Welcome to Dr. Hamid Sanatinia's Virtual Headquarters
Oncogenes, the list!

Home

Should we treat or not???
Performace Status
Antiemetics
Growth Factors
Calculations
Chemo Precautions
TOXICITY CRITERIA
Antidepressants
Chemoprotection
MESNA
Dexrazoxane
Radioprotectants
Hypercalcemia of malignancy
Mucositis
Neutropenic Fever
Palliative Care
Radiation Oncology
<<<<<<<<<>>>>>>>>>
ALL
AML
Anal
Bladder Cancer
Brain Cancer
Breast (risk category)
Breast (adjuvant)
Breast (metastatic)
Breast (Xeloda)
Breast (hormonal)
Breast Cancer Genetics
Carcinoid
CLL
CML
COLON CANCER
Endometrial
Esophagous
Gastric
Gestational Trophoblastic Disease
Germ Cell (Ovary)
Hairy Cell Leukemia
Head/Neck
Head/Neck: ChemoRT abstracts
Head/Neck: Larynx
Head/Neck:Nasopharyngeal
Hodgkins
Islet Cell Tumors
Kidney
Liver
LUNG, NSC
Stage III Unresectable NSC Lung Cancer
Lung, SC
Lymphoma, Aggressive
Lymphoma, AIDS
Lymphoma, Burkitts
Lymphoma, CNS
Lymphoma, Cutaneous
Lymphoma, Indolent
Lymphoma, MALT
Lymphoma, Mantle cell
Lymphoma, Mediastinal B-Cell
Lymphoma, Refractory NHL
Melanoma
Mesothelioma
Multiple Myeloma
MDS
NHL
Ovarian
Pancreas
Prostate
Prostate (Hormonal)
Rectal Cancer
Sarcoma
Sarcoma, Ewing's
Sarcoma, Osteogenic
Skeletal Metastasis
Testicular Cancer
Thymoma
Thyroid Cancer
Waldenstrom's
Unknown Primary
<<<<<<<<<>>>>>>>>>
Molecular Genetics
Oncogenes, the list!
Immunoperoxidase stains
Tumor Markers
Bleomycin
Cisplatin
Etoposide
Ifosfamide
Methotrexate
Temazolamide
Mechanism of Action
Dose Modifications (Renal)
Dose Modifications (hepatic)
MDR

Oncogenes:
met
ret
ErB2/Her2/neu
ras
Bcl-2
c-myc
Tumor Suppressor Genes:
Rb
P53
APC
BRCA-1
BRCA-2

NM23
----------------------------------
Other mechanisms of tumorgenesis:
HYPERMETHYLATION
ACETYLATION & DEACETYLATION
LOSS OF HETEROZYGOSITY
TELOMERASE ACTIVITY

Met Oncogene:
Its normal counterpart corresponds to the Hepatocyte Growth Factor Receptor. Individuals affected with hereditary papillary carcinomas (HPRC) have been shown to have germ line mutations in the met proto-oncogene.
Ret Oncogene:
It encodes a receptor tyrosine kinase expressed in tissues derived from the neural crest. It is implicated in a number of inherited human diseases including MEN-2A & MEN-2B, familial medullary thyroid carcinoma, & familial Hirschsprung disease. Note that in Hirschsprung disease, loss of function mutations have been identified! The ligand for this receptor is: Glial cell line-derived neurotrophic factor (GDNF), binding of which is mediated by GDNF-family receptor.
Ras Oncogene:
Ras gene product, following post-translational modification, becomes associated with the inner leaflet of the cytoplasmic membrane. They act as molecular switches alternating from inactive GDP-bound state to an active GTP-bound state. Ras activation has been shown in 15% of all human tumors. Up to 90% in pancreatic cancer. Common mutations are: codon 12, 61, 13, & 59. Ras-transformed cells exhibit loss of contact inhibition & grow to high density!


nm23
A gene that is lost in metastatic cancer. Transfection of nm23 has been shown to cause loss of the metastatic phenotype.

-------------------------------------------------
HYPERMETHYLATION
Hypermethylation of CG islands in the regulatory sequences of tumor suppressor genes has been observed. It is thought to be one of the mechanisms of tumor suppressor gene silencing.
ACETYLATION & DEACETYLATION
Acetylation of octamer histones (ie H4) is involved in activation of gene expression.
Deacetylation is associated with decreased gene expression.
LOSS OF HETEROZYGOSITY
LOH has been observed in cancer
TELOMERASE ACTIVITY
Increased activity has been observed in cancer.