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FPP Block 1 > Introduction to Neoplasia > Flashcards

Introduction to Neoplasia Flashcards

1
Q

metastasis

A

growth at a distant site

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2
Q

what is hyperplasia

A

increased number of cells

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3
Q

what is hypertrophy

A

increased size of cells

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4
Q

what is dysplasia

A

disorderly proliferation

  • change in cell structure
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5
Q

neoplasi

A

abnormal new growth

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6
Q

anaplasia

A

lack of differentiaion

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7
Q

tumor

A

originally mening swelling but now equated with neoplasia

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8
Q

what are the possible cells of origin for a tumor

A

epithelial, mesenchymal, CNS, lymphoid

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9
Q

what do we calle a tumor cell of ______ origin

  • epithelial
  • mesenchymal
  • hematolymphoi
  • melanocytic
  • CNS
  • mixed
A
  • epithelial: carcinoma
  • mesenchymal: sarcoma
  • hematolymphoi: lymphoma, leukemia
  • melanocytic: melanoma
  • CNS: Glioma, Schwanoma
  • mixed: Carcinosarcoma
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10
Q

what are the 3 type of epithelia and what are some rough functions?

A

simple squamous: protective

simple cuboidal:

Simple columnar: absorptive. cilia to increase SA for absorption

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11
Q

what is a tumor of glandular origin called

A

adeno

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12
Q

what is a cancerous epithelia called

A

carcinoma

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13
Q

what s cancer of mesenchymal origin? and what are some examples of mesenchymal cells

A

mesenchymal=below basal lamina

sarcoma

fibroblasts

blood vessels

blood cells

muscle

adipocytes

bone

cartilage

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14
Q

name the benign and malignant name for neoplasia of ______ origin

  • fibroblasts
  • adipocytes
  • smooth muscle
  • skeletal muscle
  • bone
  • caritlage
  • blood
A
  • fibroblasts: fibroma, firbosarcoma
  • adipocytes: lipoma, liposarcoma
  • smooth muscle: leiomyoma, leiomyosarcoma
  • skeletal muscle: rhabdomyoma, rhabdomyosarcoma
  • bone: osteoma, osteosarcoma
  • caritlage: chondroma, chondrosarcoma
  • blood: hemangioma, angiosarcoma
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15
Q

List the 3 categories under neoplasia of hematolymphoid cell origin

A
  • they are based upon when in the differentiation process of a hemotopoietic stem cell does the cancer formation begin

lymphoid neoplasma

myoloid neoplasms

histiocytic neoplasms

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16
Q

melanocytic neoplasm

A
  • neural crest origin
  • may be benign of malignant
    • nevus, melanoma
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17
Q

what are lymphoid neoplasms and what are some examples

A

cells resembling some normal stage of lymphocyte differentiation which serves as one of the bases for their classification

ex: non hodgkin lymphoma, hodgkin lymphoma, lymphocytic leukemia, plasma cell neoplasms

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18
Q

what are myeloid neoplasms and examples

A

arise from progenitor cells that give rise to the granulocytes, red cells, and platelets

acute myeloid leukemias, myeloproliferative disroders

myelodysplastic syndromes

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19
Q

what are histiocytic neoplasms? examples

A

proliferative lesions of macrophages and dendritic cells

ex: langerhans cell histiocytes

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20
Q

describe the difference in behavior of tumors that are benign and malignant

suffix:

morphology

growth rate

growth pattern

metastasis?

A
  • benign:
    • “oma”
    • resemble normal tissue ( well differentiatied)
    • slow growth rate
    • non-invasive, encapsulated (don’t cross basal lamina)
    • do not metastasize
  • malignant
    • carcinoma or sarcoma
    • variable morphology, normal to extremely different from typical tissue
    • variable growth pattern
    • capable of metastasizing
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21
Q

list the 4 characteristics used to differnetiate between benign and malignant neoplasms

A

differentiation and anaplasia

rate of growth

local invasion

metastasis

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22
Q

what do differentiation and anaplasia mean?

what are the categories?

A

the extent to which tumor cells morphologicall and fucntionally resemble the normal tissure counterpart

well-differentiated: resemble normal tissue

moderately-differntiatedL kind of resemble..

pooly differnetiatedL primitive, vague resemblance

anaplastic complete lack of differntiation

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23
Q

what is the difference between a well-differentiated prostate cancer and a poorly differnetiated prostate cancer?

