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Patho II > Neuroplasia part I > Flashcards

Neuroplasia part I Flashcards

1
Q

Benign tumors are defined as ?

A

o Localized lesions
o Without spread
o Patient survival (typically)
o Surgically Removable

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2
Q

Malignant tumors are described as ?

A

o Aka cancer
o Aggressive behavior
o Metastasis

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3
Q

Nomenclature for Malignant vs. Benign

A 
o	Oma (benign)
o	Sarcoma (malignant)
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4
Q

Adult Fibrous tissue: Nomenclature for Malignant vs. Benign

A

Fibroma/fibrosarcoma

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5
Q

Embryonic Fibrous tissue: Nomenclature for Malignant vs. Benign

A

Myxoma / Myxosarcoma

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6
Q

Fat: Nomenclature for Malignant vs. Benign

A

Lipoma / Liposarcoma

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7
Q

Cartilage: Nomenclature for Malignant vs. Benign

A

Chondroma / Chondrosarcoma

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8
Q

Bone: Nomenclature for Malignant vs. Benign

A

 Osteoma/ Osteosarcoma

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9
Q

Blood vessels:Nomenclature for Malignant vs. Benign

A

 Hemangioma / Hemangiosarcoma , Angiosarcoma

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10
Q

Lymph vessels: Nomenclature for Malignant vs. Benign

A

 Lymphangioma

Lymphangiosarcoma

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11
Q

Smooth Muscle: Nomenclature for Malignant vs. Benign

A

 Leiomyoma / Leiomyosarcoma

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12
Q

Striated Muscle: Nomenclature for Malignant vs. Benign

A

 Rhabdomyoma/ Rhabdomyosarcoma

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13
Q

Stratified squamous: Nomenclature for Malignant vs. Benign

A

 Papilloma, seborrheic kertatosis/ squamous cell carcinoma; epidermoid carcinoma

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14
Q

Glandular Epithelium: Nomenclature for Malignant vs. Benign

A

Adenoma/Adenocarcinoma

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15
Q

Liver: Nomenclature for Malignant vs. Benign

A

Hepatic adenoma/ hepatoceullular carcinoma

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16
Q

Kidney: Nomenclature for Malignant vs. Benign

A

 Renal tubular adenoma/ Renal cell carcinoma

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17
Q

Bile duct: Nomenclature for Malignant vs. Benign

A

 Bile duct adenoma/ cholangiocarcinoma

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18
Q

Transitional Epithelium: Nomenclature for Malignant vs.

A

 Transitional cell papilloma / Transitional cell carcinoma

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19
Q

Glial cells (of several types): Nomenclature for Malignant vs. Benign

A

 Glioma/ Diffuse astrocytic and oligodendroglial tumors

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20
Q

Nerve Cells: Nomenclature for Malignant vs. Benign

A

 Ganglioneuroma/ Neruoblastoma, medulloblastoma

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21
Q

Meninges: Nomenclature for Malignant vs. Benign

A

 Meningioma/ Malignant meningioma

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22
Q

Neoplastic cells would constitute the?

A

Tumor parenchyma

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23
Q

Supporting stroma tells you about the?

It is useful for?

A

Micro environment of the tumor cells

 Useful for predicting growth and spread of the tumor

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24
Q

Supporting stroma is composed of ?

A

o Tumor blood and lymphatic vessels, ECM (collagen and hyaluronic acid), and stromal cell constituents

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25
Q

What are the stromal cells constituents?

What is the clinical significance?

A

o Angiogenic vascular cells
o Infiltrating immune cells
o Cancer -associated fibroblastic cells
o An important influence on the malignancy outcome and treatment responses

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26
Q

What are two strategies used to remodel the tumor microenvironment to enchance cancer therapy? Describe their MOAs?

