The Common Cancer Genes

 

The Human Genome Cancer Genes

Jorma Jyrkkanen

22 July 2008

The human genome is a host to numerous genes that cause cancer and those that fight cancer. It is worth becoming familiar with them since they affect so many of us. 

Cancer occurs when cell division gets out of control. Usually, the timing of cell division is under strict constraint, involving a network of signals that work together to say when a cell can divide, how often it should happen and how errors can be fixed.

Mutations in this interconnected system can trigger cancer, be it through exposure to some of the enormous numbers of chemical carcinogens and mutagens we humans produce, natural carcinogens and mutagens or because of a genetic predisposition, or immune system compromise from other diseases or a blend of factors.

Usually, several cancer-promoting factors have to gang up before a person will develop uncontrolled growths: with some exceptions like plutonium, no one risk alone is sufficient.

The main ways for starting the cancers below are when genetic strands (DNA) break and the fixing mechanisms break down, the natural or induced transformation of a normal gene into an oncogene, a gene that aggressively promotes unrestricted growth and when tumor supressor genes stop working properly. 

The common gene linked cancers or cancer like diseases

Breast cancer.

Ovarian Cancer.

Burkitt's lymphoma(EBV)

Chronic myeloid leukemia(CML)

Colon cancer (see my other article on this)

Lung cancer(small cell)

Malignant melanoma

Multiple endocrine neoplasia

Neurofibromatosis

p53 Tumor suppressor

Pancreatic cancer

Prostate cancer

Ras Oncogene

RB Retinoblastoma

von Hippel-Lindau syndrome

The Cancer Genes and Associated Chromosomes 

Chromosome 1. HPC1 of prostate cancer (1/500 cases)

Chromosome 2. MSH2 and MSH6 mutations of colon cancer

Chromosome 3. MLH3 of colon cancer; deletion regions of 3 and other mutations associated with small cell lung cancer; VHL of von Hippel-Lindau disease of vessels

Chromosome 7.  P53 tumor suppressor gene stop signal for cell division (see also Rb and DPC4 gene)

Chromosome 8.  Myc gene for Burkitts lymphoma

Chromosome 9.  Ableson proto-oncogene ABL of CML; CDKN2 gene mutations can lead to malignant melanoma; TSC1 of tuberous sclerosis

Chromosome 11. MEN1 mutations affect calcium metabolism in a cancer like way; RAS oncogenes can make cells divide wildly when coupled to other mutations

Chromosome 13.  BRCA 2 mutations can lead to breast cancer, missing rb genes can lead to retinoblastoma

Chromosome 14. Myc translocation from chromosome 8 can lead to Burkitts lymphoma

Chromosome 16. PKD1 polycystic kidney disease; TSC2 of tuberous sclerosis

Chromosome 17. BRCA 1 mutations can lead to breast cancer.

Chromosome 18. DPC4 (Smad4) tumor suppressor gene if lost in deletion can lead to cancer

Chromosome 22. BCR of chronic myelogenous leukemia; NF2 gene of neurofibromatosis

I wish to thank the National Library of Medicine for this information and those thousands of researchers who made these discoveries. Please note that there are many mutations that are not listed here that can also facilitate the development of cancer. I have simply rearranged their data and added explanation for the lay person and drawn a few conclusions.

Conclusions

It is clear to me from the evidence above that a few conclusions can be drawn.

One is that any chemicals or pollutants or factors that induce deletions or translocations in the critical chromosomes should be viewed as a carcinogen.

A second conclusion is that cumulative mutagens should be regarded as carcinogens.

A third conclusion is that DNA repair mechanisms can stop working and we need to find out why and if they can be fixed.

A fourth conclusion is that endogenous retroviruses are not our friends and we need to find ways of removing them or blocking them.

A fifth conclusion is that clean water, air and food, healthy immune systems and most important, genetic counselling, should have priority in community and public health policy.  

A sixth conclusion is that evolution and its natural repair mechanisms should be consulted for ideas for a long term solution. Can we stop passing certain genes along?

The seventh conclusion is that the signal pathways for controlling cell division timing and for programming cell function and death are vital in preventing cancers.

Jormawankenobe

© 2008 J. Jyrkkanen