Intro to Neoplasia II (Putthoff Lect) Ch 7 Flashcards

(67 cards)

1
Q

Describe the changes in grading you would observe in various stages of cervical cancer

A

CIN I (Cervical intraepithelial grade 1) = Start to see a proliferation of cells above the basement membrane,however there is still a maturation process that can be seen

CIN I (Cervical intraepithelial grade 2) = Even more disordered proliferation than grade 1

CIN (Cervical intraepithelial grade 3) = NO MATURATION process is observable

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2
Q

What are these examples of?

A

Basal cell carcinomas

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3
Q

The coarse chromatin feature seen in cancerous cells is due to…

A

HETEROCHROMATIN

*Remeber: It is dense and inactive

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4
Q

Describe the concept of differentiation

A

The degree to which a neoplasm resembles the tissue from which it arises or is derived

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5
Q

What is the major general rule to follow for differentiation of tissue?

A

The less differentiated a malignant neoplasm, the more aggressive it’s biological behavior

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6
Q

What are some examples of well differentiated benign tumors?

A

Leiomyoma

Thyroid adenoma

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7
Q

What is the grading system for malignant neoplasms?

A

Well differentiated

Moderatley differentiated

Poorly differentiated

Undifferentiated

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8
Q

What are general characteristics of benign neoplasms?

A
  • Resemble the tissue of origin
  • Well differentiated
  • Likely to retain functions of their cells of origin
  • Slow growing
  • Circumscribed, may have a capsule
  • Remain localized at the site of origin
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9
Q

What are general characteristics of malignant neoplasms?

A

-Undifferentiated

-Sometimes aquire unexpected functions

-Faster growing

  • Poorly circumscribed, tend to invade surrounding normal tissues
  • Have capability to metastasize to distant sites
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10
Q

What is the ABSOLUTE only criteria for malignancy?

A

METASTASIS

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11
Q

INCLUDE KEY CONCEPTS on page 274 here

A
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12
Q

What are examples of cavitary lung lesions?

A

Bronchogenic carcinoma

Staphylococcal pneumonia

Fibro-caseous cavitary TB

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13
Q

What is a good GENERAL rule to follow when it comes to naming a neoplasia that is either benign or malignant?

A

Benign = -oma

Malignant = -sarcoma

*Remember. This is not a hard rule. Just GENERALLY a lot of malignant cancers have -sarcoma, however they can have -oma at the end. Haven’t seen a benign tumor with -sarcoma at the end though!

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14
Q

There is no such thing as a benign ______ tumor

A

Wilms

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15
Q

Describe the comparison b/w cancer indidence and cancer deaths between men and women

A

Incidence: Men (Prostate most common) Women (Breast most common)

Deaths: Men (Lung most common) Women (Lung most common)

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16
Q

The vast majority of cervical cancers arise from?

A

HPV

(considered a sexually transmitted cancer)

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17
Q

Cervical cancer

What type of cancer?

A

Squamous cell cancer

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18
Q

INSERT KEY CONCEPTS on pg 280 for epidemiology of cancer here

A
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19
Q

Describe development of a tumor

A
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20
Q

Clinically, how big and how many cells does a tumor contain to allow us to identify it?

A

Mass of 1 gram

1 billion cells (10^9)

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21
Q

_____________ can explain not only the natural history of cancer, but also changes in tumor behavior following therapy

A

Selection of the fittest cells

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22
Q

What is one of the most profound selective pressures that cancer cells face?

A

Effective chemo/radiotherapy given by the treating physicians

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23
Q

What are the 4 classes of regulatory genes?

A

Growth-promoting proto-oncogenes

Growth-inhibiting tumor-suppressor genes

Genes that regulate apoptosis

DNA-_repair genes_

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24
Q

How many alleles need to be converted to induce neoplasia for:

Proto-oncogene

Tumor suppressor gene

A

Proto-oncogene = will become an oncogene if ONE of the two alleles is converted

Tumor suppressor gene = will promote neoplasia ONLY IF BOTH alleles are converted. Having one of the two gene products is sufficient to inhibit neoplasia

