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Block 9 Week 3 > Pulmonary Neoplasms-Barsky > Flashcards

Pulmonary Neoplasms-Barsky Flashcards

1
Q

What is the most common cancer found in the lungs?

A

metastasis from breast, colorectal and endometrial carcinomas; and soft tissue and bone sarcomas and skin melanomas

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2
Q

The (blank) can also be a site of metastasis to the lungs, especially from breast cancer and ovarian cancer (transcoelomic spread)

A

pleura

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3
Q

Why is it important to distinguish a metastasis from a primary lung cancer?

A

Staging
-if primary Stage 1-4 but confined to lung then stage 1-2
-if metastasis stage 4
Prognosis and therapy

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4
Q

How do you distinguish between metastasis and primary lung cancer?

A
  • Microscopic appearance
  • Multiple v solitary lesion (not always discriminatory)
  • Presence of precursor lesions (mets do not have precursor lesions)
  • Organ specific immunocytochemistry
  • Molecular profiling
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5
Q

What cancer is most common in men? What cancer kills the most men?

A

Prostate
LUNG CANCER
BUT its been decreasing since 1990
Having the disease is almost predicition of dying from it

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6
Q

What is the most common cancer in women? What cancer kills the most women? Has it changed as of late?

A

Breast
lung cancer
Slight decrease but not by much

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7
Q

What are the causes (etiologies) of human cancer?

What are the 2 most dramatic causes of lung cancer?

A
  • ENVIRONMENTAL CARCINOGENS
  • UV RADIATION
  • OTHER IONIZING RADIATION
  • VIRUSES
  • LIFESTYLE, DIET, IMMUNE STATUS
  • HEREDITARY FACTORS OR GENES
  • UNKNOWN

Environmental carcinogens and ionizing radiation!

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8
Q

If you alter smoking you can alter what?

A

the incidence and mortality of lung cancer

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9
Q

How do chemical carcinogens lead to lung cancer?

A

Acts by forming DNA adducts which give rise to mutations; if mutations occur in hot spots, spots which change gene expression or protein, mutations can be carcinogenic; if mutations occur in introns or junk DNA or in the non-coding strand they can be harmless

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10
Q

If you quit smoking, do you reduce the likelihood of getting cancer?

A

if you smoke and quit you have declining risk of lung cancer but have an increased risk of disease as compared to a non smokers because you don’t lose all your DNA adducts

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11
Q

T or F

If you quit at a younger age you will have a greater benefit from smoking cessation

A

T

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12
Q

How does ionizing radiation (i.e radon) cause cancer?

A
  • forms DNA adducts

- causes single and double strand breaks

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13
Q

Next to smoking which is clearly the leading cause of lung cancer, the next leading cause of lung cancer is (blank). How do you reduce these levels?
If you get away from radon, can you reduce your risk of cancer?

A 
RADON.
air ventilation (check houses for this)

no because once you have a strand break you cannot repair this

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14
Q

What are the 5 basic categories of oncogens?

A
  • Growth factors
  • growth factor receptors
  • signal transducing proteins
  • nuclear transcription factors
  • cyclins and cyclin dependent kinases
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15
Q

What are the four types of protooncogene functions?

A

Growth inhibitory factors
Molecules that regulate cell adhesion
Molecules that regulate signal transduction
Molecules which regulate nuclear transcription and cell cycle

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16
Q

What is the most important oncogene that causes lung cancer? How can we counteract this?

A

HER-1 (EGFR)

-block the tyrosine kinase domain in HER1

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17
Q

In malignancies, overexpression or dysregulation of EGFR may increase the signaling response and result in….?

A
  • increased invasion and metastasis
  • increased survival
  • increase angiogenesis
  • increased proliferation
  • decreased apoptosis
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18
Q

(blank) is one of the most commonly mutated genes seen in virtually all types of human canceres.

A

TP53

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19
Q

What does TP53 do? If DNA cannot be repaired, apoptosis genes such as (blank) are induced.
Is it predictive for lung cancer?

A

Senses DNA damage arresting cell in GI and induces DNA repair

BAX

-no

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20
Q 
TP53 increases (blank) preventing phosphorylation of RB
It also induces (blank) which aids in DNA repair.
A 
CDKI p21 (CDKN1A)
GAD45
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21
Q

What type of tumor is this:
apex of the lung; invades sympathetic ganglion chain (unilateral sympathetic blockade to the face); rare. Anatomical description is important in terms of presentation.

A

pancoast tumor

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22
Q

What type of lung tumor is this:

easiest to diagnose by bronchoscopy

A

Central

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23
Q

What type of lung tumor is this:

diagnose via needle aspiration. Most common.

A

Peripheral lung tumor

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24
Q

What is the clinical presentation of central lung cancer?

A

cough, chest pain, hemoptysis, sputum

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25
Q

What is the clinical presentation of mid-zonal lung cancer?

A

chest pain

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26
Q

What is the clinical presentation of peripheral lung cancer?

A

Typically silent, pickd up incidentally on chest x ray or CT scan

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27
Q

What is the clinical presentation of pancoat tumor?

A

-horner’s synrome (ptosis, enophthalmos, miosis, anhidrosis) due to invasion of sympathetic ganglion and chain

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28
Q

There are OVER (blank) TYPES OF PRIMARY LUNG CANCER BUT MOST TYPES ARE MINOR TYPES THAT WE DO NOT THINK OF WHEN WE THINK OF PRIMARY LUNG CANCER (i.e. lymphoma, sarcoma, etc.).

A

70

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29
Q

What are the major types of lung cancer?

A
  • small cell carcinoma

- non-small cell carcinoma

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30
Q

What are the three types of non-small cell carcinoma?

A
  • squamos cell carcinoma
  • large cell undifferentiated carcinoma
  • adenocarcinoma
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31
Q

what are the 2 types of adenocarcinoma?

A
  • invase adenocarcinoma

- non-invasive adenocarcinoma (bronchiolaroalveolar carcinoma-BAC)

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32
Q

Central and mid-zonal primary lung cacners are often termed (blank)

A

bronchogenic CA

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33
Q

Central and mid-zonal primary lung cacners are often termed bronchogenic CA. What kind of carcinoma is this?

A

could be either small cell carcinoma or non-small cell carcinoma (squamos, adenocarcinoma or undifferentiated)

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34
Q

When does bronchogenic CA rates peak?

A

55-65 years

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35
Q

What is the leading cause of cancer death in men and women?

A

Central and mid-zonal primary lung cancers (bronchogenic CA)

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36
Q

What is the overall survival rate of central and mid-zonal primary lung cancers (bronchogenic CA)?
(blank) percent have metastases at diagnosis
Strongly linked with (blank)

A

overall 5 year survival only 14%
50%
smoking

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37
Q

How do you treat small cell carcinoma (SCLC)?

A
  • chemoTX with or without radiation

- usually not amenble to surgery

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38
Q

How do you treat non-small cell carcinoma (NSCLC)?

A
  • usually better treated with surgery

- respond poorly to chemoTX (generally)

39
Q

14-18% of primary lung cancers are this.

A

Small cell carcinoma (oat cell carcinoma)

40
Q

Where do you find oat cell carcinoma? What happens to it? What is the carcinoma derived from?

A

central bronchi

  • infiltrate widely and metastasize early (70%)
  • derived from neuroendocrine stem cells (colchiski cells)
41
Q

What does small cell carcinoma produce?

A
  • NSE, neurosecretory granules, neurofilaments

- Makes polypeptide hormones-> paraneoplastic syndromes

42
Q

A (blank) syndrome is a disease or symptom that is the consequence of cancer in the body but, unlike mass effect, is not due to the local presence of cancer cells. These phenomena are mediated by humoral factors (by hormones or cytokines) excreted by tumor cells or by an immune response against the tumor.

A

paraneoplastic

43
Q

What type of lung cancer causes paraneoplastic syndrome? What paraneoplastic syndromes are associate with small cell carcinoma?

A

All lung cancers

  • Cushings disease (ACTH like molecule)
  • SIADH (ADH-concentrated urine and hyponatremia)
  • Neuromuscular syndromes
44
Q

What are all the paraneoplastic syndromes associate with lung cancer?

