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Pathophysiology > TBL 2 > Flashcards

TBL 2 Flashcards

1
Q

what is a tumor suppressor gene?

A

a type of gene that makes a protein called a tumor suppressor protein that helps control cell growth

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2
Q

what does a normal tumor suppressor gene do and what does a mutated one do?

A

normal: represses genes essential for continuing cell cycle, apoptosis, couple cell cycle to DNA damage, cell adhesion, DNA repair proteins, vascular proliferation
mutated: affects 1 of the 6 factors in the ‘hallmark of cancer’

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3
Q

what are the 2 most well-characterized tumor suppressor genes?

A

p53 and Rb

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4
Q

what does Rb do?

A

puts the breaks on the cell cycle by preventing transcription of genes necessary for DNA replication

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5
Q

what are the p53 domains?

A

DNA-binding, oligomerization, NLS (moves the gene in and out of nucleus/cytoplasm)

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6
Q

what does the mdm domain do?

A

targets p53 for degradation

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7
Q

what is an oncogene?

A

mutation of a gene that has the potential to cause cancer

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8
Q

what is Ras?

A

oncogene that is important for the growth, proliferation, and migration of cells

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9
Q

what is Bcr-abl?

A

a translocation mutation

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10
Q

what are some examples of growth factors?

A

epidermal growth factor receptors, platelet derived growth factor receptor, vascular endothelial growth factor receptor and human epidermal growth factor

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11
Q

what are viruses made up of?

A

small number of genes in the form of dna or rna surrounded by a protein coat

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12
Q

how can a virus push a cell into becoming cancerous?

A

forces cell into S-phase

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13
Q

what are some viruses that can be linked to cancer?

A

EBV, HIV, Hepatitis B and C

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14
Q

describe how hpv can be linked to cancer

A

E7 oncogene binds to ubiquitin ligase which binds to p53 and targets it for degradation

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15
Q

what is a carcinoma?

A

malignant tumor derived from epithelial tissues

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16
Q

describe an adenocarcinoma?

A

derived from glandular epithelium that line in the insides of your organ

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17
Q

what is a sarcoma?

A

malignancy derived from mesenchymal cells

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18
Q

what do mesenchymal cells develop into?

A

connective tissue, blood vessels and lymphatic tissue

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19
Q

what is Her2 overexpressed in?

A

overexpressed in 20% of breast cancers and has also been found to be overexpressed in certain brain, lung, ovarian, stomach, and salivary glands

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20
Q

describe Her2

A

growth factor (oncogene, has tyrosine kinase activity) receptor that regulates cell growth, differentiation, and potentially angiogenesis → when overexpressed it can cause malignancy and a poor prognosis in breast cancer

monomer that dimerizes with ligand binding though no specific ligand that binds to HER2 has been identified
HER2 becomes overexpressed when HER2 heterodimers are formed which leads to enhanced responses to growth factors and oncogenic transformation.

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21
Q

how can we reduce the prevalence of cancer caused by Her2?

A

removing HER2 from the cell surface or inhibiting the enzyme activity, monoclonal antibody therapy that binds to Her2, or one that blocks it, from overexpression: Trastuzumab

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22
Q

how do you test for Her2 expression?

A

Assay testing: overexpression of Her2 protein → western blotting, ELISA, or immunohistochemistry (IHC) OR Her2 gene amplification testing by FISH, or PCR

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23
Q

what is staging used for?

A

to determine the extent of the cancer such as how large the tumor is and if it has spread

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24
Q

what does the T in TNM cancer staging describe?

A

describes the size of the tumor and any spread of cancer into nearby tissue

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25
Q

what does the N in TNM cancer staging describe?

A

describes the spread of cancer to nearby nodes

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26
Q

what does the M in TNM cancer staging describe?

A

describes metastasis

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27
Q

what is a leukemia and what are some examples?

A

cancers of white blood cells that start in the bone marrow (AML, ALL, CML, CLL)

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28
Q

what is a lymphoma and what are some examples?

A

cancers that start in the lymph system
(Hodgkins: contains Reed-Sternberg cells, Non-Hodgkin’s: no Reed-Sternberg cells)

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29
Q

what are the symptoms of acute leukemia?

A

fatigue, fever, bleeding, infection, gingival swelling, joint pain

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30
Q

what would a CBC of a patient with acute leukemia look like?

A

low to high WBCs, presence of peripheral blasts

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31
Q

what is the timeline for acute lymphocytic leukemia?

