Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neoplasia Block > MOD first 3 lectures > Flashcards

MOD first 3 lectures Flashcards

1
Q

Features of malignance

A 
METASTATIC
Invasive
Anaplasia (poor differentiation)
Pleomorphic (bizarre shaped)
Tripolar/mercedes benz mitoses
Disarray
Enlarged nucleus (incr N:C ratio)
Rapid growing (lots of mitoses), large
Necrotic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is cancer of the parenchyma? Cells involved?

A

CARCINOMA (cancer of epithelial origin)
Epith, liver, kidney, etc (fibrous, bc karkinos=hard)
(parenchyma=fxnl part of organ outside circulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is cancer of the mesenchyme called? Cells?

A

SARCOMA
muscle, bone, fat, cartilage, vessels
(CT derives from mesoderm/mesenchyme)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are neuro-endocrine cell tumors called

A 
CARCINOID tumors (eg islets of langerhans, etc) 
All carcinoid tumors are malignant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are tumors of germ cells of gonads?

testicle, 2/3 embryological tissue type

A

Testicle: SEMINOMA (still malig)
2/3 embryological tissue type (ecto/meso/endo) is
TERATOMA (ovarian teratoma common in younger women, forms cystic masses) (benign or malig)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are cancers of WBCs?

A

LEUKEMIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a mesothelioma

A

Tumor in cell of pleural/peritoneal cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hematoma

A

Bruise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Granuloma

A

Collection of immune cells in inflamm, immune sys walls off (histiocytes aka dendritic cell macrophages)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hamartoma

A

A developmental abnormality of disorg tissue of particular system (eg hamartoma of lung)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Choristoma

A

normal tissue found in wrong site (eg pancr tissue in esoph)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What level of differentiation is cancer?

A

POORLY differentiated! (hard to tell what kind of tissue tumor is derived from)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

EPETHELIUM TUMORS: (parenchymal?)
Adenoma/ adenocarcinoma
Squamous carcinoma
Papilloma/ papillary carcinoma

A

Glands
Squamous cells/linings
Papilloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q 
MESENCHYME TUMORS
Lipoma/ liposarcoma
Angioma/angiosarcoma
Chondroma/Chondrosarcoma
Leiomyoma/ Leiomyosarcoma
Rhabdomyoma/ rhabodmyosarcoma 
Osteoma/osteosarcoma
A 
Fat
Blood vessels
Cartilage
Smooth muscle
Striated muscle (eg cardiac)
Bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q 
Neuroma
Meningioma
Glioma/Glioblastoma
Lymphoma/leukemia
Nevus/ melanoma
A 
Nerve (benign?)
Meninges (benign?)
Brain (glioblastoma is most aggressive of gliomas)
Lymphocyte/WBC (always malig?)
Melanocytes in skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PARENCHYMAL MALIGNANT ONLY TUMORS

A

Urothelial carcinoma (transitional cell carcinoma)
Hepatocellular carcinoma
renal cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Neoplasia characteristics

A

Excessive uncontrolled growth/ self governing, irreversible

Monoclonal (cells come from single mother cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What 3 isoforms is clonality determined by, and what ratios characterize these?

A

G6PD Isoforms
(X-linked, 1:1 is hyperplasia, anything diff is neoplasia)
Androgen receptor isoforms
Ig Light-chain phenotype (for B cells; any K:L ratio different from 3:1 could mean neoplasia, prob lymphoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Suffixes that almost always indicate malignancy

A
  • SARCOMA

- CARCINOMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 3 types of malignant spread/metastasis

A

1 Direct (seeding of body cavities)
2 Lymphatic spread (usu in carcinomas)
3 Hematogenous spread (usu in sarcomas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Metaplasia
Dysplasia
Anaplasia

A

Meta: one cell type replaced w another (eg in esoph, bronchus)
Dysplasia: disordered cells, abnormal, pre-malig (eg in cervix, oropharynx, GI) (severe is full epith involvement, thick, may still be in situ ie not invading stroma yet)
Anaplasia: lack of differentiation, malig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cancer definition

A

A genetic disease resulting from DNA mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

WHAT 4 TYPES OF GENES ARE MUTATED IN CANCER GENESIS?

A

1) Promotors of proliferation (eg Ras)
2) Tumor suppressors (eg RB gene)
3) Apoptosis genes (eg p53)
4) DNA repair (eg BRCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

1) mutation in promotors or proliferation

A

eg RAS
protooncogene mutates to oncogene and causes continuous stim
-This is the only one that requires ONE HIT (mutation in one allele only), gain of fxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

2) mutation in TSG

A

eg RB

mutation means lose the brakes, causing cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

3) mutation in apoptosis gene

A

eg p53

mutation means cells that are supposed to die via apoptosis DON’T, so defective cells still multiply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

4) DNA repair mutation

A

eg BRCA

cannot fixed damaged DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Vogelstein’s multi-hit hypothesis for colorectal carcinogenesis

A

Need mutations in lots of types of genes!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Philadelphia chromosome in CML

A

CML is associated with the philadelphia chromosome. this is when BCR from chromosome 9 translocates to ABL on chromosome 22, forming the Bcr-abl fusion on chrom 9:22 (bcr abl is an oncogene, and expresses an abnormal tyrosine kinase which cues abnormal growth signal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What viruses can cause cancer?

