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SPM > PBL Cases 9-15 > Flashcards

PBL Cases 9-15 Flashcards

1
Q

Define Collagen.

Describe the 4 types?

A
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2
Q

Describe the compostion of collagen.

A

Repeating sequence -GLY-X-Y- (X mainly proline, and Y mainly hydroxyproline)

3 alpha helices in triple helix

Every third amino acid should be a glycine

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3
Q

What are some important structural feature of collagen?

Think H-bonds.

A

Proline important for hydroxylation → forms H-bonds → strengthens collagen structure

Hydrogen bonds between hydroxyl groups on external amino groups are weakened due to kink

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4
Q

What happens if a glycine in a collagen strucutre is substituted for another AA?

A

Substitution of glycine for another amino acid creates a kink in structure → unfolded protein (this is due to the relative flexibility of glycine when compared to other AAs)

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5
Q

Steps (7) of post translational modifications of collagen?

A

Translation of mRNA creates prepro-a-chains on RER

Steps of Post-Translational Modifications

  1. Hydroxylation: Proline and lysine can be hydroxylated, requiring O2, Fe2+, and Vitamin C).
    1. Enzyme: lysyl hydroxylase
  2. Glycosylation: Hydroxyl group of the hydroxylysine can be glycosylated, attaching glucose and galactose (ER)
  3. Assembly: Formation of the triple helix with H-bonds and disulfide bonds, forming procollagen (ER)
  4. Exocytosis: Procollagen moves through the Golgi and packaged into secretory vesicles, which is secreted into the ECM
  5. Proteolysis: specific procollagen peptidases cleave N and C terminus with disulfide bridge by N- and C-procollagen peptidases, making tropocollagen (insoluble)
  6. Cross-Link Formation: Lysine and hydroxylysine covalently bond, forming staggered tropocollagen molecules making fibrils
    1. Enzyme: lysyl oxidase

Formation of Fibers: Inter cross-links between fibrils form collagen fibers.

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6
Q

Describe the role of vitamins in collagen formation.

A

Vitamin C

  • Necessary for lysyl hydroxylase/prolyl hydroxylase.
  • Deficiency causes anemia due to poor blood vessel formation (collagen is necessary for vessels)

Copper

  • Necessary for lysyl oxidase
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7
Q

What is the most common unheritance pattern for OI?

What gene is mutated?

What are some less common genes involved with OI?

A

Most common gene affected in OI

  • Autosomal dominant mutation in COL1A1 or COL1A2 affecting alpha chains of type I collagen
  • Autosomal dominant Gly to Val mutation hinders proper triple helix formation in ½ of the procollagen. This consequentially leads to the unfolding of procollagen and a significant decrease in type 1 collagen within bone.

Other autosomal recessive gene mutations can occur that affect the hydroxylases, oxidases and folding machinery

  • CRTAP
  • LEPRE1
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8
Q

What are some example of collagen diseases that are not OI?

A
  • Ehler’s Danlos - collagen type 3 (1 and 5 may also be affected); stretchy skin; problem with crosslinking; most affected - skin, gi, blood vessels.
  • Marfan’s Syndrome - tall, thin, large bones. Defect in fibrillin 1. Major risks - mitral valve prolapse, aortic aneurysm
  • Epidermolysis Bullosa - dermis and epidermis are not linked together, lots of tearing and blistering.
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9
Q

Discuss how DNA testing is used to confirm an OI diagnosis.

A

DNA testing shows mutations in COLA1 and COLA2 genes

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10
Q

Describe the treatments available for OI.

A
  • Goal: Reduce fractures and pain and maximize mobility (physical therapy)
  • Cure: None
  • Bisphosphonates: Inhibit osteoclastic bone resorption by attaching to the hydroxyapatitte binding sites on bony surfaces, especially those undergoing active resorption.
  • Hormonal Therapies (Teriparatide): PTH (takes Ca from bone and other sources to increase serum Ca levels) intermittent exposure leads to increased bone formation
  • Supplementation: Vitamin C, Vitamin D, Calcium
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11
Q

Define X-inked inheritance.