A

Hypercalcemia (PTH – more likely squamous)
Cushing’s disease (ACTH-like molecule)
SIADH (ADH – concentrated urine and hyponatremia)
Neuromuscular syndromes
Pulmonary osteoarthropathy
-Finger clubbing

45
Q

What causes this:

  • central airway with obstruction
  • well differentiated to undifferentiated
  • tends to cavitate
  • tends to spread LN’s early out later outside of thorax
  • more common in men
A

Squamos cell carcinoma

46
Q

What are the paraneoplastic syndromes associated with squamous cell carcinoma?

A 
hypercalcemia
pulmonary osteoarthropathy (finger clubbing)
47
Q

What percent of lung cancers are large cell carcinoma

A

18-10%

48
Q

What will a large cell carcinoma look like under a light microscope? what is the prognosis?

A

undifferentiated

poor prognosis and metastasize early

49
Q

What is this:
grows slowly but metastasize early
-K-RAS (oncogene mutation) defect in 30%
-form glands

A

Adenocarcinoma

50
Q

What does 30% of adenocarcinomas have?

A

K-RAS defect

51
Q

What percent of lung cancers are adenocarcinomas? Who gets it?
Where are they generally found?

A

37-47% (most common type of lung cancer)
younger (40’s), women and nonsmokers
-generally peripheral

52
Q

What are adenocarcinomas associated with?

How does it progress?

A
  • scars and pneumonia-like pattern

- grows slowly but metastize early

53
Q

Bronchioloalveolar lung cancer (BAC) usually arises (blank)
Can be multifocal or (blank)
Can be diffuse and mimic (blank)
Can be associated with a pre-existing (blank)
Can be mucinous or non mucinous (well differentiated)
What does it usually line?

A 
peripherally
bilateral
pneumonia
pulmonary scar
alveolar spaces
54
Q

(blank) are a form of adenocarcinoma in situ. Adenocarcinoma implies (blank). Where will you find this?

A

BAC
invasion
one fins BAC areas adjacent to adenocarcinoma areas

55
Q

If you have a well differentiated cancer located in the terminal airways, what cancer is it? Does it have a strong association with smoking?

A

BAC (type of adenocarcinoma)

no

56
Q

What is lepidic spread?

What exhibits this?

A

growth of atypical cells along preexistent alveolar walls.

-BACs

57
Q

What are these:
carcinoid (neuroendocrine)
benign harmartomas (chonromas)
mesotheliomas

A

Lung tumors

58
Q

What will carcinoid tumors present with and where do they come from?

A
  • Kilchitsky cells

- Neurosecretory granules- carcinoid syndrome rare

59
Q

What are malignant carcinoids similiar to?

A

small cell cancers

60
Q

Where do most carcinoid tumors occur? (blank) percent can be either atypical carcinoids or malignant carcinoids and metastasize to (blank) and few to distant sites. Atpical or malignant lesions have more (blank and blank)

A

in main stem bronchi (so removal is easier)
30%
hilar lymph nodes and few to distant sites
mitoses and areas of necrosis
(still better to have an atypical carcinoid than some other tumors)

61
Q

What is a bronchial chondroma “coin lesion” and why are these important?

A

benign lesions that are constantly giving false positives for lung cancers.

62
Q

What are the 2 types of neoplastic diseases of the pleura?

A

Secondary-metastatic

Primary- malignant mesothelioma

63
Q

What is primary malignant lung cancer (mesothelioma) associated with? Is it associated with smoking? What is the latency period like?

A 
asbestos exposure (plaques)
no
long latentcy
64
Q

What does mesothelioma do to the lung?

A

it makes the lung encased (restrictive lung disease)

  • direct pushing invasion of the thoracic structures
  • mets are rare
65
Q

What are the three patterns of malignant mesothelioma?

A

sarcomatoid, epithelial, and biphasic

66
Q

What will you see in malignant mesothelioma?

A

Ferruginous bodies

67
Q

What does carcinoma in situ in the central bronchus originate as?

A

squamos cell dysplasia

68
Q

What does atypical adenomatous hyperplasia (AAH) in the periphery originate as?

A

adenomatous hyperplasia (AH)

69
Q

What does mesothelioma originate as?

A

pleural fibrous plaques

70
Q

What does carcinois and small cell carcinoma originate as?

A

Kulchitisky cell hyperplasia

71
Q

What percent of lung cancers are squamos cell carcinomas? What will they be preceded by?
How does it present? How differentiated is it?

A

25-32%
years of metaplasia-dysplasia-CIS
Central airway with obstruction

72
Q

What is this:

  • scar is a precursor lesion
  • adenomatous hyperplasia (AH) and Atypical adenomatous hyperplasia (AAH)
A

Peripheral adenocarcinoma and/or BAC

73
Q

What is the progression of BAC?

A

normal type II pneumocytes in alveolus-> transformed type II pneumocyte in alveolus-> differentiated BAC

74
Q

(blank) is the number of tumors, number of nodes, metastasis (i.e is it metastatic)

A

staging

75
Q

(blank) is the level of differentiation within a cell

A

grading

76
Q

Like in other organ cancers, (blank) determines prognosis and guides therapy

A

staging

77
Q

The basis of this therapeutic molecular classification centers on (blank) triggered signaling and (blank) and (blank) rearrangement tyrosine kinase signaling. These molecular alterations define non-overlapping subsets of lung cancer.

A

EGFR tyrosine kinase
ALK (ANAPLASTIC LYMPHOMA KINASE)
ROS gene

78
Q

10% OF NON-SMALL CELL CANCERS, ESPECIALLY IN NON-SMOKERS, HAVE (blank) MOLECULAR ALTERATIONS.

A

EGFR TYROSINE KINASE

79
Q

5% OF NON-SMALL CELL CANCERS, ESPECIALLY IN NON-SMOKERS, HAVE (blank) REARRANGEMENTS.

A

ALK

80
Q

3-5% OF NON-SMALL CELL CANCERS, ESPECIALLY IN NON-SMOKERS, HAVE (blank) REARRANGEMENTS.

A

ROS

81
Q

Can different non small cell cancers be distinguished pathologically?

A

`no

82
Q

10% of NSCLC cancer is dependent on the (blank) pathway being activated; due to exon deletion or point mutation.

A

EGFR (Her family)

83
Q

What are the anti-HER targeted approaches?

A
  • Her dimerization inhibitors
  • Anti-EGFR blocking antibodies
  • Antiligand blocking antibodies
  • tyrosine kinase inhibitos
  • ligand toxin conjugates
84
Q

What is an example of a HER dimerization inhibitor?

A

trastuzumab

85
Q

What is an example of anti-EGFR blocking antibodies?

What are some tyrosine kinase inhibitors?

A

cetuximab

erlotinib,geftinib, iapatinib

86
Q

What are some ligand-toxin conjugates?

A

TP-38, DAB EGF, ETA fusion toxin

87
Q

(blank and blank) are 2 ATP-competitive inhibitors of the EGFR tyrosine kinase.
Mutations in the tyrosine kinase domain that lead to increased growth factor signaling correlate with increased clinical responsiveness to these TKIs. These mutations demonstrate increased sensitivity to these 2 drugs.

A

Erlotinib and gefitinib

88
Q

Conjugates of a ligand and a cytotoxic agent (eg, TP-38 and DAB389EGF) or an antibody and a cytotoxic agent (eg, scFv-14e1-ETA fusion toxin) are another approach that may have the advantage of killing the cell after (blank), in addition to inhibiting tyrosine kinase activity.

A

internalization

89
Q

EGFR activating mutation and/or deletion result in (blank). Which exons on the EGFR domain are affected? What is wrong with these exons?
What is the effect of this?

A

oncogene addiction
19 or 21

they are either deleted or have a point mutation

the effect of either is self activation and downstream signaling

90
Q

What is the defect found in exon 19? What is the defect found in exon 21?
How can you detect this?
If you detect it then what?

A

deleted
a L858R mutation resulting in an AA sub at position 858 in EGFR from a Leucine (L) to arginine (R)

  • PCR test
  • it makes the tumor sensitive to tx with tyrosine kinase inhibitors: Tarceva or Iressa
91
Q

What are some tyrosine kinase inhibitors?

A

Tarceva or Iressa

92
Q

What is an ALK-EML4 rearrangement?

A

Chromsome 2 has an inversion which creates a EML4-ALK fusion protein-> increase cell survival (BAD) + increaase tumor cell growth (STAT, S6K) + tumor cell proliferation ( ERK, IP3)

93
Q

Tumors with ALK or ROS gene rearrangements are sensitive to (blank)

A

crizotinib

Block 9 Week 3 (6 decks)

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