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Block 1 Week 4 > Clinical Cancer 2 > Flashcards

Clinical Cancer 2 Flashcards

1
Q

3 many ways to classify tumors

A

1) organ or tissue of origin
2) cell type (nomenclature)
3) degree of differentiation (resemblance to normal counterpart)

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2
Q

Grading

A
  • level of differentiation

- is pathological

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3
Q

Staging

A
  • shows extent of the spread
  • is mostly clinical
  • most important tumor classification
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4
Q

why need grading and staging?

A

1) quantify probable clinical aggressiveness
2) determine extent & spread
3) make accurate prognosis
4) compare end results of treatment protocol, will guide treatment

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5
Q

How describe grading of a tumor based on differentiation?

A
  • provide it grade 1-4 based on differentiation of the tumor cells
  • although now prefer to use low grade vs high grade because hard to distinguish between the grades
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6
Q

Well differentiated

A
  • Grade 1 (best one to have)

- tumor cells and their arrangement closely resemble their normal tissue counterpart

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7
Q

Poorly differentiated

A
  • (Grade 3)

tumors cells lose their normal staining characteristics, organization and functions

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8
Q

Intermediately Differentiated

A
  • (Grade 2)

- in between grade 1 and 3

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9
Q

Anaplastic

A
  • (Grade 4) the worst

- tumor cells have no resemblance to normal tissue counterpart

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10
Q

how provide grading via microscopic evaluation?

A

1) degree of differentiation of tumor cells
2) number performing mitosis
3) architectural features (types of cell/tissue)
4) necrosis

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11
Q

tumors and their necrosis?

A
  • tumors eventually over grow vasculature & die due to lack of resources
  • tumors that grow fast= less necrosis
  • tumors that grow slow= more necrosis
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12
Q

When do you use staging? what does it tell you?

A
  • where is all the cancer at time of diagnosis
  • tells you extent of:
    1) local invasion (primary tumor size)
    2) regional spread (extent of spread to regional lymph nodes)
    3) distant spread (presence/absence of blood borne metastases)
    4) tumor grade (occasionally)
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13
Q

Why is Staging Important?

A

1) Determines prognosis (estimate)
2) Guides treatment strategy
3) Every cancer has a distinct set of rules; so hard to know how to stage each type, or accurately predict prognosis

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14
Q

3 types of staging?

A

1) TNM Staging
2) Summary Stage
3) clinical staging

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15
Q

TNM staging

A

T – tumor size and extent of local invasion (0-4)
N – involvement of regional lymph nodes (0-3)
M – spread to distant sites and organs (0 or 1)

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16
Q

Summary Stage

A
  • Combines T & N & M scores

- gives out put as I II III IV

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17
Q

Clinical Staging

A
  • non-invasive testing (physical exam, labs, radiologic studies)
  • pathologic staging: information gained from definitive surgery, retrieve piece of tumor to ID it
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18
Q

T in the TNM (x-4)

A

-T= tumor size and extent of local invasion
Tx-Primary tumor can’t be assessed
Tis-Primary tumor not invasive
T0-No evidence of primary tumor
T1-Small minimally invasive tumors
T2-Larger invasive tumors
T3-Very large or deeply invasive or critically located
T4-Invading adjacent distinct tissues (i.e. bone, muscle)

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19
Q

N staging

A

N =Involvement of regional lymph nodes
Based on number, size and location of cancer- containing regional lymph nodes

Nx = Cannot (or did not) assess
N0 – No regional lymph node involvement
N1 – Minimal regional lymph node involvement
N2 – Moderate regional lymph node involvement
N3 – Extensive regional lymph node involvement

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20
Q

M staging

A

M= Spread to distant sites and organs

M0-No evidence of distant spread (metastasis)
M1- Clear evidence of distant spread

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21
Q

what does each stage 1-4 mean?

A

I - Locally confined; surgically resectable for cure
II - Locally extensive, still curable & benefits from adjuvant therapy
III - Locally advanced, requires more than surgery; sometimes inoperable
IV – Metastatic (widespread)
most often not curable

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22
Q

adjuvant therapy

A

-continued radiation/chemo treatment after surgery

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23
Q

do all cancers use this staging system?

