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Pathopharmacology > Unit 2 Pathophysiology - Chapter 12 Cancer Biology > Flashcards

Unit 2 Pathophysiology - Chapter 12 Cancer Biology Flashcards

1
Q

Benign tumors

A
  • encapsulated
  • contain differentiated cells
  • organized stroma
  • do not spread
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2
Q

Malignant tumor

A
  • rapid growth
  • anaplasia (loss of maturity + functions)
  • loss of differentiation
  • no cell organization
  • no capsule
  • invade blood vessels + lymphatics + distant metastases
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3
Q

Carcinomas and leukemias arise from?

A

Epithelial tissues // leukemias

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4
Q

CIS or carcinoma in situ

A

preinvasive epithelial tumors of glandular or squamous cell origin

early stage cancers localized to epithelium and did not penetrate local basement membrane (right under epithelium) and did not invade surrounding stroma

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5
Q

Genetic changes - cancer

A

small, large DNA mutations in genes, chromosomes, non-coding RNAs, altered chemical modifications of DNA + histones (epigenetics)

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6
Q

Chromosome translocation

A

partial or whole chromosome breaks off and attaches to another

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7
Q

gene amplification

A

Increase in number of genes; maybe also more RNA and protein production from gene

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8
Q

DNA methylation

A

methylation of the DNA sequence of a gene may turn the gene off so it does not make a protein.

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9
Q

histone acetylation

A

By modifying chromatin proteins and transcription-related factors, these acetylases are believed to regulate the transcription of many genes.

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10
Q

altered expression of non–coding RNA

A

chromatin remodeling, regulate gene expression at transcriptional or post-transcriptional

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11
Q

Driver mutations

A

drive progress of cancer

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12
Q

Passenger mutations

A

random events; along for the ride hehe

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13
Q

Cancer cell can develop own mutations?

A

Yes, resulting in genomic heterogenous mixture of cancer cells w/ subsets that accumulate more mutations => increase malignant potential

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14
Q

Development of cancer analogus to what?

A

Wound healing

initial proliferation of cancer cells and enlarging tumor => creates proinflammatory mediators by cancer cells + adjacent nonmalignant cells

These mediators => recruit inflammatory/immune/tissue repair cells forming the stroma (connective, functionally supportive framework of a biological cell, tissue, or organ) that surround and infiltrate tumor

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15
Q

Stromal and cancer cells relation

A

D/t extensive paracine signaling amongst both populations

  • increased proliferation and heterogenous growth during tumor growth
  • stromal cell phenotypes that promote more cancer progressio nand metastatic potential
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16
Q

Hallmarks/enablers of genomic alterations for cancer

A
  1. sustained proliferative signaling
  2. evade growth suppression
  3. genomic instability
  4. replicative immortality
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17
Q

Hallmark secondary to genomic change

A

cellular adaptations, including angiogenesis (formation of new blood vessels) and reprogramming energy metabolism

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18
Q

Hallmark/enablers - protective mechanisms

A

apoptotic cell death, promote tumor inflammation, avoid immune destruction

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19
Q

last hall mark - most important?

A

culmination of all previously mentioned: activating invasion and metastasis

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20
Q

Cancercous cells express specifically what?

A

mutated or overexpressed proto-oncogenes (oncogenes), they are independent of normal regulators and signal uncontrolled proliferation

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21
Q

RAS oncogene

A

result from point mutation, all Ras proteins are GTPases which act as molecular switches in the cell, regulating signaling pathways and other interactions until they mutate and for cancer

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22
Q

Philadelphia chromosome in CML or chronic myeloid leukemia

A

Comes about d/t translocation that creates novels protein fusion of BCR + ABL genes and expression for unregulator promotor of cell growth

Abl is tumor suppressor gene

BCR protein may act as a GTPase activating protein (GAP). GAPs turn off (inactivate) proteins called GTPases, which play an important role in chemical signaling within cells.

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23
Q

How do Tumor suppression genes work in cancer

A

mutations of each allele, for each parent in terms of inactivating said gene

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24
Q

Common mutation in cancer cells

A

inactivation of tumor suppressor gene, tumor protein P53 (TP53) important in contrlling gene expression for DNA damage repair, suppression of cellular proliferation during genomic repair, and apoptosis initiation => resulting mutation rates and cancer

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25
Q

inheritable tumor-suppressor gene

A

TP53, retinoblastoma gene (RB) [nuclear protein that acts as a cell cycle control checkpoint at the G1 phase], or breast cancer genes [BRCA1 and BRCA2]

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26
Q

Caretaker genes

A

susceptible to disruption from inherited mutations; caretaker genes responsible for maintaining genomic integrity

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27
Q

Abnormal gene silencing

A

major factor in cancer; passed down from parent => child => single => progeny d/t epigenetic silencing

28
Q

Are cancer cells immortal?

A

Yes, when they reach critical age, cancer cells activate telomerase to restore and maintaine their telomeres, allowing to divide repeatedly

29
Q

How to fully rid of cancer in a body?

A

Target cancer stem cell

30
Q

What’s essential for tumor growth?

A

Access to vascular system

31
Q

VEGF or vascular endothelial growth factor

A

stimulate new blood vessel growth or angiogenesis when stromal or cancer cells excrete this factor

32
Q

Cancer cell division requirements?

