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Adv Patho > Exam 4-Cancer > Flashcards

Exam 4-Cancer Flashcards

1
Q

Benign tumor characteristics

A 
slow growth
well defined capsule
not invasive
well differentiated
low mitotic index
does not mets
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2
Q

malignant tumor characteristics

A 
rapid growth
not encapsulated
invasive
poorly differentiated: anaplasia
high mitotic index
can spread distantly (mets)
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3
Q

anaplasia

A

not differentiated, nucleus has irregular shape, size, tissue structure is abnormal

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4
Q

metastasis

A

spread of cancer cells from the site of the original tumor to distant tissues and organs through either blood or lymphatic vessels

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5
Q

carcinomas

A

cancers arising in epithelial tissue

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6
Q

adenocarcinomas

A

cancer arising from ductal or glandular structures

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7
Q

sarcoma

A

cancer arising from mesenchymal tissue

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8
Q

lymphoma

A

cancer of lymphatic tissue

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9
Q

blastoma

A

malignancy in precursor cells “blast”

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10
Q

leukemia

A

cancers of blood forming cells

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11
Q

carcinoma in situ

A

in its original place, cancer cells not spread beyond where they first formed

  • pre-invasive cancer; atypical cells
  • have not penetrated the basement membrane, no local invasion
  • May: remain where they are, progress to invade and metastasize, regress and go away
  • The more dysplastic the cells are, the more likely they are to be invasive
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12
Q

What type of cancer is more common in children

A

Blastoma

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13
Q

what is cancer

A

any malignant growth or tumor, cause by abnormal and uncontrolled cell division; it may spread through the lymphatic system or blood stream to other parts of the body

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14
Q

Cancer cell behaviors

A
  • normal cells transform and become cancer cells
  • behave autonomously, not following usual cell control mechanism (long life span, can grow in suspension, can grow even when they come in contact with other cells.
  • lack differntiation
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15
Q

Metabolism of cancer cells

A
  1. rapidly dividing, able to survive in sub optimal environment that normal cells cant
  2. b/c dividing rapidly, use nutrients that are then not available to normal cells
  3. have ability to perform glycolysis without using mitochondria to generate “usual” ATP-but able to generate “normal: number AtP molecules
  4. despite anaerboic metabolic pathway, able form lipids and other cell building blocks
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16
Q

How do cancer cells make cellular building blocks

A

by consuming large quantities of glucose which support rapid proliferation

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17
Q

How do normal tissues make energy?

A

Oxidative phosphorylation to turn glucose into CO2 and energy in the form of ATP

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18
Q

What is heterogenieity

A

quality or state of being diverse in character or content

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19
Q

Hallmarks of cancer cells:

A
  1. evading growth suppressors
  2. enabling replicative immortality
  3. tumor promoting inflammation
  4. activating invasion and metastasis
  5. genomic instability
  6. inducing angiogenesis
  7. resisting cell death
  8. deregulating cellular energetics
  9. sustaining proliferative signaling
  10. avoiding immune destruction
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20
Q

Paraneoplastic syndromes

A

are rare disorders that are triggered by an altered immune system response to a neoplasm. They are defined as clinical syndromes involving nonmetastatic systemic effects that accompany malignant disease.

  • group of rare disorders that are triggered by an abnormal immune system response to a cancerous tumor known as a “neoplasm.” Paraneoplastic syndromes are thought to happen when cancer-fighting antibodies or white blood cells (known as T cells) mistakenly attack normal cells in the nervous system.
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21
Q

What is the tumor marker for

HEPATIC, GERM CELL–

A

ALPHA FETOPROTEIN (AFP)

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22
Q

What is the tumor marker for –

MULTIPLE MYELOMA, CLL

A

BENCE JONES PROTEIN

23
Q

What is the tumor marker for –

BREAST, OVARIAN

A

BRCA1 AND BRCA2

24
Q

What is the tumor marker for –

GI, PANCREAS, LUNG, BREAST, ETC

A

CARCINOEMBYRIONIC ANTIGEN (CEA)

25
Q

What is the tumor marker for **

GERM CELL, CHORIOCARCINOMA

A

BETA-HUMAN CHORIONIC GONADOTROPIN

26
Q

TNM staging

A 
Tumor- primary tumor
T0-no tumor
T1-lesion <2 cm
T2-lesion 2-5 cm
T3-skin and or chest wall invasion

Nodes-lymph node involvement
N0-no axillary
N1-mobile nodes involved
N2-fixed nodes involved

Metastases-extent of distant mets
M1-not mets
M2- demonstratable mets
M3-suspected med

**the higher the number in each stage, the more extensive the cancer

27
Q

What is the tumor marker for

PROSTATE**

A

PROSTATE SPECIFIC ANTIGEN (PSA)

28
Q

What is the tumor marker for small lung cancer and neuroblastoma **

A

NEURON-SPECIFIC ENOLASE (NSE)

29
Q

Multistep nature of Metastases

A
  1. aggresive phenotype
  2. prerequisites
  3. microenvironment
  4. intravasation
  5. life in transit
  6. distant accomplices
  7. homing
  8. extravasation
  9. micrometastases
  10. co-opted stroma
  11. full colonization
30
Q

Role of inflammation in cancer

A
  1. goal of inflammation, immune response is to recognize cancer cell surface antigens and destroy
  2. inflammation both protective or potentially harmful
  3. Role in cancer progression
    - cancer cells use inflammatory response to their benefit, especially healing and proliferative pathways to support growth and progression
    - have ability to produce chemotactic signals&raquo_space;attract macrophages&raquo_space; produce mediators&raquo_space; decrease inflammation, increase proliferation, and increase angiogenesis
    - macrophages decrease cytoxic response therefor not kill cancer cells
    - T regulatory cells change&raquo_space; no cell destruction + produce cytokines&raquo_space; proliferate, spread
31
Q

Clinical manifestations of cancer

A
  1. paraneoplastic snydromes
  2. cachexia
  3. fatigue
  4. immune suppresion
  5. pain
  6. thromnbocytopenia
  7. Leukopenia
  8. systemic effects of cancer
32
Q

Goal of cancer treatement

A
  1. remove cancer cells
  2. stop cancer cell growth
  3. kill cancer cells
33
Q

Immune therapy: interferons

A

such as interferon alpha (Roferon‐A [2a], Intron A [2b], Alferon[2a]). Side effects of interferon treatment may include flu‐like symptoms, an increased risk of
infection, rashes, and thinning hair.