A

-no;
1) hematologic malignancies have their own system (leukemias/lymphomas)
2) alternative (very old) systems for prostate, colon melanoma
3) brain cancer lacks staging
TNM always preferred!!!!

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24
Q

what does the primary tumor characteristic in breast cancer tell us?

A
  • some tumor characteristics predict chance of distant spread & prognosis
    1) tumor size
    2) tumor grade
    3) number of lymph nodes (more= worse prognosis)
    4) positive for cancer
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25
Q

8 ways to diagnose type of cancer & TNM?

A

1) Clinical information
2) Histologic methods
3) Cytologic methods
4) Immunohistochemistry (IHC)
5) Flow cytometry
6) Tumor markers
7) Molecular & cytogenetic diagnostics
8) Circulating tumor cells

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26
Q

Histological cancer diagnosis?

A

1) Biopsies

2) Frozen section: rapid evaluation

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27
Q

what do biopsy’s need to be/have?

A
  • must be
    1) adequate in size
    2) representative (take from actual tumor)
    3) properly preserved in formalyn so doesn’t dry out
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28
Q

what do histological frozen sections tell us?

A

histology= study of tissues

1) nature of the lesion
2) it’s margins
3) adequate material
4) decide additional studies, as needed

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29
Q

what is cytology and it’s two types?

A
  • the study of cells
    1) cytologic smears (exfoliative cytology)
    • screen for carcinomas in cervix
    • any sites that shed cells
      2) Fine-needle aspiration (FNA)
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30
Q

Immunohistochemistry (IHC) tells us what about the cancer?

A
  • uses immunologic principles (antigen-antibody complexes)
    1) categorization of undifferentiated malignant tumors
    2) determination of site of origin of metastatic tumors
    3) detection of molecules that have prognostic or therapeutic significance

-help us define treatment

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31
Q

IHC & categorization of undifferentiated malignant tumors?

A
  • undifferentiated tumor cells look nothing like original tissue and can be distant from initial tissue
  • use antibodies to ID specific tissue antigens within the tumor to determine where it initially came from
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32
Q

what do we use flow cytometry for?

A
  • Identify cell antigens expressed by “liquid” tumors (leukemia/lymphoma)
  • Multiple antigens can be assessed simultaneously
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33
Q

How else can you obtain liquid tumor to do flow cytometry?

A

-can take any solid tumor make suspension of cells and run this, ID on DNA content

34
Q

flow cytometry & CBC lab tests?

A
  • When get complete CBC blood count from patient they run blood through flow cytometry
  • light scattered by cells will tell size of cell, size of nucleus irregularities of nucleus, size of cytoplasm
35
Q

what can tumor markers be used for?

A
  • can’t be used for definitive diagnosis of cancer, but:
    1) help w/ detection of cancer
    2) determine effectiveness of therapy
    3) determine appearance of recurrence
  • hcG, PSA, AFRP etc
36
Q

Circulating Tumor Cells

A
  • if tumor invasive, assume it is circulating in blood/lymph
  • doesnt meant it will metastasize in other tissue, just more likely to
  • this testing allows us to do assays of circulating tumor & see if DNA is being shed into bodily fluids
37
Q

What does molecular & cytogenetic diagnostics help us with?

A

1) diagnosis & prognosis of malignant neoplasms
2) detection of minimal residual disease
3) diagnosis of hereditary predisposition to cancer
4) guiding therapy with oncoprotein-directed drugs
* this is personalized med*

38
Q

How determine molecular profiles of tumors?

A

1) DNA microarrays

2) Next gen sequencing

39
Q

gene expression in malignant cells?

A

1) malignant diff from healthy cells in the ratio of normal to mutated genes expressed
2) cancer cells phenotype & genotype based on pattern of genes expressed in malignant tissue
3) similar cancers can vary widely in their prognosis & treatment response

40
Q

what is the hypothesis about understanding pattern of gene expression in cancer cells?

A
  • detailed analysis of pattern of gene expression of a patient’s cancer would enable accurate prediction of rates of response to therapy, risk of relapse, & may suggest novel therapeutic targets
  • this is personalized medicine
41
Q

How is detailed analysis of gene expression accomplished?

