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Peds Patho Exam 3 > Oncology > Flashcards

Flashcards in Oncology Deck (30)
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1
Q

Tumor definition

A

Gradual increase in the number of dividing cells creates a growing mass of tissue called a “tumor” or “neoplasm.” If the rate of cell division is relatively rapid, and no “suicide” signals are in place to trigger cell death, the tumor will grow quickly in size; if the cells divide more slowly, tumor growth will be slower. But regardless of the growth rate, tumors ultimately increase in size because new cells are being produced in greater numbers than needed. As more and more of these dividing cells accumulate, the normal organization of the tissue gradually becomes disrupted.
*Becomes a problem when it invades tissues or organs

2
Q

Invasion vs. Metastasis

A

Invasion refers to the direct migration and penetration by cancer cells into neighboring tissues.

Metastasis refers to the ability of cancer cells to penetrate into lymphatic and blood vessels, circulate through the bloodstream, and then invade normal tissues elsewhere in the body.

3
Q

Benign vs. Malignant Tumors (3)

A
  1. Benign tumors are tumors that cannot spread by invasion or metastasis; hence, they only grow locally.
  2. Malignant tumors are tumors that are capable of spreading by invasion and metastasis. By definition, the term “cancer” applies only to malignant tumors.
  3. A malignant tumor, a “cancer,” is a more serious health problem than a benign tumor because cancer cells can spread to distant parts of the body. For example, a melanoma (a cancer of pigmented cells) arising in the skin can have cells that enter the bloodstream and spread to distant organs such as the liver or brain. Cancer cells in the liver would be called metastatic melanoma, not liver cancer. Metastases share the name of the original (“primary”) tumor. Melanoma cells growing in the brain or liver can disrupt the functions of these vital organs and so are potentially life threatening.
4
Q

Grading and staging of cancer

A

Microscopic examination provides information regarding the likely behavior of a tumor and its responsiveness to treatment.
Cancers with highly abnormal cell appearance and large numbers of dividing cells tend to grow more quickly, spread to other organs more frequently, and be less responsive to therapy than cancers whose cells have a more normal appearance. Based on these differences in microscopic appearance, doctors assign a numerical “grade” to most cancers. In this grading system, a low number grade (grade I or II) refers to cancers with fewer cell abnormalities than those with higher numbers (grade III, IV).
1. Staging
2. Grading

5
Q

Oncogenes (4)

A
  1. Oncogenes are genes whose PRESENCE in certain forms and/or overactivity can stimulate the development of cancer. When oncogenes arise in normal cells, they can contribute to the development of cancer by instructing cells to make proteins that stimulate excessive cell growth and division.
  2. Oncogenes are related to normal genes called proto-oncogenes that encode components of the cell’s normal growth-control pathway. Some of these components are growth factors, receptors, signaling enzymes, and transcription factors. Growth factors bind to receptors on the cell surface, which activate signaling enzymes inside the cell that, in turn, activate special proteins called transcription factors inside the cell’s nucleus. The activated transcription factors “turn on” the genes required for cell growth and proliferation.
  3. Oncogenes arise from the mutation of proto-oncogenes. They resemble proto-oncogenes in that they code for the production of proteins involved in growth control. However, oncogenes code for an altered version (or excessive quantities) of these growth-control proteins, thereby disrupting a cell’s growth-signaling pathway.
  4. By producing abnormal versions or quantities of cellular growth-control proteins, oncogenes cause a cell’s growth-signaling pathway to become hyperactive. To use a simple metaphor, the growth-control pathway is like the gas pedal of an automobile. The more active the pathway, the faster cells grow and divide. The presence of an oncogene is like having a gas pedal that is stuck to the floorboard, causing the cell to continually grow and divide. A cancer cell may contain one or more oncogenes, which means that one or more components in this pathway will be abnormal.
6
Q

Tumor suppressor genes (3)

A

1.Tumor suppressor genes are normal genes whose ABSENCE can lead to cancer. In other words, if a pair of tumor suppressor genes are either lost from a cell or inactivated by mutation, their functional absence might allow cancer to develop.