A

peak incidence occurs in early childhood

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32
Q

what is the timeline for acute myelogenous leukemia?

A

usually occurs >50

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33
Q

what does CAR-T stand for?

A

Chimeric Antigen Receptor T-Cells

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34
Q

what are CAR-T cells?

A

T-lymphocytes that are genetically modified to replace the T-cell receptor (TCR) with synthetic receptors, s-CARS, to recognized and eliminate cancer cells independent of major histocompatibility complex (MHC)

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35
Q

what is the function of CAR-T cells?

A

antibody specific properties, proliferation, cytokine production and elimination of targeted cells, allows the modified T cell to recognize more extensive targets than the natural TCRand enables T cell expansion, withstands tumor related immunodeficiency and avoids tumor escape by HLA down regulation

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36
Q

what is the structure of a CAR-T cell?

A
  1. an extra cellular Ag binding domain; it contains an Ag recognition regions of an Ab single-chain variable fragment that binds specifically to the target molecule expressed on the surface of the tumor cell
  2. an extracellular hinge region: it is made of Ig like CD8, CD28, IgG and assists in signal transduction
  3. a transmembrane domain
  4. an intracellular signaling or T-cell activation domain: it is the functional part of the CAR and consists of CD3 chain of TCR which provides the activating signal.
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37
Q

how long does the process of developing CAR-T cells take?

A

about 3 weeks

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38
Q

what is the process of developing CAR-T cells generally?

A

obtaining a T-cell from a patient and converting them outside the body and reinsertion of the modified cells into the human body to target cancer cells

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39
Q

what are the steps of developing CAR-T cells?

A
  1. T cell collection by leukapheresis
  2. T cell activation
  3. T cell expansion
  4. Genetic modification to create CAR T cells
  5. Expansion in ex-vivio
  6. Transfusing the appropriate dose of the expanded CAR T cells back into the patient
40
Q

what have CAR-T cells shown improvements in?

A

hematologic malignancies, including relapsed and refractory B-cell malignancy, such as B-cell non-Hodgkins lymphoma (NHL), acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL)

41
Q

what was the first target of CAR-T cells?

A

CD19

42
Q

what is Tisagenlecleucel approved for?

A

treatment of relapsed and or refractory B cell precursor ALL in children and adults with DLBCL

43
Q

what is Axicabtagene ciloleucel (Yescarta) approved for?

A

treatment of adults with relapsed or refractory large B-cell lymphoma including diffuse large B-cell lymphoma (DLBCL)

44
Q

what are toxicities associated with CAR-T cells?

A

Cytokine release syndrome (CRS) is the most common adverse side effect which manifests as a systemic inflammatory response and neurotoxicity (CAR related encephalopathy) is the second most common (altered level of consciousness, seizure, aphasia, coma and cerebral edema

45
Q

how is cytokine release syndrome reversed?

A

IL-6 blocking Ab (tocilizumab and corticosteroids)

46
Q

how is neurotoxicity reversed?

A

anti-epileptics and steroids

47
Q

describe acute lymphocytic leukemia

A

most common cancer in children, proliferation of of immature nonfunctional WBCs - leading to pancytopenia
May develop extremely high WBC count, increasing risk for leukostasis and DIC

48
Q

what is the generalized treatment regimen for ALL?

A

chemo regimen of high dose and low dose cycles - can use allogeneic stem cell transplants if prognosis is poor or if chemo fails

49
Q

what is the initial phase of ALL treatment and what is the timeline for it?

A

Induction therapy using systemic chemo, average duration of induction chemo for ALL is 4-8 weeks
would eventually lead to consolidation chemo lastsing 4-8 months, then maintenace chemo of 2-3 years

50
Q

what chemotherapy regimen is commonly used to treat ALL?

A

hyper-CVAD - cyclophosphamide, vincristine, daunorubicin (Adriamycin) and dexamethasone

51
Q

what are the main classes of drugs used in initial treatment of ALL?