A

o Vascular normalization strategy
 Reduces the pore sizes  improves perfusion  improves the delivery of drugs
 It gets the chemotherapy more efficiently to the tumor so its not leaking out of the blood vessels

o Stress alleviation strategy
 By decreasing stromal expression of TGF- as well as other fibrosis inducing signaling molecules  improves the delivery of drug
 Decrease the pressure on the blood vessel that is causing stenosis of the blood vessel

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27
Q

What does differentiation mean?

A

Differentiation: How closely tumor cells histologically and functionally resemble their normal cell counterpart (cytologist can look at the cytoplasm of the cell and determine its origin- this is a good thing) THIS IS A GOOD THING YOU WANT TO LOOK LIKE THE PARENT CELL

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28
Q

Lack of differentiation is called?

A

Lack of differentiation is called anaplasia (malignancy’s hall mark) (cell loses its cytoplasm and cytologists can determine where the cell is coming from)

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29
Q

Metaplasia means?

A

Replacement of one cell type with another cell type

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30
Q

Dysplasia means?

A

Loss of cellular uniformity and architectural organization

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31
Q

Carcinoma in situ means?

A

Marked dysplastic changes involving the entire thickness of the epithelium

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32
Q

Invasive carcinoma means?

A

The basement membrane is broken, and all the dysplastic cells can leave

33
Q

No local invasion is defined by?

A

Most benign tumors develop a surrounding rim of condensed connective tissue, or capsule

34
Q

Local Invasion is defined by?

A

Malignant tumors are invasive and infiltrative, destroying surrounding normal tissues with no capsule

35
Q

Metastasis is ?

A

o Single most important feature distinguishing benign from malignant*
o Invasion of lymphatics, blood vessels, or body cavities by tumor, followed by transport and growth of secondary tumor cell masses

36
Q

What describe the tumor spread when it is seeding of body cavities and surfaces ?

A

o Dispersion into open spaces like peritoneal, pleural, pericardial, subarachnoid and joint space

37
Q

Most carcinomas spread?

A

Lymphatically

38
Q

Most sarcomas and (renal carcinoma) spread?

A

the blood vessels (lung and liver most common sites of spread)

39
Q

Define Tumor metastatic tropism?

A

o A tumor tendency to metastasize to specific organs

• The tropism indicates the cancer cells ability to adopt to and colonize in the secondary tissues

40
Q

Mechanisms of tumors organ tropism:

A

o Some tumor cells have adhesion molecules
o Some tumor cells have chemokine receptors
o The microenvironment of an organ might not be suitable

41
Q

Prostate cancer are more likely to spread to what organ?

A

Bone Marrow

42
Q

Primary Colon cancer is most likely to spread to what organ? Why?

A

Primary colon cancer mainly metastasizes to liver due to the portal vein drainage from the colon directly into the liver

43
Q

Breast cancer is most likely to spread to what organ?

A

Bone marrow and lung

44
Q

Pancreatic cancer is most likely to spread to what organ?

A

Liver

45
Q

What plays a great influence in where tumors metastases too?

A

The circulation layouts may also greatly influence the metastatic site

46
Q

What are the environmental factors that in risk your risk for cancer?

A
  • Infectious agents
  • Smoking
  • Alcohol Consumption
  • Diet
  • Obesity
  • Reproductive history
47
Q

Why does reproductive history cause an increased risk for cancer?

A

o Starting period at young and age and then going into menopause later in life
 You are exposed to estrogen for a long period of time which is find if you have progesterone to counterbalance it

48
Q

Why does aging cause an increased risk for cancer?

A
  • Due to accumulation of somatic mutations

- Decline of immune response

49
Q

Why does Chronic inflammation increase your risk for cancer?

Chronic inflammation plus ___________ puts you at a higher risk for cancer?

A

o Increases the pool of stem cells that are very prone to mutations
o Chronic inflammation also increases growth factors and cytokines and ROS species

-higher cancer risk with infectious causes

50
Q

What is an example of a precursor lesion that could increase your risk for cancer? Why?