A
  • gene expression array analysis

- this is personalized medicine

42
Q

how does gene expression array work?

A

1) compare the level of all expressed genes in a cancer cell with the level of expression of all expressed genes in a same tissue non cancer cell
2) compare variations in patterns of expressed genes in a cancer cell from the same cancer in diff patients

43
Q

which version of the gene expression array is most useful?

A
  • comparing variations in patterns of expressed genes in cancer cells from the same cancer in diff patients
  • can help explain why patients respond differently
44
Q

how can gene expression array help determine treatment & prognosis?

A
  • if know higher expression of gene A= worst prognosis, and patient has elevated gene A expression then need to give more aggressive treatment & know that prognosis is poor
45
Q

what does gene expression array help determine?

A

1) prognosis (chance of death/recurrence)
2) treatment options
3) personalized medicine if possible for patient

46
Q

Next Generation DNA sequencing

A
  • rapid, inexpensive DNA sequencing
  • sequence human genome in 1 day for ~ $1000
  • sanger had to do one base at a time, next gen does it all at once so goes faster
47
Q

three things can do with next gen?

A

1) Whole genome sequencing
2) exon sequencing (just expressed genes)
3) transcriptome sequencing; just trxned genes (is RNA sequencing)

48
Q

Whole genome sequencing in cancer can tells us?

A 
-structural changes
(translocations, deletions)
-gene copy number changes
-point mutations 
-gene expression level changes
49
Q

Exome sequencing in cancer can tells us?

A
  • copy number changes

- point mutations

50
Q

Transcriptome sequencing in cancer can tell us?

A
  • structural variations like fusion proteins
  • translocations
  • siRNA variation
51
Q

What is goal w/ next gen sequencing and cancer treatment?

A
  • want to do sequencing on many patients w/ same cancer, and compare
  • realize that tumors are genetically heterogenous
  • assign personalized treatment to every patient, so treat that persons type of cancer, not cancer generally
52
Q

3 types of Cancer Treatments?

A

1) surgery: resect visible tumor with margins
2) Radiation: lethally irradiate all detectable tumor & include a rim of normal tissue
3) Systemic Therapy: treatment reaches malignant cells throughout body

53
Q

four types of systematic therapy?

A

1) Chemotherapy
2) Hormonal therapy
3) Immunotherapy
4) Targeted Therapy

54
Q

Chemotherapy

A
  • drugs that act through chemical rxt to disrupt normal cell functions & lead to apoptosis
  • attack cells in cell cycle
  • first line of cancer defense
55
Q

Hormonal Therapy:

A

-Drugs that bind to intracellular hormone receptors to block or overstimulate normal gene expression and lead to apoptosis

56
Q

Immunotherapy

A
  • drugs which target or stimulate components of normal immunity to destroy malignant cells
  • enhance immune system
  • antigen specific cancer cell, but also kill healthy cells w/ same antigen
57
Q

targeted therapy

A

drugs that act by interfering w/ specific cell processes unique to the cancer cell
–typically less toxic, more specific than cytotoxic chemo

58
Q

most common chemo targets?

A
  • DNA, RNA, & microtubules

- need rapidly dividing cells to be effective, means if tumor has stopped progressing, then will be less effective

59
Q

normal vs malignant cell damage w/ chemo?

A

-normal cell damage does happen but is easily reversible while malignant cells have lost DNA repair mechanisms therefore they die

60
Q

general trend of tumor growth

A
  • tumors grow w/ gompertzian kinetics
  • means they have fast (exponential) initial phase and slow (quasi linear) in late phase

-this happens cuz tumors outgrow nutrients & oxygen supply so mature tumors are experiencing necrosis

61
Q

chemotherapy and tumor growth issue?

A
  • when tumor is at most rapid point (best for chemo) it is undetectable
  • once reach detectable point only have a small window b4 tumor hits plateau, stops dividing, & is immune to chemo and patient dies
62
Q

how many cancer cells does systematic therapy have to destroy to be effective?