A
  • HPV 16 and 18 can cause squam cell carcin of uterine and oropharynx (most common)
  • Epstein barr virus (EBV, a herpes virus) can cause nasophar carcin and lymphoma (like burkitt)
  • HHV8 (human herpes virus 8) can cause kaposi sarcoma and lymphomas in AIDS pts
  • Hep B&C: hepatocell carcinoma
31
Q

Bacteria and parasites that can cause cancer?

A
  • H pylori: gastric MALT lymphoma and gastric adenocarcinoma

- Clonorchis sinesnsis: fluke that can cause bile duct carcinoma

32
Q

What is a lymphoma

A

WBC cancer! (can include enlarged lymph nodes etc)

33
Q

What is Familial Adenomatous Polypsis (FAP) syndrome?

A

germline mutation in APC (adenomatous polypsis coli) gene, a TSG), develop many colorectal ademonas early, need colectomy or eventually dev carcinoma

34
Q

Diff b/n labile, permanent, and quiescent stable cells?

A
  • Labile always profli (eg marrow)
  • permanent: non-dividing, dont give rise to neoplasms (eg neurons and cardiac myocytes)
  • quiesecent stable: in g0 phase, not dividing normally but can enter cell cycle or acquire mutations to give neoplasm (eg liver and renal tube cells)
35
Q

Tumor detectable size

A

1cm (palpation, xray), 1 billion cells, takes 30 divisions (exponential amplification)

36
Q

What is growth fraction and what can decrease this

A

proliferative pool, can be decr by chemo

37
Q

What is the mitotic figure count (histo, eqn)

A 
# mitoses/fields= grade 
(proliferation/mitotic index PI and flow cyometry not done as much anymore)
38
Q

What is immunohistochemistry in measuring cancer prolif rate?
What marker is impt in breast cancer?

A

Use antibodies to prolifreration markers, eg PCNA
Ki-67 (MIB-1) is impt marker in BC (use an ab to this, so if ab binding shows 20% are ki-67 positive, this means theres 20% growth fraction, and these cells are prolif)
-used to determine type of tumor, her-2 also

39
Q

Neoplasia sx

A

asymptomatic
high WBC count
painless lump, fatigue, wasting (cachexia), paraneoplastic syndromes (sx of immune resp against tumor)

40
Q

What are some examples of paraneoplastic sydnromes?

A

any sx really,

carcinoid syndrome, hypercalcemia

41
Q

Carcinoid syndrome?

A

Tumor cells rel serotonin, diarrh, bronchospasm, flushing/sweating, heart failure, GI tract and can flow to liver

42
Q

Hypercalcemia in cancer?

A

squamous cell carcinoma in lung
PTH like hormone rel by tumor cells
abnormal clotting (trosseau’s sign), clot, DIC (small vessel clots)

43
Q

GRADE vs STAGE?

A

grade: differentation and number of mitoses, necrosis (higher grade =more aggro)
Stage: tumor size/spread (MORE impt for prognosis!), higher stage means more extensive spread

44
Q

What are 3 ways of dx neoplasia?

A
  • Monoclonal protein (immunoglobulin, myeloma (plasma cell cancer)/lymphoma)
  • Endocrine/hormones: increased lvls may mean tumor is secreting excess hormones
  • Serum tumor markers (elevated, shed into circ often by tumor in later stage)
45
Q

Examples of serum tumor markers?

A

CEA (carcinoembryonic ag; colon/pancr/lung carcin)
AFP (alpha fetoprot; liver carcin, and testis/ovary/yolk sac tumors)
PSA (prostate specific ag; prostate carcin)
CA-19-9 (cancer ag; pancr adenocarcin)
CA-125 (ovarian carcinomas)

46
Q

Biopsy methods

A

Look @ histology from frozen section

Look @ cytology from needle aspiration or pap smear (less invasive)

47
Q

What does brown stain cytokeratin positive on histo mean

A

carcinoma (keratin, int filament in epith cells)

48
Q

Is meningioma benign?

A

Yes, but can still be fatal (so can hormone producing tumors)

49
Q

Most important prognostic factor of malignant tumor

A

STAGE!

50
Q

Driver vs passenger mutations?

A

DNA mutations that promote tumor development (mutations w no effect are passenger)

51
Q

Primary, immortal, and transformed cells?

A

Primary: divide a limited amoutn of times before senescence
Immortal: divide indefinitely
Transformed: divide indef and other abnormal things like are indep of GFs, anchorage indep; immortal cells can become transformed and cause tumors

52
Q

Evidence that cancer is multistep>?

