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Copy of Cancer/HIV Lecture

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1 Copy of Cancer/HIV Lecture
BIT 120 Copy of Cancer/HIV Lecture

2 Cancer DEFINITION Any abnormal growth of cells that has malignant potential i.e.. Leukemia Uncontrolled mitosis in WBC Genetic disease caused by an accumulation of mutations over a lifetime not inherited (may exhibit strong predisposition); disease of elderly These cells can form a TUMOR –localized, abnormal, growing mass of tissue not normally found in portion of body Tumors can metastasize-cells break of from original mass; enter bloodstream-move to other parts of body; this called CANCER

3 Loss of Normal Growth Pattern
TWO CAUSES 1. uncontrolled cell growth 2. loss of a cell's ability to undergo "apoptosis." Apoptosis "cell suicide" or “programmed cell death” the mechanism by which old or damaged cells normally self-destruct.


5 Classes of Cancer Cancer can originate almost anywhere in the body.
Carcinomas the most common types of cancer arise from the cells that cover external and internal body surfaces. Lung, breast, and colon Sarcomas arise from cells found in supporting tissues bone, cartilage, fat, connective tissue, and muscle.

6 Types of Cancer Lymphomas
arise in the lymph nodes and tissues of the body's immune system. Leukemias immature blood cells that grow in the bone marrow and tend to accumulate in large numbers in the bloodstream. Uncontrolled mitosis in white blood cells


8 Naming Cancers TABLE 14.1, p. 314 Names are created by using different prefixes that stand for the name of the cell type involved. prefix "osteo” = bone osteosarcoma - cancer of bone prefix "adeno" = gland, adenocarcinoma - cancer of gland cells/breast

9 Tumors (Neoplasms) Growing mass of tissue
New cells are being produced in greater numbers than needed. organization of the tissue becomes disrupted. Immune system can destroy if cell surface proteins are different enough from self to be detected

10 Transformation Definition:
change of a normal cell into a cancerous one due to a deregulation of growth rate of cell proliferation has increased

11 What causes tumor growth?
A. Proto-oncogenes proteins involved in growth and cell-cell interactions B. Viruses contain ONCOGENES Cancer genes which cause cell proliferation despite signal saying ‘STOP’ many cancers have no viral association Insert into our chromosomes -Transforms GOOD GENE undergoes mutation BAD GENE Epstein-Barr Virus --> Burkitt’s Lymphoma Papillomaviruses --> cervical cancer

12 What causes Tumor Growth?
C. Tumor Suppressor Genes Normal gene prevents cells from dividing when mutated loss of function Cells divides Out of Control

13 Traits of Tumor Cells A. Distinctive Appearance loss of orientation
different shape B. Immortal in culture C. Interact with neighboring cells differently from normal cells Tumor cells LOSE Contact Inhibition Density-dependent growth inhibition

14 Traits of Tumor Cells D. Do Not attach to surfaces
E. Altered cell surfaces different proteins in plasma membrane F. May have chromosomal mutations Figure 14.2, p.317 G. Secrete proteins Growth factors to make blood vessels for ANGIOGENESIS Proteases

15 Microscopic Appearance
Cancer cells have Distinctive appearance a large number of dividing cells variation in nuclear size and shape variation in cell size and shape loss of specialized cell features loss of normal tissue organization


17 Malignant vs. Benign Benign tumors that cannot spread by invasion or
metastasis; hence they only grow locally. Malignant tumors that are capable of spreading by invasion and metastasis. ”Cancer" applies only to malignant tumors.

