Neoplasms9-13 Flashcards
Which protooncogene is associated with a t(14:18) translocation?
Bcl-2
BRAF V600E mutations
Melanoma (40-60%)
What is the function of BRAF?
BRAF is a protein kinase involved in the activation of signaling pathways for melanocyte proliferation.
What type of necrotic pathology would you see after ischemia to the brain?
Liquefactive necrosis
Lysozymes has completely digested and removed all of the necrotis tissue and formed a cystic cavity.
Name the genes (1, 2, & 3) involved in the adenoma to carcinoma sequence.
Normal epithelium(1)>Early adenoma(2)>Late adenoma(3)>Adenocarcinoma
- APC: tumor suppresor; located on chromosome 5; causes the formation of a small polyp
- K-RAS: proto-oncogene; increases the size of polyps
- p53: tumor supressor; allows cells with genomic errors to enter cell cycle; last hit (along with DCC gene)
List the four (4) non-neoplastic colonic polyps.
- Hyperplastic: well differentiated mucosal cells forming glands and crypts
- Hamartomatous: mucosal glands, smooth muscle and connective tissue
- Inflammatory: regenerating intestinal mucosa
- Lymphoid: intestinal mucosa infiltrated with lymphocytes
Pathogenesis:
Tumor lysis syndrome
When tumors with a high cell turnover rate are treated with chemotherapy, intracelluar content (potassium, phosphorous, & uric acid) spills over into the serum.
Diagnosis:
Autosomal recessive, UV specific endonuclease deficiency
xeroderma pigmentosum
Treatment:
Tumor lysis syndrome
- Hydration
- Alkalinize the urine
- Allopurinol ā> to reduce uric acid production during the breakdown of tumor cells.
Name the metabolite of tumor nucleic acid that is soluble at physiological pH, but can precipitate in the kidney.
Uric acid is a metabolite of tumor nucleic acid. It can precipitate in the acidic environment of the renal distal tubule and collecting duct.
What is the best prognostic indicator for patients with malignant melanoma?
Breslow thickness: the measure of depth invasion (vertical)
You biopsy an abnormal lymph node and see monoclonal T-cell receptor gene rearrangements. What is this indicative of?
A monoclonal lymphocytic proliferation is strong evidence of MALIGNANCY.
What determines the prognosis of colorectal adenocarcinoma?
The STAGE, or extent of tumor expansion, NOT the grade, or degree of tumor differentiation!
Proto-oncogenes vs. Anti-oncogenes
ras, N-myc, ERB-B1, ERB-B2, TGF_, sis, abl
proto-oncogenes (tumor promoters)
Proto-oncogene vs. Anti-oncogene
BRCA-1, BRCA-2, NF-1, APC/_-catenin, DCC, p53, RB, WT-1
anti-oncogenes (tumor supressors)
Pathogenesis:
How do aflatoxins cause hepatocellular carcinoma?
High levels of dietary aflatoxin exposure is associated with a Cā>T transversion in the p53 gene. p53 mutations have been identified in most individuals with hepatocellular carcinoma.
What is the name of the molecule responsible for cachexia (wasting syndrome) in cancer patients
TNF-_
Another name for TNF-_ is cachectin.
Clinical Manifestation:
Cachexia
- anorexia
- malaise
- anemia
- weight loss
- generalized wasting
Myeloproliferative disorders associated with JAK2 mutations
chronic myeloproliferative disorders
- Polycythemia vera
- Essential thrombocytosis
- Primary myelofibrosis
Myeloproliferative disorders associated with persistant activation of signal transducers and activator of transcription (STAT) proteins
Chronic myeloproliferative disorders; associated with JAK2 mutations
