responses are partial, unpredictable, more options are needed. Cancer mortality from 4 major killers has decrease in the past century: male stomach, female stomach, colorectal, uterine cancer has decreased, reasons: improvements in food storage practices, decreased h. pylori infection rates, improved screening (early detection) Target: hormone receptor: anti-endocrine therapies, tamoxifen (anti estrogen therapy in breast cancer, anti-androgen therapy in prostate cancer.

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Causes of Abnormal Plasma Urea Concentration HAPTER 12 Nonprotein Nitrogen Compounds Congestive heart falure Shock, hemorrhage Dehydration Increased protein cataboliom High-protein diet Acute and chronic renal failure Renal disease, including glo- CASE STUDY TABLE 12.1.1 Laboratory Reis- First Admission Urea N (Img/d) Creatinine (mg/dl) 1.8 13 Urea N/creatinine 25 Renal merular nephritis and tubular 18.5 122 7.50 48.7 Urinary tract obstruction 744 Decreased Concentration Low protein intake Severe vomiting and diarrhea Liver disease pO, (mm Hg o,sat (%) 328 576 51.391.0 protein cin catabolism, such as occurs in stress, fever, major diuresis. This treatment brought about a illness, corticosteroid Because of severe respiratory distress, the patient was transferred to the intensive care unit, placed on a respirator and given diuretics and intravenous (IV) fluids to promote d therapy, and Gl hemorrhage, may signiÅicamt increase the urea concentration. Decreased urea concentration as a result of compromised urea excre- ed renal function causes an increase in plasma improvement in both cardiac output and renal function. as shown by laboratory results several days later (6/3).After 2 additional days on a respirator with IV therapy, the patik of elevated urea include acute anbere within normal limits (67), renal function had returned to normal and, at discharge, his dmitted 6 months later because of intrinsic renal disease (see Chapter 27). Postrenala temia can be due to obstruction of urine flow anywhere in the urinary tract by renal calculi, tumors of the bladder or prostate, or severe infection. increasing inability of his family to arouse him. On admis sion, he was shown to have a tremendously enlarged heart with severe pulmonary disease, heart failure, and prob- able renal failure. Laboratory studies on admission were The major causes of decreased plasma urea concen- as shown in Case Study Table 12.1.2. Numerous attempts tration include low protein intake and severe liver dis- were made to improve the patient's cardiac and pulmonary ease. Plasma urea concentration is decreased during late f pregnancy and in infancy as a result of increased protein synthesis. The conditions affecting plasma urea concentra function, all to no avail, and the patient died 4 days later Differentiation of the cause of abnormal urea concentration CASE STUDY TABLE 12.1.2 Laboratory Results is aided by calculation of the urea nitrogen/creatinine (urea Second Admission N/creatinine) ratio, which is normally 10:1 to 20:1. Prerenal conditions tend to elevate plasma urea, whereas plasma creati- nine remains normal, causing a high urea N/creatinine ratio. A high urea N/creatinine ratio with an elevated creatinine is Uric acid (mg/dl) usually seen in postrenal conditions. A low urea N/creatinine Urea N/creatinine ratio is observed in conditions associated with decreased urea production, such as low protein intake, acute tubular necrosis, pH tion are summarized in Table 12.3. 90 Urea N (mg/dl) 3.9 12.0 23 7.35 59.9 pCO: (mm Hg) pO, (mm Hg) O, sat (96) 34.6 and severe liver disease. 63.7 CASE STUDY 12.1 e chronic obstructive lung disease, renal insufficiency, 1. What is the most likely cause of the patient's clevated and 65-year-old man was first admitted for treatment urea nitrogen? Which data support your conclusion t laboratory data on au significant cardiomegaly. Pertinent (5/31) are shown in Case Study Table 12.1.1.

Neutron activation has an important application in analyzing the trace elements from a sample. It can also be employed in the treatment of brain tumors where is consumed in the form of medicine or intravenous injection. This isotope is attracted by tumor cells and activated by neutrons. The isotope captures the neutrons (1 n 0), forming radioactive boron, which disintegrates into lithium and alpha particles ( 4 a 2 or 4 He 2 ). This disintegration produces energy in the form of gamma radiations (y) that kills the tumor cells in the vicinity of boron nuclei. This form of cancer treatment is known as boron neutron capture therapy (BNCT).Part BBNCT relies on the initial targeting of tumor cells by an appropriate chemical compound tagged with 10 B 5, which preferentially concentrates in tumor cells. During the irradiation of the tumor site by neutrons (1 n 0) the 10 B 5 absorbs a low-energy neutron (1 n 0), and it ejects an energetic short-range alpha particle ( 4 a 2 or 4 He 2 ) and lithium ion along with gamma radiation (y). This radiation deposits most of its energy within the cell containing the original 10 B 5 atom. Therefore, if a higher concentration of 10 B 5 exists in tumor cells relative to other normal tissues, a concomitantly higher dose will be delivered to the tumor cells during neutron irradiation.What is the nuclear reaction that takes place in the tumor cell?

I need help with the pre lab questions:)

Experiment 8: Determination of k 45 Exp 8: Determination of Logkow Values for Four Drugs Objectives . Discover how compound polarity affects absorptiorn e Perform extractions Calculate and compare partition coefficients (Olog Kp)of four different pharmaceutical Intreduction Pharmaceutical drug design involves creating a molecule that will target a general region or site and have a therapeutic effect on the patient. Such properties depend on the drug's structure as well as its affinity for different phases in the body. When orally ingested, a drug moves from the stomach into the small intestine. From there, a drug must pass through a layer of cells before it can enter the bloodstrcam (this process is called absorption) and be distributed throughout the body. This requires crossing through largely non-polar cell membrane twice, first to enter the cell from the intestine side and then to exit the cell for entry into the bloodstream Solubility properties have a large influence on the drug's ability to navigate this trek. The drug must be polar enough to convey water solubility so that it does not precipitate out in the water solution that is well, us. For it to be absorbed into the bloodstream, however, a drug mast be non-polar enough to pass through a non-polar lipid bilayer that forms the membranes of cells. A lipid is an organic molecule that can be extracted from living tissues using non-polar organic solvents. A lipid bilayer is a thin membrane made of two lipid layers; the bilayer forms a spherical non-polar barrier separating the inside of a cell from the outside of a cell. The types of lipids that are found in cell membeanes (most commonly phospholipids (Figure 1)) are amphiphilic molecules consisting of hydrophobic ("water-fearing") and hydrophilic ("water-loving") parts. In lipid bilayers, these amphiphilic molecules arrange themselves such that the inside of the bilayer is hydrophobic while the outside (which faces the aqucous intracellular and extracellular environments) is hydrophilic (Figure 2) Figure 1: A phospholipid containing a hydrophilic head and two hydrophobic tails Figure 2: A cartoon representation ofa layer of cells separating the intestne from the bloodstream. An orally-ingested drug must pass through a cell to enter the Noodstream, cncountering both hydrophobic and hydrophilic environments in the process. Diffusion of Drug

PHC320H1 Lecture : Targeted cancer therapies

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