FINAL EXAM part 6 - Neoplasia Flashcards

1
Q

Malignant tumor cells characteristic:

A
  • Undifferentiated cell
  • Do not look like their tissue of origin
  • Heterogeneous (change, diverse–> difficult to tx)
  • Loss of normal feature
  • Pleomorphic (multiple shapes and sizes)
  • Little evidence of normal function
  • Can spread (metastasis) and produce new blood vessels into the tumor (angiogenesis)
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2
Q

Systemic effects of malignant tumors:

A

Cachexia (total body wasting)

  • Paraneoplastic syndromes (biochemical, neurological, hematoligical derangements caused by abnormal compounds that tumors can release)
  • Immunosuppression (more susceptible to infections)
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3
Q

Histological grading of tumors with the:

A

Gleason Scale:
Grade I (well differentiated)
Grade II (moderately differentiated): increase mitoses and variation in size and shape.
Grade III and IV (poorly differentiated)

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4
Q

Cancer cell at the beginning:

A
  • Initial cancer cell has to multiply about 30 doublings before you have the smallest detectable tumour mass.
  • Because of the exponential phenomenon, it only take 10 more doublings before you are dead.
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5
Q

Proto-oncogenes are:

A

Genes that are involved in normal cell growth

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6
Q

3 differents ways Proto-oncogenes can be altered:

A
  1. Gene amplifications: more receptors –> more growth
  2. Translocation/transposition: relocation of a gene that is now next to a new promoter which increase production of a protein –> stimulate growth
  3. Point mutation: too much of a normal growth-stimulating protein or an abnormal hyperactive or degradation resistant protein –> hyperactive growth and act for a long period
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7
Q

Burkitt lymphoma

A

Burkitt lymphoma is caused by Epstein Bass Virus (EBV/HHV4) (B lymphocytes) combined with malaria

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8
Q

Cancer cells are able to resist cell death because of

A

The BCL-2 is overexpress–>block apoptosis by blocking the normal signaling mechanisms

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9
Q

RB Gene (Governor of the Cell Cycle) is:

A
  • The RB genes codes for a protein that suppresses cell growth.
  • It attaches to the transcription factor that binds DNA to block transcription.
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10
Q

P-53 Gene (Guardian of the Genome) is:

A
  • A sensor of multiple forms of stress (DNA damage, activated oncogenes, hypoxia, RNA depletion, telomere erosion) –> Major defenses against cancer
  • P53 will either cause the cell to die by triggering apoptosis or it will stop cell division to try to allow the cell to fix itself.
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11
Q

Colorectal cancer development:

A

Adenomatous polyp–> clonal expansion

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12
Q

Familial adenomatous polyposis (FAP) is

A
  • Born with one abnormal APC gene which causes thousands of polyps throughout the GI tract. (will not take long before getting a second defective enzyme)
  • APC regulates B catenin (needed to regulate the cell growth)
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13
Q

The majority of breast cancer is in origin:

A

Ductal

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14
Q

Sentinel Lymph nodes are:

A

The lymph node that drains the area of the tumor

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15
Q

One of the method for evaluating prognosis of breast cancer:

A

Is to see whether or not the tumor cell still has the normal receptors or not.

  • If the estrogen receptors are still present, it gives physicians a way to tx the cancer with hormone blocking agents. (better prognosis)->Tamoxifen
  • If the HER2 is overexpressd at the surface of the tumor cells (prognosis is grimmer)->MAB
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16
Q

4 ways the tumor can resist the hormone therapy:

A
  1. De novo androgenesis: it makes its own androgens
  2. Overexpression of the androgen receptor: even tiny amount of androgens can keep it going
  3. Non-specific ligand recognition: will start reponding to other ligands besides the androgen to stimulate its growth
  4. Ligand independent activation: does not need androgens at all anymore, completely independent.
17
Q

Brachytherapy is;

A

radioactive units inserted aroung the region of the tumor cells is, release radiation and kill locally the cancer cells.

18
Q

HPV (human papillomavirus) can cause cervical cancer: mechanisms:

A

Viral protein inactivates RB and P53