A

Alkylating agents, Anthracyclines, Antimetabolites, Enzyme therapy, Alkaloids and Glucocorticoids

52
Q

describe alkylating agents

A

Alkylizizes DNA (adds chemical groups to it) to damage DNA and decrease DNA replication (Cyclophosphamide, Cisplatin, Ifosfamide)

53
Q

describe anthracyclines

A

inhibits topoisomerase and DNA and RNA synthesis, DNA intercalation breaks DNA strands and decreases DNA replication, does DNA strand excision, makes free radicals to cause DNA damage (Daunorubicin, Doxorubicin)

54
Q

describe antimetabolites

A

interferes with cellular division, impairs DNA replication by destroying the machinery and deoxynucleotides needed for DNA synthesis (Cytarabine, Methotrexate, 6-mercaptopurine)

55
Q

describe enzyme therapy

A

cleaves off AA of L-asparagine and is cytotoxic to leukemic cell (L-asparaginase)

56
Q

describe alkaloids

A

inhibits beta-tubulin from polymerizing into microtubules - therefore preventing mitotic spindle formation and causes mitotic arrest of the cell in metaphase (Vincristine)

57
Q

describe glucocorticoids

A

reduces immune response, especially after a bone marrow transplant (prednisone, dexamethasone)

58
Q

what are the typical symptoms of ovarian cancer?

A

Abnormal vaginal bleeding/discharge, Pelvic pain/pressure, Dyspareunia, Abdominal/back/leg pain, Bloating/swelling, Change in bathroom habits, GI, Loss of appetite

59
Q

what are risk factors of ovarian cancer?

A

BRCA ½, Prolonged estrogen exposure, Endometriosis

60
Q

what are the subtypes of ovarian cancer and their percentage of occurrence?

A

germ cell - 5%
ovarian stromal cell - 5%
epithelial - 90%

61
Q

describe germ cell

A

forms in eggs, usually unilateral, most common in teenage girls and young women under 20

62
Q

describe ovarian stromal cell

A

in structural connective tissue that produces estrogen/progesterone, seen in adolescents and young adults

63
Q

describe epithelial

A

starts in surface layer/lining of ovary, >40 years, 50% in women 65+

64
Q

what is the primary risk factor for developing cervical cancer?

A

HPV

65
Q

how does HPV use passive evasion?

A

HPV can evade detection by minimizing antigen production while it is in its vegetative state, In early phase, expresses small amt of proteins and the ones that are expressed are promptly transferred to the nucleus
Doesn’t allow enough time for detection
During late phase, expresses immunogenic capsid proteins BUT these are shed quickly from the outer epithelium, few APC here

66
Q

how does HPV use aggressive evasion?

A

Expresses oncoproteins E6 and E7, target cell cycle control center, controls apoptosis, facilitates DNA damage, high binding affinity to immune regulators, keratinocytes, innate leukocytes, langerhans , block immune-related gene expression and signaling, downregulates MHCI and interferon synthesis
Results in overall immunosuppressive environment that promotes cancer

67
Q

what are the symptoms of cervical cancer?

A

Often asymptomatic, vaginal bleeding after intercourse, between periods, after menopause, heavier/longer periods, water, bloody vaginal discharge, may be heavy, may have foul odor, pelvic pain or pain during intercourse

68
Q

describe the USPSTF guidelines for cervical cancer screenings

A

21-65 years old
21-29: pap smear every 3 years
30+: pap every 3 years OR primary HPV testing alone every 5 years OR pap and HPV testing together every 5 years

69
Q

what is a colposcopy?

A

diagnostic procedure in which a colposcope (dissecting microscope) is used to provide illuminated, magnified view of cervix, vagina, vulva, and anus → typically used as a follow up test from abnormal cervical cancer screenings

70
Q

what is the primary goal of a colposcopy?

A

identify precancerous or cancerous lesions to be treated early (most notably for cervix)

71
Q

what are contraindications for a colposcopy?

A

cervicitis, anticoagulation diathesis, pregnancy, and immunosuppression

72
Q

what area does a colposcopy mostly focus on?

A

squamocolumnar junction and transformation zone

73
Q

why is the transformation zone at a greater risk for neoplasms?

A

area of squamous metaplasia that contains embryonic cells that may be more vulnerable to infection, like HPV → cancers

74
Q

what would a biopsy following a colposcopy be looking for?

A

cervical intraepithelial neoplasia
Grade 1: abnormal cells in deep third of epithelium
Grade 2: abnormal cells make up 2/3 of epithelium
Grade 3: abnormal cells make up greater than 2/3 of epithelium

75
Q

what is carcinoma in situ?

A

the entire epithelium is made up of abnormal cells but do not make it past the basement membrane (like in invasive cervical cancer)

76
Q

what is the follow up if no cervical intraepithelial neoplasia is found?