A

X-linked Inheritance: any mutation that lies on the X-chromosome, and therefore is more likely to be present in males

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12
Q

Define anticipation.

A

Anticipation: The signs and symptoms of some genetic conditions tend to become more severe and appear at an earlier age as the disorder is passed from one generation to the next.

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13
Q

What is X-inactivation?

How does it relate to Mosaicism?

A

X-Inactivation: One chromosome can be inactivated in a way that it has heterochromatin – an inactive form of DNA.

  • Condensing of on X chromosome into barr bodies that are not expressed
    • Mosaicism
      • Xist RNA inactivates the X chromosome via methylation
      • Inactive X chromosomes can be at least partially reactivated in vitro by administering 5-azacytidine, a demethylating agent.
      • Skewing favors the wild type over the defective
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14
Q

Explain dosage compenstation.

A
  • Dosage compensation – most gene products coded by the X chromosome are present in equal amounts in males and females,
    • Males have one X chromosome
    • Females have two X chromosomes - one of which is inactivated.
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15
Q

Describe how females can manifest an X-linked disorder.

A
  • Each cell in a female will inactivate or turn off one of its two X chromosomes.
  • If a large proportion of the cells turn off the X chromosome with the Fragile X mutation, then most of the cells will have an active X chromosome that can produce FMRP. As a result, the impact of Fragile X syndrome will be limited.
  • If a large proportion of the cells turn off the X chromosome with the working FMR1, then there will be few cells able to produce FMRP. As a result, the impact of Fragile X syndrome will be more pronounced.
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16
Q

Descibe the symtpoms of Fragile X?

A
  • Symptoms in Full Penetrance Individual
    • Intellectual disability/autism
    • Large testes, ears, jaw, face
    • Mitral Valve prolapse
    • Seizures
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17
Q

Describe the sympotms who carrier the premutation for Fragile X.

A
  • Symptoms in Pre-mutation
    • Premature menopause in women who are carriers (Fragile X related ovarian insufficiency)
    • Tremor/Ataxia (Fragile X Ataxia-Tremor Syndrome) - histone acetylation
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18
Q

What protein is involved with Fragile X?

What is that protein’s normal function?

A
  • The FMR1 gene codes for the FMRP protein which is important for synaptic plasticity and brain development.
    • FMRP also acts as an mRNA chaperone → regulation of translation
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19
Q

What is the mechanism of mutation for Fragile X?

A

Genetic Mechanism: DNA polymerase slips due to the number of CGG repeats and a loop of unreplicated DNA forms

Fragile X syndrome is due to hypermethylation of 5’ UTR of DNA due to trinucleotide repeats (CGG)

More repeats = more methylation

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20
Q

Define the terms pre-mutation and full mutation and describe the range of phenotypes and genotypical differences associated with these mutations.

A

Pre-mutations: less triplets of a triplet expansion disease

50-200 repeats = pre-mutation

Full-mutation: large number of triplets causing silencing of gene in triplet expansion disease

>200 repeats = gene silencing

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21
Q

What gene is affected in DMD and BMD?

What is the function of the protein it codes for?

A

Dystrophin is a cytoskeletal protein that binds actin filaments inside sarcomeres to a protein complex at the sarcolemma, which in turn bind glycoproteins and collagen. It acts as a cohesive protein, connecting the cytoskeletons of skeletal muscle cells to help keep structure. N-terminus binds actin, cytoskeleton. C-terminus binds extracellular matrix.

DMD gene.

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22
Q

Why do mutations in DMD casues muscle wasting phenotype?

A

The muscle membrane is susceptible to damage and muscle fiber deterioration occurs, resulting in cycles of regeneration and degeneration that result in fibrosis and fatty replacement of muscle.

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23
Q

Why does elevated serum creatine phosphokinase indicate muscle damage?