18 Diagnosis 1. Blood Tests 2. PAP test
microscopically observe cervical cells 3. Biopsy surgical removal of a small piece of tissue for microscopic examination. 4. Genetic Diagnosis Screen for oncogene or tumor suppressor mutations 5. MRI Magnetic Resonance Imaging *PROSTATE CANCER prostate-specific antigen (PSA) produced by cells of the prostate gland. PSA circulates in the blood and can be detected and measured with a simple blood test. *Other proteins Proteases secretes in blood aid in detection * Tumor cells Since the 1930s, early detection using the Pap test has helped lower the death rate from cervical cancer more than 75 percent MRI Examine internal organs without invasive surgery

19 Treatments Remove mass surgically
need to remove before tumor has done damage to organ Chemotherapy – chemicals used to destroy mitotically dividing cancer cells Table 14.3, p. 327 Radiation – use X-rays or gamma rays to kills cancer cells ONLY chemotherapy works for metastasizing tumors

20 Side Effects Lowers immune response no increase in WBC
need antibiotics Intestinal Disorders Nausea Vomiting Loss of hair Side affects result because treatment prefers ACTIVELY DIVIDING CELLS

21 Where does Biotech Come In?
1. Gene Therapy 2. Antisense Technology 3. Immunological Approaches

22 Gene Therapy Deliver Killer genes Issue: Selective Delivery
Procedure: Figure 14.5, p. 330 Genetically engineer retrovirus with a gene encoding and envelope protein specific for the cell receptor of the Tumor cell

23 Antisense Technology Add antisense DNA to cancer cell
This makes antisense mRNA Complements with mRNA of oncogenes Antisense mRNA would bind the sense oncogene mRNA and prevent translation of the oncogene

24 Immunological Approaches
A. Tumor Infiltrating Lymphocytes (TILs) Isolated from blood Treated to proliferate -ILs Reintroduce to body to fight tumor Called adoptive immunotherapy B. Magic Bullets monoclonal antibodies (against Tumor cell antigen) conjugated to toxin MOST of these treatment require that you ‘know’ the tumor cell antigens/receptor

25 high risk areas

26 Drug Trials for Cancer No Phase I – cytotoxic therapy will make people sick Therapies allowed to be used prior to launch- special circumstances Placebo

27 HIV Human Immunodeficiency Virus
Virus that causes AIDS (acquired immune deficiency syndrome) 30 to 40 million infected Prolonged infection Primary effect of HIV infection: reduction in TH cells

28 HIV Results of TH cell depletion: HIV mutates rapidly
opportunistic infections tumors develop HIV mutates rapidly HIV is a retrovirus – encodes genome in RNA Member of lentivirus – “slow virus”

29 HIV Lentivirus: Persist lifelong High mutation rates
Variation in disease presentation Variation in time of onset of disease Infect non-diving cells 3 infection stages acute latent high levels of viral production


31 Progression of HIV Infection


33 Life Cycle of HIV 1. Virus attaches and penetrates host cells- gp120 binds CD4 TH cells 2. Viral RNA converts to viral DNA 3. Viral DNA integrates into human chromosome 4. Infected host cells produce new virus particles 5. New virus particles bud from host cell one-by-one, taking host cell's membrane along as envelope HIV high mutation rate impedes immune response

34 Development of HIV Disease
Time Periods: 1. weeks 1-3: virus enters body, circulates, and makes infected person contagious 2. weeks 1-8: acute viral syndrome short term mild or severe flu-like symptoms fever, fatigue, rash, aching muscle and joints, sore throat, enlarged lymph nodes

35 Development of HIV Disease (cont’d)
3. 6 weeks - 6 months +: positive HIV antibody test seronegative: negative test seropositive: positive test for HIV 4. 2 yrs: onset of longer-lasting symptoms 5. 6 months-15 yrs: development of AIDS

36 Diagnosis of AIDS ELISA test Western Blot PCR test

37 HIV Therapy Strategies
Boosting immune response insufficient Interfere with: HIV attachment to Cells HIV integration into the host cell genome Virus replication Assembly of new virus particles

38 Possible HIV Therapies
Preventing assembly of HIV virus HIV protease Inhibit reverse transcription AZT (azidothymidine) Other nucleotide analogs Gene Therapy Antisense RNA Introduce into stem cells Preventing entry of HIV into uninfected cells gp120/viral envelope CD4 on the cell surface Vaccines – recombinant or attenuated virus (risky?)

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