INTRO to neoplasia - EXAM 1 Flashcards

1
Q

What does neoplasm mean

A

new growth thats either benign or malignant

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1
Q

what is hyperplasia

A

an increase size of an organ due to an increased number of cells

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2
Q

what is metaplasia

A

substitution of one type of adult tissue to another type of adult tissue

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3
Q

what is dysplasia

A

an abnormal proliferation that results in loss of normal architecture

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4
Q

What is carcinoma

A

malignant neoplasm of squamous epithelial cell origin

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5
Q

what is anaplasia

A

a loss of structural differentiation. Cells dedifferentiate

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6
Q

what is adenocarcinoma

A

adeno= from glands
malignant neoplasm that started in glandular tissue

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7
Q

what is sarcoma

A

malignant neoplasm that started in mesenchymal tissue (bone, fat, muscle)

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8
Q

lymphoma and leukemia

A

malignant neoplasms of hematopoietic tissues

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9
Q

Melanoma

A

type of cancer of pigment production cells in the skin or the eye

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10
Q

blastoma

A

malignancy in precursor cells - commonly seen in children

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11
Q

teratoma

A

a germ cell neoplasm made of several different differentiated cells and tissue types
(can look real wonky)

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12
Q

Question
A 6 month old boy is determined to have a systemic malignancy originating from precursor cells of the nervous system. the pathology report would state?
A. Adenocarcinoma
B. Neuroblastoma
C. leukemia
D. Metastatic sarcoma

A

B. Neuroblastoma

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13
Q

Numerical staging system:

A

0: in situ carcinoma, no signs of local invasion (hasn’t left the tissue it was first diagnosed in)

I: microscopic invasion of surrounding tissue (not in lymph node but has traveled to surrounding tissues)

II: 4-9 surrounding lymph nodes are involved

III: 10 or more surrounding lymph nodes are involved

IV: distant metastases are detected

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14
Q

TNM staging
Primary Tumor (T)

A

TX: Primary tumor cannot be evaluated
T0: no evidence of primary tumor
Tis: carcinoma in situ
T1,T2,T3,T4: size and or extend of invasion of the primary tumor

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15
Q

TNM staging system
Regional lymph nodes

A

N1,N2,N3 - degree of regional lymph node involvement

16
Q

TNM staging system
Distant metastasis (M)

A

MX: distant metastasis cannot be evaluated
M0: no distant metastasis
M1: distant metastasis is present

17
Q

TNM staging system example
A breast cancer is found to be a large tumor that has spread outside the breast to nearby lymphy nodes but not to other parts of the body

A

T3 N2 MO

18
Q

Question 2
A 48 year old woman has a routine physical examination. A 4cm diameter non-tender mass is palpated in her right breast. the mass appears fixed to the chest wall. Another 2cm non-tender mass is palpable in the left axillary node. A chest radiograph receals multiple 0.5 to 2cm nodules in both lungs. Which of the following TNM classifications best indicates the stage of her disease?
A. T1 N1 M0
B. T1 N0 M1
C. T2 N1 M0
D. T3 N0 M0
E. T4 N1 M1

A

E. T4 N1 M1

19
Q

SEER staging
Summary staging

A

In situ: abnormal cells are present only in the layer of cells in which they developed

Localized: cancer is limited to the organ in which it began, without evidence of spread (primary site)

Regional: cancer has spread beyond the primary site to the lymph nodes or tissues and organs

distant: cancer has spread from primary site to distant tissues or organs or to distant lymph nodes

Unknown: There is not enough information to determine the stage

20
Q

Tumor Grading

A

Gx: grade cannot be assessed
G1: well differentiated
G2: moderately differentiated
G3: poorly differentiated
G4: undifferentiated

21
Q

Oncogene

A

Oncogenes are what initiate cancer and the first example was v-Src

22
Q

Proto-oncogene

A

Gene that has the capacity to cause cancer but hasn’t yet

23
Q

Tumor suppressor

A

Some cancers form from the deletion or mutation of a single proton which is known as tumor suppressor and these tend to fun in families

24
Q

RB1

A

this is a tumor suppressor

25
Q

BRCA1 and BRCA2

A

These are tumor suppressor genes that encode for proteins invovled in the DNA repair

26
Q

How will genome sequencing change personalized cancer treatment

A

oncogenes show a better response to targeted therapies whereas tumor suppressors respond better to chemotherapies

27
Q

Importance of cell cycle in cancer chemotherapy

A

G1: Mitogentic signaling
- G1 is trageted by kinase inhibitors and hormone inhibitors
S: DNA replication
- Targeted by anti-metabolites, anti-folates, and topol inhibitores
G2: Sister chromatid seperation
- targeted by topo2 inhibitors
M: Chromosome segregation
- targeted by microtubule inhibitors

28
Q

Understand how chemotherapies target cancer growth and cancer survival

A

in cancer cells they have lost the checkpoints inbetween each cycle so when chemotherapy causes damage to the DNA in a normal cell it will stop and repair the damage, but in cancer cells they will continue on with the cycle even with the damage which eventually triggers apoptosis

29
Q

Kinetics of cancer cell proliferation (rate of tumor growth, growth fraction, doubling time) and kinetics of cancer cell killing by chemotherapy

A

Tumor cells have lost cell cycle control mechanisms and leads to increased cell proliferation and checkpoints in-between the stages of the cell cycle are often lost

30
Q

Major mechanisms of drug resistance in cancer chemotherapy

A
  1. the cells increase efflux pumps which pushes the drug outside of the cell leaving the drug ineffective
  2. reduce transport into the cell
  3. decreased activation of prodrug
  4. increased detoxification of drug molecule
  5. can also increase amount of cell receptors so that the drug is unable to block all receptors and thus becomes less effective
  6. can change the type of receptor which means the drug can no longer bind to the receptor
31
Q

Most common dose-limiting toxicities resulting from cancer chemotherapy

A

Hematopoietic - WBC - infections, platelets- hemostasis, RBC- anemia
nausea, vomiting, diarrhea, loss of appetite

32
Q

Principles of combination chemotherapy

A

it is impossible to kill all tumor cells with a single dose of drug
Giving dose dense and combination of drugs with distinct mechanisms has shown to improvement in treatment according to norton- simon hypothesis

33
Q

PARP inhibitors

A

Examples: Olaparib, rucaparib, niraparib, talazoparib, veliparib

These are used for cancers with BRCA1/2 mutations (tumor suppressor genes)

they work by trapping PARP to DNA which makes it unable to move to other damaged DNA and repair it which leads to buildup of damaged DNA and usually cell death in the cancer cell

34
Q

Chemotherapy that interferes with DNA synthesis is
A S-phase specific
B G1-phase specific
C cell cycle non-specific D M-phase specific

A

A. S-phase specific

35
Q

Which phase of the cell cycle do you think is targeted by Palbociclib (the CDK4/6 inhibitor)?
A. G1
B. S
C. G2
D. M

A

A. G1

36
Q

What is the most common reason for resistance to multiple chemotherapies at once?
A. Decreased activation of prodrugs
B. Drug transport out of cells
C. Cell cycle changes
D.Mutations in drug targets

A

B. Drug transport out of cells