A

Creatine phosphokinase is very concentrated within muscle cells and should remain inside the cytoplasm of myocytes. When the membrane is damaged, CPK may leak out of the cell and into the blood. Phosphocreatine is used in muscle as an ATP reserve for short term storage to buffer the levels of ATP present in the muscle. If not present in the blood, probably a neurological problem.

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24
Q

Difference between DMD and BMD?

A

Duchenne is a quantitative issue, no dystrophin is transcribed due to a frameshift mutation. Beckers is a qualitative issue, the dystrophin made retains some function due to an inframe mutation, typically a premature stop codon.

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25
Q

How is muscle damage caused DMD?

A
  1. Dystrophin – connects extracellular matrix with sarcolemma membrane and associated cytoskeleton
    1. Defect in Dystrophin gene causes MD
    2. X-linked disease
  2. Ca++ entry from extracellular fluid causes proteolysis – inducing muscle damage
  3. Creatine Kinase – muscle breakdown causes leak out of muscle and becoming elevated in the blood
  4. Myofibrils are replaced with fatty tissue. Therefore, muscles are not fully repaired.
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26
Q

How is repair of muscles affected in DMD?

A

MD patients cannot go through muscle regeneration repair fast enough

  • Pts with MD lack to ability to completely repair the muscle fibers. It is thought that the satellite cells are either unable to repair the muscle fibers or are not fast enough to repair it.
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27
Q

Define atrophy.

A

Atrophy is the decrease in muscle strength due to a decrease in muscle mass, or the amount of muscle fibers. Can be due to diseases, starvation, or disuse.

28
Q

Define hypertrophy.

A

Hypertrophy is an increase in the size of a muscle through an increase in the size of its component cells. Hypertrophy can occur through increased sarcoplasmic volume or increased contractile proteins. Can be due to strength training or anaerobic training. Changes occur due to adaptive responses to increase ability to generate force or resist fatigue

29
Q

Name some disease asscoited with Ashkenzi Jews.

A

CF, Tay-Sachs

30
Q

What are the most common molecular genetic defects associated with Tay-Sachs? What protein does the HEXA gene encode?

A

Beta-hexosaminidase A, encoded by HEXA, plays a critical role in the brain and spinal cord (central nervous system). Within lysosomes, beta-hexosaminidase A forms part of a complex that breaks down a fatty substance called GM2 ganglioside.

31
Q

What are gangliosides?

A
  • Gangliosides are sialic acid-containing glycosphingolipids that are most abundant in myelin of the nervous system. The hydrocarbon motif embeds in the cell membrane and the rest is exposed to the cell surface. On the cell surface, they participate in cell-cell recognition, adhesion, and signal transduction.
  • They are continually synthesized and broken down. The sugars cause water to come in so if it is not broken down the cells can swell - causes brain problems.
32
Q

What is the differenece between different LSDs?

A
33
Q

What are symptoms of Tay-Sachs?

A
  • Cherry red spot on macula
  • Startle Response
  • Seizures
  • Hypotonia
  • Normal at birth but progress to a vegetative state with early death between around 2 yo
34
Q

Explain heritable versus non-heritable retinoblastoma.

A
  • Non-heritable form: Unilateral RB → two sporadic mutations
  • Heritable form: Bilateral RB → loss of heterozygosity (“second hit” after germline mutation)
35
Q

What is the difference in frequecy between inherited Rb to somatice Rb?

A
  • The frequency of RB in an inherited Rb proband will be higher than in a somatic Rb proband.
36
Q

Outline the testing for Rb.

A
  • Testing
    • Ophthalmic Exam: Complete visualization of the retina and identification of multifocal tumors; Can detect leukocoria
    • WBC Analysis: In heritable forms of retinoblastoma, molecular testing of peripheral white blood cells can identify the germline mutation in 90 to 95 percent of cases
      • More likely to get metastatic form of the cancer
37
Q

Expliain the inheritance pattern (recessive/dominat) of Rb?

What is the two hit hypothesis?