  1. Individuals who inherit an increased risk of developing cancer often are born with one defective copy of a tumor suppressor gene. Because genes come in pairs (one inherited from each parent), an inherited defect in one copy will not lead to cancer because the other normal copy is still functional. But if the second copy undergoes mutation, the person then may develop cancer because there no longer is any functional copy of the gene.
  2. Supposed to work to suppress normal genes if there is an absence in normal genes
  3. Some reason they mutate or inactivate the cells and escape through the immune system and tumor can grow
  4. Tumor suppressor genes are a family of normal genes that instruct cells to produce proteins that restrain cell growth and division. Since tumor suppressor genes code for proteins that slow down cell growth and division, the loss of such proteins allows a cell to grow and divide in an uncontrolled fashion. Tumor suppressor genes are like the brake pedal of an automobile. The loss of a tumor suppressor gene function is like having a brake pedal that does not function properly, thereby allowing the cell to grow and divide continually.
7
Q

p53

A

One particular tumor suppressor gene codes for a protein called “p53” that can trigger cell suicide (apoptosis). In cells that have undergone DNA damage, the p53 protein acts like a brake pedal to halt cell growth and division. If the damage cannot be repaired, the p53 protein eventually initiates cell suicide, thereby preventing the genetically damaged cell from growing out of control.

  1. P53 = tumor suppressor gene mutation
  2. See in sarcoma = p53 only one
8
Q

DNA Repair Genes (5)

A
  1. DNA repair genes code for proteins whose normal function is to correct errors that arise when cells duplicate their DNA prior to cell division. Mutations in DNA repair genes can lead to a failure in repair, which in turn allows subsequent mutations to accumulate. People with a condition called xeroderma pigmentosum have an inherited defect in a DNA repair gene. As a result, they cannot effectively repair the DNA damage that normally occurs when skin cells are exposed to sunlight, and so they exhibit an abnormally high incidence of skin cancer. Certain forms of hereditary colon cancer also involve defects in DNA repair.
  2. Body stops cancer from growing
  3. Repair or replace DNA
  4. Repair genes do not work – they mutate
  5. Immune system should come in but don’t work that way
9
Q

Common pediatric cancers (8)

A

3 Most Common:

  1. Leukemia*** - most common
  2. Brain and Central Nervous System Tumors
  3. Neuroblastoma

Other Types:

  1. Lymphoma
  2. Rhabdomyosarcoma
  3. Wilms Tumor
  4. Bone Cancers – i.e. Osteosarcoma and Ewing’s Sarcoma
  5. Germ Cell Tumors
10
Q

Genes causing pediatric cancers (5)

A

KNOW THESE

  1. NPM-ALK fusion genes associated with anaplastic large cell lymphomas
  2. ALK point mutations associated with a subset of neuroblastomas
  3. BRAF and other kinase genomic alterations associated with subsets of pediatric gliomas
  4. Hedgehog pathway mutations associated with a subset of medulloblastoma
  5. ABL family genes activated by translocation in a subset of acute lymphoblastic leukemia (ALL)
11
Q

Hematopoiesis definition (2)

A
  1. Production, multiplication, and specialization of blood cells that occurs in the bone marrow
  2. Abnormal leads to cancer*
12
Q

Hematopoiesis blood types (4)

A

a. White Blood Cells – abnormal WBCs (usually leukocytes cause leukemia)
b. Red Blood Cells
c. Platelets
d. Abnormal Hematopoiesis can lead to malignancy

13
Q

definition of blood types (3)

A
  1. Leukocyte: white blood cells with subtypes:
    - Granulocytes - neutrophils
    - Monocytes – develops to macrophage; responsible for phagocytosis
    - Lymphocyte - main cells for immune response; B and T cells
  2. Megakaryocyte: giant cell of bone marrow containing a greatly lobulated nucleus, from which mature blood platelets originate.
  3. Erythrocyte: red blood cells
14
Q

Leukemia definition and types (4)

A
  1. Definition: malignancy of abnormal or immature blood cells produced in blood cell producing tissue mainly the bone marrow, that invade the periphery (circulating blood cells)

Types

  1. Acute Lymphoblastic Leukemia (ALL); Most Common
  2. Acute Myeloid Leukemia (AML)
  3. Acute Promyeloctic Leukemia (APML)
  4. Type of leukemia is based on the cell line from which the abnormality is derived.
15
Q

Leukemia Classifications (3)

A
  1. Acute vs. Chronic
    * Pediatric Leukemia- primarily acute
    * ALL – 75 – 80%
    * AML - ~20%
  2. Lymphoid vs. Myeloid
    - Therapy based on primary cell lineage
    - Morphology of bone marrow cells
  3. Bone marrow aspirate/biopsy
    - essential to diagnose leukemia because as many
    - 20% of patients lack circulating blast cells at diagnosis
    - Morphology of leukemic cells in peripheral blood may differ from that in marrow
16
Q

ALL (5)

