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gen path- exam 1 > Neoplasia 3- evasion of apoptosis > Flashcards

Neoplasia 3- evasion of apoptosis Flashcards

1
Q

_______ is the prototypic anti-apoptosis gene

A

BCL2

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2
Q

how can the BCL2 gene be activated?

A

Can be activated by translocation from chromosome 18 to the Ig heavy chain locus on chromosome 14

(shift from chromosome 18 to 14)

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3
Q

what is the result of BCL2 over-expression? where is this situation usually seen?

A

Results in steady accumulation of cells (prevents apoptosis)

– often seen in “low-grade” lymphomas

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4
Q

p53 will upregulate ____, which triggers apoptosis

A

upregulates BAX gene

its a balancing game between BLC2 and BAX

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5
Q

Tumors cannot grow larger than 1 or 2 mm in diameter unless what occurs?

A

they are vascularized

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6
Q

how does Angiogenesis facilitates metastases ?

A

it provides the neoplastic cells access to the vasculature

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7
Q

what are the 2 major steps in invasion/metastasis?

A

1) invasion of the extracellular matrix

2) vascular dissemination and adhesion/homing of tumor cells

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8
Q

how do tumor cells invade the extracellular matrix?

A
  1. Detachment of tumor cells from one another
  2. Attachment of tumor cells to matrix components
  3. Degradation of extracellular matrix
  4. Migration of tumor cells
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9
Q

how can the distribution of tumor metastasis be predicted?

A

can generally be predicted by the location of the primary tumor and its vascular or lymphatic drainage

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10
Q

lung cancer spreading to adrenal glands, but almost never to skeletal muscle, is an example of what?

A

organ tropism

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11
Q

what 2 ways can organ tropism occur?

A

A) Adhesion molecules:
-Organ-specific endothelial adhesion molecules bind tumor cell ligands

B) receptor mediated homing:
-Chemokine receptors on tumor cells home to sites where specific ligands are readily produced

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12
Q

what is Hereditary nonpolyposis colon cancer syndrome? what causes it?

A
  • familial cancers of the colon
  • resulting from defective genes involved in DNA mismatch repair
    • and evidence of microsatellite instability (MSI).
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13
Q

microsatellite instability (MSI) is seen in ____% of colon cancers

A

15%

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14
Q

what is Xeroderma pigmentosum? what causes it?

A
  • defective nucleotide excision repair system
  • Sunlight (UV light) causes pyrimidine cross-linking in DNA, halting replication

**inability to repair UV damage

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15
Q

what (4) disorders are associated with characterized by hypersensitivity to DNA damage (AKA “fragile DNA” diseases)

A

Bloom syndrome
ataxia telangiectasia
Fanconi anemia
familial breast cancers (BRCA1 & 2)

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16
Q

what is meant by the concept of “Multistep Carcinogenesis ”?

A

Cancers typically exhibit multiple genetic alterations including activation of several oncogenes and two or more cancer suppressor genes

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17
Q

what characteristic change as tumors progress through successive “generations”? (how do daughter cells differ)

A
  • they change due to the acquisition of multiple mutations during tumor growth
  • results in numerous “subclones” with different characteristics
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18
Q

CML (“Philadelphia chromosome”) is an example of what Karyotypic change?

A

Balanced Translocations

  • translocation between chromosome 22 and 9. As a result, 22 appears shortened
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19
Q

what types of cancers result from karyotypic deletions?

A

– retinoblastoma (Rb)

  • colon cancer
  • oral cancer
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20
Q

neuroblastoma and breast cancers are both the result of what Karyotypic change?

A

Gene amplification

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21
Q

chronic myelogenous leukemia is the result of balanced _________

A

translocation

  • ALB onconogene is translocated from chromosome 9, onto the BCR locus of chromosome 22
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22
Q

During CML, the BCR-ALB hybrid gene will code for what to be produced?

A

Tyrosine kinase

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23
Q

what are the 3 major classes of carcinogens?

A

1) chemical
2) radiant energy
3) onconogenic viruses

24
Q

Percival Pott was the first to discover __________

A

chemical carcinogens

  • linked scrotal cancer (ouch) to the soot from chimneys
25
Q

what are “indirect carcinogens”

A
  • chemical carcinogens

- they become active only after metabolic conversion

26
Q

what are procarcinogens ? what are ultimate carcinogens ?