A
  • Tumor suppressor genes are recessive, loss of function
  • Retinoblastoma exhibits haploinsufficiency, only requires one mutated allele + loss of heterozygosity (only one WT allele left)
  • Retinoblastoma is dominant because one allele can lead to the disease (“second hit”), but it is genotypically recessive
  • Two-Hit Hypothesis: In a tumor suppressor gene, a mutation in one allele will cause genomic instability. This can lead to a mutation in the second allele and ultimately “two-hits”.
38
Q

What is the transcriptional control of the cell cycle?

A

Transcriptional Control:

  • Rb attaches to E2F (a transcription factor)
  • When Rb is phosphorylated by Cdks → E2F is active
  • p21/p16/p27 deactivate cyclin → dephosphorylating Rb → E2F is inactive
    • p53 transcribes p21
  • [Cdk] stays constant. [Cyclin] varies.
39
Q

What cyclin controls each checkpoint?

A

G1/S Checkpoint

  • Cyclin E

S/G2 Checkpoint

  • Cyclin A

G2/M Checkpoint

  • Cyclin B

M/G1 Checkpoint

  • Cyclin E

G0 Checkpoint

  • Cyclin D
40
Q

How do these classes of drugs target the cell cycle in cancer cells?

DNA Damage

Inhibition of DNA synthesis

Inhibition of Microtubule Function

A
41
Q

Explain why the risk for additional cancers is higher in retinoblastoma patients.

A

Children with germline mutations have a higher risk for other types of cancer. This is due to the fact that the body has an abnormal RB1 tumor suppressor gene, which would normally stop some of these cancers from forming. This is not true for non-hereditary.

42
Q

What is the inheritance pattern of BCRA1/2?

What type of cancers are these proteins related to?

A
  • Most inheritance is due to germline mutations in BRCA1 or BRCA2, which is inherited as an autosomal dominant fashion.
    • Mutations in BRCA1/BRCA2 often cause breast cancer in women and can possibly cause prostate cancer in men.
  • These genes produce tumor suppressor proteins → help in repair of damaged DNA
43
Q

What is the molecular function of BRCA1 and 2?

A

Overall, BRCA1 makes sticky ends and BRCA2 localize RAD51 to resected DNA and work as homologous recombination (HR) transcription factors. In BRCA-deficient cells, non-homologous end-joining (NHEJ) takes over as the primary form of double stranded break repair, which is faulty and can result in mistakes/somatic mutations that lead to mutations, genomic instability, and transformation.

44
Q

When is Tamoxifen used?

What does it do?

A
  • ER-positive breast cancer drug
  • Competitively binds to estrogen receptor at the ligand binding site → Preventing estrogen molecules from binding → doesn’t change receptor’s shape so coactivators are unable to bind → genes that stimulate cell proliferation can’t be activated
  • Antagonist on breast tissue; agonist at uterus, bone
45
Q

When is Anastrozole used?

What does it do?

A
  • aromatase inhibitor that inhibits synthesis of estrogen by binding reversibly to aromatase enzyme through competitive inhibition
  • inhibits conversion of androgens to estrogens in peripheral tissues
  • ONLY for postmenopausal women (postmenopausal women the ovaries are no longer making estrogen. This is why anastrazole is used in these women.)
46
Q

Explain the significance of HER2/neu (her 2 or c-erbB2) overexpression in breast cancer, and its relevance for breast cancer therapy.

A

HER2/Neu Receptor binds to a partner receptor to form a dimer with tyrosine kinase domains. The partner receptor can come from the EGFR family of growth factor receptors, and HER2 has high affinity for all monomers. HER2 has no specific ligand. HER2/Neu overexpression will cause it to competitively bind to EGFR family monomers, causing cell proliferation and cell cycle disregulation through PI3K activation.

47
Q

Explain the rationale for using PARP inhibitors for treating BRCA-mutant tumors.

A

PARP is important in SSB repair. If BRCA1/2 is mutated, tumor cell is dependent on PARP for all DNA repair. PARP inhibitors prevent this DNA repair in cancer cells and since BRCA 1 cannot help the cell undergo homologous recombination → apoptosis occurs

48
Q

How does radiation and chemotherapy work as cancer treatments?