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25
What type of modifications include: DNA methylation Histone modifications
Epigenetic modifications
26
What is the effect of **DNA methylation** on gene expression?
Silence gene expression
27
What are examples of **proto oncogenes** that are categorized as _growth factor receptors?_
EGF ALK
28
What are examples of **proto oncogenes** that are categorized as _proteins involved in signal transduction?_
RAS ABL BRAF SHH/WNT
29
What is an example of a **proto oncogene** that is categorized as a _nuclear regulatory protein?_
MYC
30
What is the most common type of abnormality involving **proto-oncogenes** in human tumors?
RAS mutations
31
What pathway is crucial for the development of the **bilaterian** feature of humans?
The Hedgehog (HH signaling) pathway along with one of its key regulators (Sonic SHH)
32
General rule for the term **blastoma?**
Generally its a familial cancer seen in **pediatric pop'n**
33
Which proto-oncogene is VERY important and involved in nearly all human tumors?
MYC
34
What is the general description of **MYC?**
A major transcriptional regulator of **_cell growth_** It activates many of the _genes_ that are involved in cell growth
35
What is a unique feature of **MYC?**
Can act to reprogram somatic cells into **pluripotent stem cells**
36
INSERT KEY CONCEPTS PAGE on MYC Oncogene pg 290 here
37
What are the two major tumor suppressor genes?
p53 Rb
38
Table 7-7 What are the inhibitors of **mitogenic signaling pathways?**
APC (AD) NF1 (AD) NF2 (AD) PTCH
39
Table 7-7 What are the inhibitors of **cell cycle progression?**
RB (AD)
40
Table 7-7 What are the inhibitors of **pro-growth programs of metabolism and angiogenesis?**
VHL (AD)
41
Table 7-7 What are the inhibitors of **invasion and metastasis?**
CDH1 (E-cadherin)
42
Table 7-7 What are enablers of **genomic stability?**
TP53 (AD)
43
Table 7-7 What are the **DNA repair factors?**
BRCA1 BRCA2 MSH (AR)
44
What is referred to as the "gaurdian of the genome"? ALSO is the most frequently mutated gene in human cancers
p53
45
What is aka "gatekeeper of colonic neoplasia"?
APC
46
What is related to certain **CNS tumors, renal cysts, neuroendocrine tumors** and **renal cell carcinoma?**
VHL
47
What is commonly known as the "governor of the cell cycle"?
RB
48
What is the difference b/w **familial and sporadic RB mutations?**
*_Familial_* = children inherit one defective copy of the RB gene in the _germline_ (the first hit), and the other copy is normal. Retinoblastoma develops when the normal RB allele is mutated as the result of a spontaneous _somatic_ mutation. *_Sporadic=_* Both normal RB alleles must undergo **somatic** mutation in the same retinoblast (two hits). The probability of this occuring is LOW!
49
What chromosome and where on the chromosome is **p53** found?
Chromosome 17p13.1
50
What happens with a **loss of p53** function?
- DNA damage goes unrepaired - Driver mutations accumulate in oncogenes - Cell is on a dangerous path leading to malignant transformation
51
Loss of p53 is heavily associated with which particular syndrome mentioned in class?
Li-Fraumeni syndrome
52
Where is **WT1** found?
Chromosome 11p13
53
What is loss of **WT1** associated with forming?
Wilms tumor Pediatric kidney cancer \*WT1 was named for the disease it causes when it's non-functional! WT=Wilms tumor
54
What is a major immunotherapy mechanism used to treat cancer?
Use of monoclonal antibodies that target either **PD-1/****PD-L1/CTLA-4** This will boost the immune response to cancer cells
55
Describe the concept of **angiogenesis** in cancer formation
Development of blood supply to the newly formed mass
56
Table 7-8 State the translocation _Chronic myelogenous leukemia (CML)_
(9;22) (q34;q11)
57
Table 7-8 State the translocation **Acute myeloid leukemia (AML)**
(8 ; 21) (q22 ; q22) | (15; 17) (q22 ; q21)
58
Table 7-8 State the translocation **Burkitt lymphoma**
(8 ;14) (q24; q32)
59
Table 7-8 State the translocation **Mantle cell lymphoma**
(11 ; 14) (q13 ; q32)
60
Table 7-8 State the translocation **Follicular lymphoma**
(14, 18) (q32, q21)
61
What are the most frequent **radiation induced cancers?**
Myeloid leukemias
62
Microbial carcinogenesis What is the **ONE oncogenic RNA virus?**
HTLV-1
63
Microbial carcinogenesis What are examples of **Oncogenic DNA viruses?**
HPV EBV HBV Merkel cell polyomarvirus (MCV) HHV-8
64
What are **paraneoplastic syndromes?**
Tumor cells themselves elaborate certain substances that have effects
65
What is the most common **paraneoplastic syndrome?**
Endocrinopathy
66
What is **chromothripsis?**
Widespread chromosomal issues are occuring with cancer "Genome instability characterized by _tens to hundreds of locally clustered rearrangements_ affecting one or more chromosome(s) in cancer cells. This phenomenon, is likely due to a single **catastrophic event** leading to the simultaneous formation of multiple double-strand breaks, which are repaired by error-prone mechanisms"
67
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