**man made proteins (aka interferons) that tell immune cells to attack cancer cells

34
Q

Immune therapy: interleukins

A

It is used to treat kidney cancer and skin cancer, including melanoma. Common side effects of IL‐2 treatment include weight gain and low blood pressure,flu‐like symptoms.

** Interleukin-2 is systemic therapy, which means that the treatment reaches all parts of your body through the bloodstream. tell immune system to kill cancer cells and shrink tumor growth

35
Q

Metastasis

A
  • not all cancer cells have ability to be tissue specific
  • epithelial-mesenchymal transition
  • in order to move to distant sites
  • outgrow, alter immediate limiting environment -access to local blood, lymphatic vessels
  • survive in circulation
  • attach, grow in new environment (may survive but not proliferative)
36
Q

How do tumor cells evade the immune system

A

Tumors may evade the immune response by losing expression of antigens or major histocompatibility complex (MHC) molecules or by producing immunosuppressive cytokines or ligands for inhibitory receptor on T cells.

37
Q

Purpose of biologic tumor markers

A
  1. surveillance, diagnosis, therapy, assess recovery, assess recurrence
  2. produced by benign and malignant tumor cells
  3. generally found on (or in) tumor cell, serum, spinal fluid, urine
  4. if marker causes symptoms, paraneoplastic syndrome
38
Q

What are tumor suppressing genes

A
  • genes that inhibit or decelerate proliferation

- suppress oncogenes-decrease cell growth, mutation, replication

39
Q

What are oncogenes

A
  • prot-oncogenes: genes encode components of receptor mediated pathways designed to regulate normal cellular proliferation
  • oncogenes: mutated or over expressed prot-oncogenes, which are independent of normal regulatory mechanism
  • may amplify, making numerous copies of mutated genes-important in prognosis of therapy
40
Q

Examples of oncogenes

A

RAS, MYC, P13K, D cycling, HER2 (ERBB-2)

41
Q

Behavior of cancer cells

A
  1. heterogeneity

2. cancer stem cells

42
Q

Cachexia

A
  • a multi-organ syndrome that has been discussed as a type of energy balance disorder where energy intake is decreased and energy expenditure is increased.
  • loss of skeletal muscle and adipose tissue that affects the heart, brain, gut, liver, and heart
43
Q

Genetic basis of cancer

A
  • change in cell’s genes cause the cell to become a cancer cell
  • basic theory: gene change occurs fairly constant over time. when a critical number of mutations occur, it becomes cancer
  • as mutations occur and cells become a cancer»has advantage over normal surrounding cells>.clonal proliferation»cancer in titu»potential for advancing
  • oncogenes
44
Q

Multistep nature of metastasis

A
  1. aggressive phenotype-oncogenic mutations. Epi/genome instability
  2. prerequisites-self renewal, invasivness, motility, detachment survival
  3. Microenvironment: angiogenesis, inflammation, cancerized stoma
  4. Intravasation: epithelial to mesenchymal transitions
  5. Life in Transit: platelet association, embolism, vascular adhesion
  6. distant accomplice: vascular progenitors, metastatic niche precursors
  7. Homing: attachment; attraction to survival signals
  8. Extravasation: motility, vascular remodeling
  9. Co-opted stroma: angiogenesis; inflammation; cancerized stroma
  10. Full colonization: organ specific mets factors and functions
45
Q

Pattern of metastsis

A

Lung, colorectal, testicular, prostate, breast, head and neck, ovarian, sarcoma, and melanoma cancers

46
Q

Breast cancer usually spreads to ___

A

bones via the bloodstream

47
Q

Lymphoma spreads to spleen, but not to_____

A

bone

48
Q

Immunotherapy

A

treatment that boosts the body’s natural defenses to fight cancer. it uses substances made by the body or in a lab to improve or restore the immune system function.

49
Q

Immunotherapy may work by:

A
  1. stopping or slowing the growth of cancer cells
  2. stopping cancer from spreading to other parts of the body
  3. Helping the immune system work better at destroying cancer cells
50
Q

Types of immunotherapy:

A
  1. monoclonal antibodies
  2. non-specific immunotherapies
  3. oncolytic virus therapy
  4. T cell therapy
  5. cancer vaccines
51
Q

Monoclonal antibodies

A

Are made in a laboratory.
Can be used as targeted therapy by blocking an abnormal protein in a cancer cell.
Can be used as immunotherapy

52
Q

Most common cancer in children

A

Leukemia and brain tumor

53
Q

Most common cancer in adolescents

A

lymphomas, leukemia, brains, and germ cell tumors

54
Q

Children cancer etiology

A

genetic factors: mutations in oncogenes or tumor suppressor genes

environmental factors: prenatal exposure to xray, drugs, pesticides, childhood exposure to ionizing radiation, drugs, virus, radon, formaldehyde

Adv Patho (23 decks)

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