A

Radiation - causes more mutations helping lead to apoptosis

Chemotherapy: combination of different drugs to treat different classes of breast cancer

49
Q

What are the STAGES of breast cancer?

A
  • Stage 0: Noninvasive cancers
  • Stage I: The tumor is small, and the cancer has not spread to the lymph nodes under your arm or to other sites beyond your breast.
  • Stage II: The tumor is a little larger, or the cancer has spread to the lymph nodes under your arm. Stage I or II cancers may be called early-stage cancers.
  • Stage III: This is a more advanced cancer, but it is still confined to your breast, surrounding tissues, and lymph nodes.
  • Stage IV: Cancer has spread or metastasized
50
Q

Correlate drug therapies with the different classes of breast cancers.

PARP, Trastuzamab, Lapatinib, Anastrozol, Tamoxifen, Fulvestrant

A

BRCA1/2 (+) – PARP Inhibitors

HER2/Neu (+) – Trastuzamab (antibody)/Lapatinib

ER/PR (+) Post-Menopausal – Anastrozole (aromatase inhibitor)

ER/PR (+) Pre/Post-Menopausal – Tamoxifen (SERMS → modulates receptor) Fulvestrant (SERD→ degrades receptor)

51
Q

What are the four clinical presentations of Lynch Syndrome?

A
  • 3 or more relatives with Lynch Syndrome
  • 2 or more successive generations affected
  • 1 or more cancers in the first degree relative before the age of 50
  • Presence of different types of cancers
52
Q

What are the two diagnostic techniques used in diagnosing Lynch Syndrome?

A
  • Microsatellite Instability Testing
    • MSI testing is performed using polymerase chain reaction (PCR) to amplify a standard panel of DNA sequences containing nucleotide repeats
  • Immunohistochemistry
    • The mutations in the MMR genes that cause Lynch syndrome typically result in a truncated or lost MMR protein that can be detected as loss of staining of the protein on tumor IHC testing
      • Then need to make sure there is no methylation by checking for BRAF-V600E. This is not considered Lynch Syndrome because it is an epigenetic modification
53
Q

What are the two genetic characteristics of Lynch Syndrome?

  • What five genes are affected?

What percentage of CRCs are caused by Lynch Syndrome?

A
  • Genetic Characteristics
    • Loss of Heterozygosity - genotypically recessive, but inherited in an autosomal dominant fashion
    • Mutations in any of the MMR genes causes LS:
    • MSH2, MSH6, MSH3, MLH1, PMS2
  • Epidemiology
    • 2-3% of all colorectal cancers
54
Q

What is the step-by-step mechanism of MMR?

A
  1. MSH2 dimerizes with MSH6 to form hMutSα, which scans the double strand DNA for mismatches
  2. Once mismatch is located, MLH1 and PMSC will dimerize (forms hMutLα) and join hMuTSα
  3. Activates Helicase and recruits exonuclease 1 that recognizes nicks on lagging strand and removes long strand of DNA nucleotides containing mismatch
  4. DNA polymerase will then use leading strand as template to create correct sequence fragment
  5. Ligation by Ligase
55
Q

What is the normal function of DNA MMR and what happens in Lynch Syndrome?

A
  • Normal Function: DNA mismatch repair allows for repair of mismatches and DNA loops
  • Lynch: A MMR gene is mutated, so cannot properly repair
    • Gut epithelial cells have a high turnover rate. So mismatches/loops accumulate and lead to cancer
56
Q

Define microsatellites and microsatellite instability.

A
  • Microsatellite Instability: common areas of hypermutation due to DNA polymerase slippage
    • MSI can inactivate tumor suppressor genes resulting in cancer.
  • Microsatellite is a tract of repetitive DNA in which certain DNA motifs (ranging in length from 2–13 base pairs) are repeated, typically 5–50 times as a result of DNA slippage
    • Similar to Insertion and Deletion loops (IDLs)
    • Normally, MMR would removes these microsatellites
57
Q

Describe epigenetic modification of DNA and its role in Lynch Syndrome.