A
  • virtually every cancer cell capable of dividing
  • remission induction treatment, then treat throughout remission (immune system increasing here too) to remove all cancer cells or else will come back
63
Q

how do you optimize systematic treatment?

A

1) maximize dose intensity
2) optimize treatment duration & schedule
3) combine agents w/ non overlapping toxicities & differing mechanisms of action

64
Q

3 uses of chemotherapy?

A

1) primary therapy for chemo-sensitive localized cancers
2) induction therapy for advanced malignancies
3) adjuvent therapy for distant micrometers

65
Q

chemo toxicity?

A
  • toxic to all dividing cells; so see:
    1) hair loss
    2) mucosistis in GI tract
    3) bone marrow depression
    4) gonadal dysfunction (infertility)
  • nausea & vomiting
66
Q

targeted systematic therapy

A

-goal is to block the signaling progression from extracellular receptors to intracellular proliferation signals to prevent growth signals and cell will die

67
Q

how targeted systematic therapy work?

A

-inhibting growth factor signaling by using immune system (antibodies) to block either growth factor itself, the receptor for growth factor or intracellular action of the receptor

68
Q

Targeted Therapy Strategy of attack (4)

A

1) Target the extracellular signaling molecule
2) Target a cell surface receptor
3) Target a novel oncogene
4) Target intracellular signal transduction components

69
Q

chromic myelogenous leukemia (CML)

A

due to translation of chrom 9 & 22. t(9;22)

  • creates a chimeric fusion protein (BCR-ABL) completely unique to cancer; not in body normally
  • protein involves an intracellular tyrosine kinase
70
Q

treatment of CML?

A
  • Imatinib mesylate (Glibic)
  • STI571 signal transduction inhibitor
  • selective & specific inhibitor of tyrosine kinase activity in:
    1) BCR-ABL
    2) c-kit
    3) PDGF-Ra
  • so does have side effects in some healthy cells
71
Q

effects of imatinib mesylate (Glibic)?

A
  • inhibits TK activity
  • good responses in CML accelerated phase & blast crisis
  • effective in low grade GI sarcoma (GIST)- attacks c-kit
  • oral drug w/ few side effects
  • effective in hypereosinophilic syndrome
72
Q

STI571 Mechanism of Action

A

healthy: atp binds BRC-ABL and phoshphorylates substrate on tyrosine kinase, activate downstream stuff
cancer: STI571 binds the ATP binding pocket so can’t phosphorylate substrate and growth halts

73
Q

Support for Patients with Cancer:

A

1) medications
2) nutrition support
3) transfusions
4) blood cell growth factor injections (red, white, & platelets)

74
Q

medications to support cancer patients?

A

1) pain control
2) stool softeners
3) antidepressants
4) energy stimulants – caffeine, ritalin, provigil

75
Q

Nutrition supporter cancer patients?

A

1) calorie & protein rich diet
2) appetite stimulants (due to cahcexia)
3) gastrostomy tube feeding

76
Q

transfusions done to cancer patients?

A

1) red cells, platelets

2) rarely white cells

77
Q

red blood cell growth factor injections?

A
  • erythropoietin
  • stimulates erythropoiesis (RBC production)

-mass produced by recombinant DNA method

78
Q

white blood cell growth factor injections?

A
  • granulocytes – monocytes
  • GCSF (granulocyte colony stimulating factor)
  • GMCSF (granulocyte/monocyte colony stimulating factor)

-mass produced by recombinant DNA methods

79
Q

platelet growth factor injections?

A

not so much

80
Q

Prevention measures for cancer patients?

A

1) Intravenous hydration
2) Antibiotics and G-CSF or GM-CSF
3) Anticoagulation (prevent blood clots)
4) Transfusion & Erythropoietin for low RBC (anemia)

81
Q

Support for Ppatient with cancer?

A

1) cancer support groups
2) emotional support from cancer specific counselors & oncologist
3) palliative Care
4) hospice

82
Q

Palliative Care

A
  • specialty care focusing on relieving physical symptoms & emotional stress from cancer during treatment & after effective treatments have been exhausted & the cancer continues to grow and spread
  • partners w/ Cancer Treatment Specialists who focus on quality of life

Block 1 Week 4 (7 decks)

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