A

another pap and HPV test in 12 months, if both are negative a repeat is done in 3 years, if negative again individual can resume routine testing

77
Q

what are the substages of stage 1 cervical cancer?

A

1A1: less than 3mm
1A2: bigger than 3mm, less than 5mm
1B1: bigger than 5mm, less than 2cm
1B2: bigger than 2cm, less than 4cm
1B2: bigger than 4cm

78
Q

what are the substages of stage 2 cervical cancer?

A

2A1: cancer has spread past cervix but is still less than 4cm
2A2: bigger than 4cm
2B: cancer has spread to connective tissue surrounding the uterus

79
Q

what are the substages of stage 3 cervical cancer?

A

3A: cancer has spread to lower vagina
3B: cancer has spread to pelvic wall
3C: can be any size, has spread to lymph nodes

80
Q

what are the treatment options for carcinoma in situ?

A

Excision, can use loop electrical excision procedure or cold knife colonization
Ablation through cryotherapy or laser
Total abdominal hysterectomy and bilateral salpingo-oophorectomy if childbearing is not wanted

81
Q

what are the treatment options for stage 1A1?

A

Total hysterectomy
Radical hysterectomy
Conization

82
Q

what are the treatment options for stages 1A2, 1B and 2A?

A

Combined external beam radiation with brachytherapy
Modified radicial hysterectomy with bilateral pelvic lymphadenectomy
Chemotherapy or radiation can be used if risk of recurrence

83
Q

what are the treatment options for stages 2B and 3?

A

Radiation therapy and chemotherapy especially Cisplatin-based

84
Q

what is the treatment option for metastatic cervical cancer?

A

Systemic chemotherapy
Radiation

85
Q

what are the risk factors for prostate cancer?

A

The most important risk factor is increasing age, African American followed by white, diet, high fat, high red meat, high dairy, obesity (not more likely to develop prostate cancer but more likely to develop an aggressive form), positive family history, BRCA 1 and 2, Vietnam Veterans due to agent orange exposure

86
Q

what would prostate cancer look like on a DRE?

A

may be a palpable hard mass, induration, or unilateral enlargement of the prostate, DRE can only detect tumors in the posterior and lateral aspects of the prostate gland

87
Q

what is the most accurate test for prostate cancer?

A

Transrectal ultrasound (TRUS)-guided prostate biopsy

88
Q

what are the risk factors for testicular cancer?

A

Caucasians, Klinefelter’s syndrome, Hypospadias, Men 15-35, Cryptorchidism can have a 4-10x increased risk in both undescended and normal testicles

89
Q

what is the clinical presentation of testicular cancer?

A

Painless testicular mass, does not transilluminate, testicular swelling or firmness, testicular heaviness or dull pain, cough, SOB, hemoptysis if metastasized

90
Q

what are common lab markers for testicular cancer?

A

Increased alpha-fetoprotein in Nonseminoma and not elevated in pure Seminomas, Increased beta-hCG in Nonseminoma
Lactate dehydrogenase (LDH) can be assessed for metastasis

91
Q

Seminoma vs Nonseminoma

A

Seminoma (hypoechoic mass), Nonseminoma (cystic, non-homogenous mass)

92
Q

what are the risk factors for colorectal cancer?

A

Primary risk factors: age, family history, lifestyle, IBD ,
Ethnic backgrounds: African American and Jews of Eastern European descent, Adenomatous polyps

93
Q

what is the clinical presentation for colorectal cancer?

A

Iron deficiency anemia (fatigue, weakness), rectal bleeding, abdominal pain & change in bowel habits
Most common cause of large bowel obstruction in adults

94
Q

what are the risk factors for pancreatic cancer?

A

Age, Having non-O blood type, Smoking, High intake of fat or meat

95
Q

what is the clinical presentation for pancreatic cancer?

A

Abdominal pain and weight loss with or without jaundice, pain is mid epigastric and can also have pain in the back which is worsened by laying flat or eating, light stool color due to absence of bile, physical signs include jaundice, signs of weight loss, a palpable gallbladder (Courvoisier’s sign), hepatomegaly, an abdominal mass, and even an enlarged spleen

96
Q

what are the risk factors for bladder cancer?

A

Smoking, Exposure to industrial chemicals
Occurs more in men than women

97
Q

what is the clinical presentation for bladder cancer?

A

uncomfortable voiding (irritative voiding sx) , Hematuria (blood in urine)

Pathophysiology (1 decks)

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