A

o Cancer rarely can rise in the previously benign tumors
 Gastric Reflux – squamous epithelium goes through metaplasia and turns into columnar epithelium because these cells are better suited for the acidic environment. Over time this can become fertile soil for esophageal cancer growth (this has a inflammation component)

51
Q

What disease that causes an immunodeficiency states can increase your risk for cancer?What is it directly related to?

A

HIV-directly related to the T-Cells (nothing to do with inflammation)

52
Q

How does cancerous tumors avoid immune destruction?

A

• Mainly cell-mediated immunity:
o Cytotoxic T cells (CD8+)
o Natural Killer Cells (NK)
o Macrophages
• Tumors won’t produce any antigens that will be recognized by t-cells
• Tumors can produce immunosuppressive proteins
• Tumors can express inhibitory cell surface proteins

53
Q

What is the function of tumor suppressor genes ?

A

• Tumor suppressor genes: slow down cell divisions, repair DNA mistakes and activate apoptosis

54
Q

How does loss of heterozygosity of the tumor suppressor gene correlate to carcinogenesis?

A

• mutation of both alleles of tumor suppressor genes are needed for carcinogenesis
• Examples: RB and p53
o RB: need two mutated alleles of p53  persistent cell cycling  childhood tumor retinoblastoma
o P53 protein “guardian of the genome” because it induces cellular apoptosis for DNA damage that cannot be repaired
 50% of all human cancers is related to p53 mutation

55
Q

What are the purpose of telomeres and telomerase and how do tumor use these concepts to protect themselves?

A

• Telomeres protect the end of chromosomes (they are short DNA sequences at the end of the chromosome)
• When telomere length critically shortens cell undergoes senescence and/or apoptosis
• Telomerase is an enzyme that builds telomeres on the endo of the chromosomes
• In most tumor cells, telomerase is active
o Cancer cells produce telomerase to protect themselves from being killed because they won’t lose their telomeres so they won’t go through apoptosis and they can replicate forever

56
Q

Tumor-promoting cytokines can ?

A

Exacerbate the growth of the tumor

57
Q

Tumor promoting immuninity can?

A

Block our immune system

58
Q

How can cancer therapy induce inflammation?

A

o Necrosis of malignant cells → the release of necrotic products and DAMPs (damage associated molecular pattern’s- produce cytokines and signals to activate immune system) → activate inflammatory cells (immune system produces cytokines)
o Cytokines activate pro-survival genes in residual cancer cells (the tumor cells that weren’t affected by the therapy)→ cancer cells become resistant to following rounds of therapy

59
Q

What is the process of metastasis

A

• Metastatic Cascade:
o Invasion of ECM
o Vascular spreading and homing of tumor cells
• Invasion of ECM
o Detachment and loosening of intracellular junctions
o ECM degradation: by proteases
o Migration: tumor cells have increase locomotion due to cytokines and motility factors

60
Q

What are some theories of how metastasis can occur?

A

o The clonal evolution model  rare variant clones in the primary tumor
 Not all cells have the ability to metastasize so variant clones are produced that have this ability
o Some tumors have high frequency of cells with a “metastasis signature”
 The majority of the cells have the ability to metastasize
o Metastatic variants exist in a tumor with a metastatic signature
 Combination of first and second theory
o Role of tumor stroma which influences angiogenesis, local invasiveness, and resistance to immune defense of the host
 Stromal cells influences angiogenesis and makes the environment suitable for metastasis to happen

61
Q

Genetic risk factors for breast cancer are in what genes?

A

o Mutations in BRCA1 or BRCA2 (DNA repairing genes)

62
Q

What specific cancers involve the mutations of BRCA2?

A

Prostate, pancreas, stomach cancers

63
Q

What are the dual effect that angiogenesis has on tumor growth?

A

• Angiogenesis: new blood vessel growth

• Angiogenesis’ duel effects on tumor growth
o Stimulate tumor growth through endothelial cell production of growth factors
o Influences metastatic potential
• Hypoxia  upregulation of VEGF  Favor angiogenesis
o When tumor cells become crowded, Vascular endothelium growth factor becomes upregulated which favors angiogenesis

64
Q

What type of cells are primed for apoptosis ?