A
  • In the tumor, MLH1 promoter is methylated, thus it does not get transcribed. This often happens in endometrial cancers and sporadic colon cancer tumors. Most microsatellite instability (MSI) cancers are caused by MLH1 methylation (~75%)
  • MSI is also associated with BRafV600E mutation, which is associated with non MMR mutation, so this would not be part of the Lynch Syndrome.
58
Q

For DNA repair mechanisms, what are the:

  • Causes
  • Effect (Damaged Caused)
  • Relevant Proteins Involved
A
59
Q

List the two major classes of genotoxic carcinogens in tobacco smoke and describe how they form DNA adducts and induce mutagenesis and carcinogenesis.

A
  • PAH - polycyclic aromatic hydrocarbon → BPDE creates mutations in p53 & Kras by forming guanine adducts
    • Main type: Benzo(A)pyrene
    • Activated by AHH and EH (types of cytochrome p450)
  • Nitrosamines (NNK) - burning of nicotine forms NNK
    • N-nitrosamines, as alkylating agents, act directly on DNA bases to induce cross-linking → adducts
60
Q

Describe the biochemical pathways by which tobacco carcinogens are metabolically activated and metabolically detoxified.

A
  • Activation: cytochrome p450s
  • Detoxification: glutathione-S-transferases (GSTs) - glutathione reduces ROS
61
Q

Describe in general terms the common components and the rationale of the AJCC staging system for patients with cancer.

A

Remember: M1 = Stage IV

62
Q

Provide an example and mechanism of action of one drug from each of the following classes of chemotherapeutics: alkylating agent, topoisomerase inhibitor, small molecule tyrosine kinase inhibitor.

A
  • Etoposide (Topoisomerase II Inhibitor)
    • Forms ternary complex with DNA and topoisomerase type II, trapping complex in the cleavable state
  • Cisplatin (Alkylating Agent)
    • Platinum-based chemotherapeutic
    • Forms monoadducts and bis adducts with guanine
    • Non-specific nucleophilic attack damages all macromolecules, but damage to DNA is the most crucial
    • Severe side effects: anemia, GI problems, hair loss
  • Erlotinib (RTK inhibitors) (-nib = tyrosine kinase inhibitor)
    • Selective and competitive EGFR inhibitor
    • Competes for the ATP binding site of EGFR
    • Typically used after failure of 1 prior chemotherapy
63
Q

Describe the cytotoxic mechanism of radiation and explain the concept of chemotherapeutic agents as “radiation sensitizers”.

A
  • Cytotoxic Mechanism of Radiation
    • Causes ds breaks by direct (breaking of phosphate bonds) and indirect (formation of oxygen radicals that act on the DNA)
    • Destroys all cells in the area
  • Chemotherapeutic agents that are highly responsive to ionizing radiation and enhance the effectiveness of radiation treatment are termed radiation sensitizers
    • This is possible by interfering with DNA repair mechanisms and checkpoints
64
Q

Describe (in general) the usefulness and limitations of surgery in the treatment of malignancy.

A
  • Inoperability
    • Age-related issues
    • Encroaching on nearby critical structures - not encapsulated
    • Comorbidity issues (obesity, heart failure)
  • Surgical resection is the first-line treatment in non-small cell lung carcinoma (NSCLC), as chemotherapy typically is not effective as it is on SCLC.
65
Q

Outline the stages of the metastatic cascade and the obstacles that tumor cells overcome to form metastases.

A
66
Q

Discriminate between Phase I, II, and III clinical trials.

A

Phase

Purpose

Phase 1

  • Find a safe dose
  • Decide appropriate route of administration
  • How treatment affects the human body
  • How treatment fights cancer

Phase 2

  • Determine if treatment has effect on specific cancer
  • How treatment affects the human body
  • How treatment fights cancer

Phase 3

  • Compare the new treatment with current treatments

Phase 4

  • Evaluate side effects not apparent in phase 3 trials

SPM (17 decks)

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