A
  1. Malignancy of white blood cells
  2. Increased production of immature white blood cells (blasts) in the bone marrow
    a. Blasts in periphery
  3. Blasts released into peripheral circulation
  4. Decreased mature white blood cells (neutrophils or segs)
  5. Immunosuppression
17
Q

ALL Increased storage in…(3)

A
  1. Liver
  2. Spleen
  3. Lymph nodes
18
Q

AML (4)

A
  1. Malignancy of the blood that starts in the bone marrow
  2. Blocks differentiation of HST
  3. Causes unchecked cell proliferation
  4. Results in accumulation of myeloblasts and decreased healthy hematopoietic precursors
19
Q

Acute Promyelocytic Leukemia (7)

A
  1. Increased promyelocytes
  2. ONC EMERGENCY** give arsenic and they are cured
  3. Secondary to arrest of leukocyte differentiation
  4. Caused by translocation of chromosome 15 and 17
  5. Healthy blood cells to do their jobs, patients are at high risk for infection or bleeding.
  6. APL is a subtype of the cancer acute myeloid leukemia (AML).
  7. APL diagnosis should be considered a medical emergency.
    - Thrombocytopenia
    - DIC
    - Coagulopathy
20
Q

APL Statistics (6)

A
  1. ~1 percent of all childhood leukemias are APL
  2. ~4 to 8 percent of all childhood AML is acute promyelocytic leukemia
  3. Hispanic or Mediterranean descent.
  4. Very rare in children < 3 yo; average age of diagnosis is 8 to 10 years.
  5. Overall excellent prognosis
  6. ~90% cured
21
Q

lymph nodes and leukemia (2)

A
  1. reactive or hyperplastic nodes – enlarged nodes from infection or inflammation; usually tender
  2. Non-tender node = red flag
22
Q

Lymphoma definition

A

Cancer of immune system cells

23
Q

Hodgkin lymphoma

A

Marked by the presence of a type of Reed-Sternberg cell

24
Q

Non-Hodgkin lymphoma (4)

A
  1. Includes large, diverse group of cancers of immune cells

Further divided into:

  1. Indolent (slow-growing) course
  2. Aggressive (fast-growing) course
  3. Subtypes affect behavior and response to treatment
25
Q

Humoral Immunity (4)

A

1) Respond to antigens
- Producing antibodies ( immunoglobulins)
- Bind to the specific antigens (matching).
- Triggers signal to T-cell to release cytokine
- B cell produces clones

2) Plasma cells
- produce antibodies that tag antigens

3) Memory cells
- prolonged life span
- remember specific antigen
- Activates immune system for repeat attack

4) B-Cell Lymphoma
- B-Cells mutate and become cancerous

26
Q

T-cell mediated immunity (2)

A

1) Differ from other Lymphocytes:
- special receptor on their cell surface
- T cell receptors(TCR)

2) Respond to antigens by producing:
- cytokines
- Interleukin
- Interferon
- Growth factor
- DO NOT produce antibodies

27
Q

T-helper cells (2)

A
  1. Provides help cells of the immune response by:
    i) Recognizing foreign antigens
    ii) Secreting cytokines that activate cytotoxic T cells and B cells.
  2. Activated by
    - Phagocytosis a bacteria, virus macrophage or dendritic cell
    - Present them on their surface (antigen presenting cells)
28
Q

pathogenesis of lymphomas (2)

A
  1. process involving the accumulation of multiple genetic lesions
  2. affecting proto-oncogenes and tumor suppressor genes
29
Q

Neuroblastoma (6)

A
  1. Arises from the developing cells of the sympathetic nervous system
  2. 65% are located above the kidney but can begin anywhere
  3. Other sites
    a) Chest
    b) Neck
    c) Pelvis
  4. Spreads from its “primary” location:
    a) Bone marrow
    b) Bones
    c) Lymph nodes.
  5. Most common solid tumor outside of the brain in children
  6. Diagnosed as mainly as toddlers
30
Q

Neuroblastoma Stage 1, 2a, 2b, 3, 4, 4s

A

1: localized tumor. complete gross total resection
2a: unilateral with incomplete gross total resection. ipsilateral and contralateral lymph nodes negative
2b: unilateral with complete or incomplete gross total resection with positive ipsilateral lymph nodes and negative contralateral lymph nodes
3: tumor across the midline w/ or w/o regional lymph node involvement
4: dissemination of disease to distant lymph nodes, bone marrow, liver or other organs/bones except as defined in 4s
4s: localized primary tumor (per stage 1 and 2) with dissemination limited to liver, skin, and bone marrow (<10% marrow involvement)