A

Can often occur in hypoxic and acidic environment; cancer genes also encourage aerobic glycolysis and high gluce utilization

33
Q

defects in intrinsic or extinsic pathways

A

provide resistance to apoptotic cell death

34
Q

Increased BCL-2

A

blocks apoptosis in most follicular B-cell lymphomas

family proteins are the regulators of apoptosis, but also have other functions. This family of interacting partners includes inhibitors and inducers of cell death.

35
Q

Chronic inflammation

A

can l/t increased risk of cancer; e.g gastric cancer and infection w/ Helicobacter pylori

36
Q

Tumor-associated macrophage (TAM)

A

usually M1 or classic proinflammatory macropahge is the primary one in acute inflammatory response

While M2 macrophage creates during healing:
* antiinflammatory mediators to suppress inflammation
* induce cellular proliferation
* angiogenesis
* wound healing

TAM mimics M2

37
Q

Cancer-associated fibroblasts (CAFs)

A

synthesize extracellular matrix that surrounds and permeates tumor; contribute to spread + metastasis

38
Q

Viruses + cancer

A

Viruses associated w/ 15% of all human cancers. Cervix and hepatocellular carcinoma account for 80% of virus-linked cancer cases

39
Q

Human papillomavirus (HPV) anad hepatitis B virus (HBV)

A

These vaccines against oncogenic viruses are expected to protect against initial infection and develop of cervical + liver tumors respectively

40
Q

T cells and NK cells for cancer

A

They can recognize unique antigens + markers on tumors cells l/t destruction

41
Q

How do cancer cells avoid immune system?

A
  • Produce immunosuppressive factors
  • Immunosuppresive T-regular cells
  • Evolviing tumor-antigen negative variants
  • suppression of antigen-presenting MHC class 1 molecules
42
Q

Metastasis

A

Requires cells to have many new abilities
* invade
* survive
* proliferate in new environment

43
Q

Traits for Invasion in cancer

A
  • loss of cell-to-cell contact
  • degrade ECM
  • migration of tumor cells to vascular or lymphatic systems
  • Stromal cells are important (TAMs or tumor associated macrophage)
44
Q

Epithelial-
mesenchymal transition

A

Carcinomas undergo this process where many epithealial-like characteristics are lost (such as polarity, adhesion to basement membrane), resulting in:
* increased migratory movement
* increased apoptosis resistance
* dedifferentiated stem cell-like state that favors foreign (lose specialized characters) microenvironments
* create metastasis

45
Q

Cancers move purposely?

A

Can move to specific sites d/t particular receptor expression for ligands expressed by cells

46
Q

Paraneoplastic syndromes

A

rare symptom complexes d/t biologically active substanes released from tumor or by an immune response triggered by tumor; manifest sx not directly caused by local effects of cancer

47
Q

Clinical manifestations of cancer

A

pain, cachexia (wasting, weakness of body), anemia, leukopenia, thrombocytopenia, and infection

48
Q

Pain

A

late stage of cancer; pressure, obstruction, invasion of structure sensitive to pain, stretching, tissue destruction, inflammation

49
Q

Fatigue

A

most frequently reported sx of cancer and cancer tx

50
Q

Cachexia

A

multiorgan syndrome
* anorexia
* muscle wasting (involves many protein signal pathways and inflammatory mediators)
* thermogenesis
* altered heart + liver fx
* gut malabsorption
* early satiety/taste alterations
* altered metabolism (protein, lipid, carbohydrate)

51
Q

Anemia w/ cancer

A

d/t malnutrition, chronic bleeding, resultant iron deficiency, chemotherapy, radiation, and malignancy in blood forming organs

52
Q

Leukopenia

A

d/t chemothrapy (toxic to bone marrow) or radiation (kills circulating leukocytes

53
Q

Thromobocytopenia d/t cancer

A

chemotherapy or bone marrow malignancy

54
Q

Infection and cancer

A

Leukopenia, immunosuppresion, or debility

55
Q

GI tract + cancer

A

d/t chemotherapy and radiation => malabsorption, oral ulcers (stomatitis), diarrhea

56
Q

Alopecia and skin d/t cancer

A

hair loss d/t chemotherapy on hair follicles

while for skin, decreased renewal rates => l/t skin breakdown and dryness

57
Q

Examination of tumor tissue by pathologist

A

Diagnosis of cancer, uses variety of tests

58
Q

Tumor staging

A

T (tumor spread), N (node involvement), and M (metastasis) system

59
Q

cancer classification methods

A

immunohistochemical analysis for protein express + molecular analysis of tumors

60
Q

Tumor markers

A

found in cancer cells, blood, spinal fluid, or urine; includes hormones, enzymes, genes, antigens, antibodies => help diagnose and follow course of cancer

61
Q

Cancer therapy

A

surgery, radiation therapy, and chemotherapy, or combination w/ limitations

62
Q

Surgical therapy

A

for nonmetastatic disease and a palliative measure to alleviate symptoms

63
Q

Radiation therapy

A

ionizing radiation cause cell damage; goal is to damage tumor w/o excessive toxicity or damage to other structures

64
Q

Chemotherapy

A

vulnerability of tumor cells in various stages of cell cycle; current tx uses combinations of drugs with different targets and toxicities

65
Q

Immunotherapy

A

modify immune system into destructive condition

Pathopharmacology (99 decks)

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