A

pro-carcinogens: the inactive chemicals that must be metabolized to become carcinogenic

ultimate carcinogens: the compounds created after metabolism of pro-carcinogens

27
Q

All chemical carcinogens are highly reactive _________, affecting mainly _______

A
  • highly reactive electrophiles

- mainly affect DNA

28
Q

__________ have little inherent mutagenicity, but drive cells to divide, possibly immortalizing DNA alterations

A

Promoters

29
Q

Dentists who held their patients’ films for radiographs often developed what kind of cancer?

A

squamous cell carcinoma of the index finger

30
Q

Survivors of the atomic bombs have had a markedly increased incidence of ________ as well as other cancers

A

leukemia

31
Q

what is an example of a RNA oncogenic viruses ?

A
  • Human T-Cell Leukemia Virus Type I

- endemic in parts of Japan and Caribbean basin

32
Q

HPV and EBV (epstein-barr virus) are both ___________ viruses. what types of cancer are they responsible for

A

DNA onconogenic viruses

  • HPV = cervical cancer
  • EBV = Burkitt lymphoma
33
Q

the ______ virus is responsible for Kaposi’s sarcoma

A

HHV8

34
Q

hepatocellular carcinoma has been linked to what virus?

A

Hepatitis B

35
Q

what is “immune surveillance”

A

refers to the recognition and destruction of non-self tumor cells when they appear

36
Q

what are some examples of tumor-specific antigens? what about tumor-associated antigens?

A

Tumor-specific: Cancer-testis antigens, MAGE-1 (melanoma-associated antigen)

Tumor-associated: prostate-specific antigen (PSA)

37
Q

_____________ antigens are expressed on normal cells, but will be overexpressed on cancer cells

A

Tumor-associated antigens

38
Q

________________ mechanisms are ways by which the body kills tumor cells

A

Antitumor Effector Mechanisms

39
Q

what cell types are involved in anti-tumor effector mechanisms?

A
  • cytotoxic T cells (CD8+)
  • natural killer cells
  • macrophages
  • humoral factors
40
Q

the Selective outgrowth of _____________ variants in tumors helps them evade the bodies immune system

A

antigen-negative

41
Q

what is the effect of a tumor cells tendency to lose or reduce the expression of histocompatibility antigens (HLA antigen)?

A

a lack of HLA antigen means they can avoid attack from cytotoxic T-cells

42
Q

T cells need _____________ molecules to initiate immune response to foreign antigen

A

co-stimulatory molecules

  • sensitization requires 2nd signal together with foreign antigen
  • tumor cells will not produce these molecules, thus avoiding destruction
43
Q

why would certain benign tumors be more serious than others? (assuming neither will metastasize)

A

LOCATION of the tumor

  • benign tumors that are located in critical areas (such as the pituitary) can be very serious.
44
Q

adenomas and carcinomas arising from the beta cells of the pancreatic islets may produce _______________

A

hyperinsulinism

45
Q

Hormone production is more frequent with what type of tumor?

A

well-differentiated, benign tumors

46
Q

what is “Cachexia” characterized by?

A

Characterized by progressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia and anemia

47
Q

__________ is usually a terminal event associated with advanced cancer

A

cachexia

48
Q

why is Paraneoplastic syndrome important in the treatment of cancer?

A
  1. May represent an early manifestation of occult disease
  2. May pose significant clinical problems for affected patients
  3. May mimic metastatic disease and thereby confound treatment
49
Q

what are some examples of paraneoplastic syndromes?

A

A) hypercalcemia
B) Cushing’s syndrome
C) nonbacterial thrombotic endocarditis
D) paraneoplastic pemphigus

50
Q

what is a disease prognosis?

A

defining the grade and stage of a malignancy, we attempt to predict the course of the disease, both with or without treatment

51
Q

grading attempts to assess the _______________ of a malignancy

A

aggressiveness

52
Q

how are malignancies graded?

A
  • Grades can range from I to IV, depending on the particular type of cancer
  • Grade I representing the most differentiated and Grade IV, the least.
53
Q

_________ is a method of estimating cancer size or EXTENT

A

staging

54
Q

how is cancer staging assessed?

A

the size of the primary lesion

lymph node involvement

and metastatic spread (TNM system)

55
Q

what biochemical assays are used to diagnose cancer?

A

prostate-specific antigen (PSA)

carcinoembryonic antigen (CEA)

α-fetoprotein

56
Q

what molecular diagnosis are used to diagnose cancer?

A

FISH

PCR

57
Q

Paraneoplastic syndromes are seen in what % of cancer patients?

A

10-15%

gen path- exam 1 (10 decks)

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