A

well-differentiated resembles benign porostate tissue morphologically. poorly differentiated does not. the tissues do not grow with any sort of pattern. usually poorly differentiated is much more aggressive

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24
Q

describe 3 features of well differentiated neoplasm

A

resembles normal histology

evidence of maturation

evidence of functionality

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25
Q

what are some histological features associated with malignancy

A

cellular nuclear pleomorphism

coarsely clumped chromatin

hyperchromatic nuclei

high nuclear to cytoplasmic ration (nucleus gets big!)

large nucleoli

atypicaly, bizzare mitoses

loss of tissue polarity

tumor giant cells

26
Q

why is this tissue malgnant?

A

nuclear pleomorphism-typically large

coarsely clumped chromatin

27
Q

what about these tissues makes them malignant?

A

hyperchromatic nuclei

28
Q

what about this tissue makes it malignant

A

nuclear pleomorphism with tumor giant cells

29
Q

what about this tissue makes it malignant?

A

atypical mitoses

30
Q

what is polarity and how is it relate to classification of benign v malignant?

A
  • nuclei line up, basal orientation, apical cytoplasm
  • if you flip a slide upside down n a microscope you would still knwo what was up and down. when you lose polarity you lose all 3 of these things!
  • malignant cells often have no polarity
31
Q

how is maturation related to malignancy

A

cell mature to develop their function. for example in the cervix as cells get closer to the surface they get thinner and flatter. in cancer a lto of times cells don’t amture. so instead of seeing the natural progression to flatter cells, the cells look all the same from the basement membrane to the surface. this is cancer!

32
Q

what are 3 features of malignancy

A
  1. cytological atypia
  2. histological dysplasis: architectural anarchy
    1. loss of polarity
    2. loss of maturation
    3. loss of architecture
    4. loss of organization
  3. varies from mild to severe forms
33
Q

what is a benign mixed tumor?

A

a tumor that is both epithelial and mesenchymal. it has multiple morphological components

ex: pleomorphic adenoma

34
Q

what is a malignant mixed mullerian tumor (MMMT)

A

a tumor that invades the myometrium superficially. tumor pushes apart the cervical canal and swells out of the cervix

35
Q

what is a teratoma

A

predominately benign tumor

composed of tissue derive from multiple germ layers-totipotent cells ( as opposed to previous tumors)

36
Q

Hamartoma

A
  • mass of disorgaized, mature tissue which is specific to the site of developemtn
  • represents anomalous development
    • ex: lung hemartoma
37
Q

what is a choriostoma

A

ectopic tissue in a foreign location

ex: gastric heterotopia

38
Q

cancer can either be ______ or invasive

A

in situ or invasive

39
Q

what are the two classifications of invasive cancer

A

locally invasive: potentially curable

metastatic: unlikely curable

40
Q

what does a carcinoma in situ mean? (CIS)

A
  • pre-invasive lesion
  • frequently seen in roximity to invasive tumor
  • malignant cells do not penetrate beyond basement membrane
  • full thickness dysplasia
    • dysplasia: disrodered growth

cancer can be invasive or not. in situ basically means non-invasive

41
Q

Describe on a molecular level how cancers can cross the basement membrane

A
  • Loosening of interacellular junctions (loss of E-cadherin function)
    • inactivation of E-cadherin
    • activation of beta-cadherin
    • NAIL or TWIST (TFs)
  • Degradation of basement membrane
    • matrix metalloproteinases (MMP)
  • Change in attachment of tumor cells
  • Migration through the membrane!! (typically when the intracellular links are disturbed that would trigger apoptosis, but in cacner it doesn’t)
42
Q

what is metastasis

A

a criterion for malignancy

benign tumors do not metastasize, but malignant tumors do

43
Q

where does metastass occur and describe its path/process

A
  • the process of metastais is predictable. based upon:
    • blood flow
    • adhesion molecules
    • chemokines
  • sites of metastasis
    • lymph nodes
    • lungs
    • liver
    • bone
    • brain
  • (colon cancer-liver)
  • (lung-brain)
44
Q

what is the most common pathway for metastasis spread?

A

lymphatic metastasis is the most common pathway for carcinoma spread! however it is raer for sarcomas. LN involvement is predictable based upon normal lymph draineage pathways.

45
Q

what is a sentinel node

A

the first LN to drain the tumor. the start of it all. important for staging cacner

46
Q

besides lymph spread what is another way that cancer can spread throgh the body

A
  • tumor cells implant and/or invade serosal surfaces
  • peritoneal cavity commonly invaded by ovarian cancer ( carcinomatosis)
  • pleural surfaces and pleural effucions in lung cancers
47
Q

what is cancer staging

A
  • process of determining how much cancer is in the body and where it is located
  • describes the serverity of the cancer
    • magnitude/size of the primary
    • extent of spread of the body
  • provides a common language to effectively comunicate about a patient’s cancer and collaberate on the best course of treatment
48
Q

What is the TNM staging system and how do you stage cancer?

A
  • TNM classification system was developed as a tool to stage different types of cancer based upon standardization criteria
    • T-tumor size
    • N-nodal involvement
    • M-metastais
  • note that each cancer type has its
49
Q

WHat are 4 common host reactions to cancer

A
  1. local effects
    1. compression of vital structures (pituitary)
    2. ulceration (bleeding, infection)
  2. Cachexia
    1. cytokine release causes weight loss ex: TNF
  3. Hemotologic abnormalities
    1. anemia, hypercoagulability
  4. paraneoplastic cyndromes-release hormones
50
Q

What is the first step in establishing a targeted therapy regimen for a patient with lung adenocarcinoma?

A

MOIDX Testing

  • two testing techniques: cytogenetic and sequencing (NextGen)
  • basically the next step is to test the genetic sequence to look for common mutations
51
Q

What do EGFR mutations lead to?

A

they alter EGFR kinase activity

52
Q

there are different exons within an EGFR mutation that either predict reactiveness or resistance to EGFR targeted therapy drugs. list the exon(s) that lead to reactivity and the exon(s) that lead to resistance to the drugs

A

Reactivity: Exon 19, Exon 21

Resitance: Exon 20

53
Q

What sequencing did they used to use for assesing EGFR mutation therapy

A

They used to use Dideoxy sequencing which took 2 days and had a lot of steps and was very labor intensive. interpretations and deletions are difficult to precisely interpret

54
Q

what sequencing do they use now to design targeted therapy for lung adenocarcinoma

A

NextGen sequencing.

the depth of coverage is the number of times a base is interrogated by overlapping reads and adequate depth of coverage is essential for accurate variant detection.

55
Q

What s variant reporting

A
  • this is when the genetic variants that nextgen spits out are given clinical meaning.
  • there are rules to approach reporting variables
    • clinical history
    • gene panel (lung, colon, melanoma aka where the gene is located changes the meaning)
    • clinical decision making information
  • there are databases to help!
56
Q

what do you get after you do sequencing and asses the variants for clinical significance?

A
  • actionability aka using the variant to impact treatment
  • you make a form stating the exon and whether or not it will increase reactivity to the drug or resistance and then a recoomended treatment plan including possible clinical trials. this should all occur within 10 work days
57
Q

Describe EGFR as an example of targeted therapy

A
  • if a person has mutant EGFR they can either be treated with target therapy or traditional cytotoxic therapy
    • the type of mutation is how you decide whether targeted therapy is the best choice.
    • certain exon mutatiosn (19 and 21) make targeted therapy better whereas exon 20 means regular therapy is the best choice
58
Q

What are the drugs that are used for Exon 19 and 21 EGFR mutation lung adenocarcinoma

A

Getfitinib (1st gen)

Erlotinib (1st gen)

Afatinib (2nd gen)

59
Q

Describe selective pressure that is put upon tumors with EGFR mutations that are treated with immunotherapy and the significance of this selective pressure

A

when a EGFR mutated tumor has exon 19 or 21 it is treated with immunotherapy. this kills all the tumor cells that are sensitive to these drugs. then all that is left would be the few cells that may not be sensitive to the drug. those cells divide and now all you have left are the cells that are resistant! Then you need to reasses your drug choice bc you have a tumor that is resitant to your drug!

60
Q

What does tumor plasticity and selctive pressure lead to

A

resistance to EGFR TKIs

61
Q

What drug do you use when you have exon 20 T790M

A

Osimertinib

62
Q

Most commone spread of sarcoma

A

hematogenous spread. veins more than arteries

FPP Block 1 (18 decks)

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