A

• Cells that have a predominance of proapoptotic proteins are considered primed for apoptosis

65
Q

What type of cells are unprimed for apoptosis ?

A

• Tumor cells that have a predominance of antiapoptotic proteins are relatively unprimed to go through apoptosis

66
Q

Tumors need lots of energy to proliferate, how do they manifest all the ATP they need?

A

• In proliferating cancer cells: aerobic glycolysis
o Shunting the pyruvate away from the O2 -PHOSYPHORYLATION
o 85% pyruvate in malignant cells are fermented into lactate and only 5% pyruvate enters into TCA cycle (krebs cycle)- do this at rapid speed faster than normal cells to generate lots of ATP

67
Q

Normal cell proliferation involves the following steps?

A

o Growth factor binding to cell surface receptor
o Activation of signal transduction proteins
o Initiating DNA transcription

68
Q

What are proto-oncogenes and how do mutations affect them?

A
  • Mutations convert proto-oncogenes(normal-associated with cell growth) into oncogenes
  • Oncogenes are genes that promote autonomous (abnormal) cell growth
69
Q

What does tyrosine kinase-mediated signal transduction cause? Mutation of it could lead to?

A

• Tyrosine kinase-mediated signal transduction causes cellular growth, apoptosis and cell migration
• Mutation or abnormal signaling through kinases can inappropriately activate signaling pathways causing neoplastic growth
o Too much activation can cause tumor cells to proliferate

70
Q

What gene is the most commonly involved in human tumors?

A

MYC oncogene

71
Q

How does the MYC oncogene play a role in Burkitt lymphoma?

A

• MYC translocations in Burkitt lymphoma
o An aggressive type of B-cell lymphoma most often in children and young adults (due to the translocation of chromosome 8 and 14 causes MYC overexpression leads to malignancy)

72
Q

If you expose the cell to enough doses of carcinogen there will be?

A

Permanent DNA damage

73
Q

How do Direct acting agents affect DNA?

A

Direct-acting Agents: No metabolic conversion is needed (there are no metabolites needed, agent directly damages DNA)

74
Q

How do indirect acting agents affect DNA?

A

Indirect-acting agents: metabolic conversion is needed

-Ex: Cigarette smoke- produces hypoxide (metabolite) causes changes in cellular structure of DNA

75
Q

How can promotion affect tumors?

A

• Promotion: Can induce tumors in previously initiated cells by stimulating cellular proliferation (agents that cause damaged cells to start expanding)
o Short-lived, reversible and non-tumorigenic by themselves

76
Q

What are the general events in Chemical Carcinogenesis?

A
  1. Carcinogen -metabolic activation
  2. Binding to DNA: Adduct formation
  3. Permanent DNA lesions: Initiated cell
  4. Cell proliferation
  5. Preneoplastic clone
  6. Malignant Neoplasm
77
Q

What cause radiation carcinogenesis?

A

o UV rays of sunlight
→ UV-B: most carcinogenic
→ UV-C absorbed by ozone layer
→ UV-A: produces ROS species

o Ionizing Radiations:
→ Radiations from electromagnetic (x-rays and gamma rays) and particulate (alpha and beta particles, photons, and neutrons) are all carcinogenic

78
Q

How does UV-B rays of sunlight cause carcinogenesis?

A

• How UV-B causes Damage
o The most toxic, mutagenic and carcinogenic UV light-induced DANA photoproducts
 Cyclobutane pyrimidine dimers (CPD’s)
 (6-4) pyrimidine-pyrimidone photoproducts (6-4PPs)

79
Q

How does Ionizing radiation cause carcinogenesis?

A
  • Damage the nucleotides or DNA sugar moieties
  • Cause double strand breaks in DNA
  • Indirect DNA damage by increasing ROS in a cell

Patho II (12 decks)

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