A

Incidence incr with age (so multiple events req)
Transfection expts (introduce foregin DNA to transform cells and growth)
Oncogene synergy (tumors dev faster if multiple oncogenes activated, eg both myc and fos)
(cancer genes were also ID’d with transforming retroviruses, and genetic sequencing etc)

53
Q

Protooncogene
TSG
definitions

A

Protooncogene is normal gene that becomes oncogene when mutated
TSG prevents tumor formation when activated

54
Q

Diff between proto-oncogene and TSG

A

protoonco: need ONE mutation, gain of fxn (dominant), mutated allele not inherited (eg in germline)
TSG: req TWO mutations, loss of fxn (recessive), often inherited (thru germline), if inherited usu has tissue preference

55
Q

Examples of TSGs

A

RB, APC

two mutations in these can cause inherited cancer syndromes

56
Q

What can mutations in Ras oncogenes do?

A

Can cause it to stay active in GTP-bound form and continually transmit growth signal
(single base substitutions v common)
May be issue with GAP (GTPase activating prot) causing issue with GTPase (which normally conv GTP to GDP)

57
Q

Amplification can occur where on chrom?

A

extra chrom dna called double minutes, or in HSR (homogenously stained region)

58
Q

Burkitts lymphoma mutation

A

c-myc 8:14 translocation, expressed constitutively

59
Q

TYPES OF MUTATIONS in cancer

A

Point mutation (eg ras, SBS’s)
Amplification
Translocation on chrom (eg bcr-abl)
Insertion (Retroviruses ingtegrate near proto-onco, causing synth of abnormal prot, but rare)

60
Q

6 CLASSES OF PROTO-ONCOGENES

A

1) Growth factors
2) Growth factor receptors
3) Signal transducers
4) Transcription factors
5) Inhibitors of apoptosis
6) Cell cycle regulatory proteins

61
Q

1) growth factors

A

overexpression of PDGF, TGF-a of EGF family, etc causing increased cell growth

62
Q

2) growth factor receptors

A

bind growth factors and transmit growth signals via tyrosine kinase activity, eg Her2 receptor can mutate and be const activated, EGF R can have deletion etc

63
Q

3) signal transducers

A

inner memb, transmit growth signals to cytoplasm prots
eg Ras, activated by GNFRF/GEFs and GTP, inactivated by GAPs (???), and Akt (tyrosine kinase which prevents apoptosis and can increase activity if activated)

64
Q

4) Transcription factors

A

const active transcription of cell cycle stuff

eg Myc TF if increased then increases cell cycle prots and cancer

65
Q

5) Inhibitors of apoptosis

A

eg Bcl-2 overexpr decreases apoptosis, (preventing cytochrome C rel from mito, Bax induces apop)

66
Q

6) Cell cycle regulatory proteins

A

eg cyclins combine with CDKs for cell cycle to progress, if cyclin D is overexpressed then faster cell cycle

67
Q

TSG can be inactivated by

A 
point mut
chrom transloc
deletion/insertion
DNA METHYLATION (whereas oncogenes are activated by above stuff and amplification), eg p16 TSG deleted/silenced
68
Q

4 CLASSES OF TUMOR SUPPRESSORS

A

1) cell adhesion
2) Signal transduction
3) transcription regulators
4) DNA repair proteins

69
Q

1) cell adhesion

A

eg e-cadherin loss of fxn allows tumor cells to escape and metast (common in epith cancers)

70
Q

2) signal transduction (3)

A

NF-1 GAP that inactivates RAS by inr GTP hydrolysis, if lost then Ras is const active, icnr cell prolif
Beta-catenin incr transcr /cell cycle w/ Wnt, where APC binds to beta-cat then causes degrad, loss of APC incr transcription and cell cycle progression)

71
Q

3) transcription regulators (2)

A

Rb binds and inactivates TF E2F
CDK can inactiv8 Rb to activate E2F by phosphorylating Rb (loss of Rb fxn inc transcr and cell cycle)
Loss of p53 results in incr survival (normally would prevent dna dmg, incr p21 and bax
-activates mdm-2, a protooncogene that inhibits own p53 fxn

72
Q

4) DNA repair proteins (and cell cycle prots?)

A
  • p16 is CDK inhibitor (inhibits cell cycle), loss of this causes cell cycle incr
  • ATM is a protein kinase activated by double strand breaks in dna, which phosphorylates and activates p53 causing cell cycle arrest, loss of ATM decr p53 activation
  • hMSH2 is dna MMR prot, loss causes accum of mutations
73
Q

STUDY TIPS

A

CLICKER Q’s (molec aspects lecture)
This year’s notesets-review
Practice q’s (canvas, etc?)
IMAGES (gross and histo) in neoplasia 1 lecture

Neoplasia Block (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions