PROOF OF CONCEPTS: THE CASE OF PANCREATIC CANCER

1.  "P" ARM VERSUS  "Q"
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As you look at the location of Genes, one will quickly notice that various genes have their family counterpart not close on the same chromosome. But instead on a different chromosome altogether.  In general we almost treat this  information in a profane manner in that we overlook the meaning of this.  Nature, however, has no place for randomness. Everything has deep meaning and NUANCES OR MINIMAL VARIATIONS can make a world of difference. Should you doubt this statement, ask the people with Sickle cell, they are not laughing about that nuance in Hemoglobins.  So when a family member has put in a different chromosome, there is no pun intended.

ERBB1 is on chromosome 7p12 (involved in Glioblastoma and Squamous cell head and neck cancers)
ERBB2 is on chromosome 17q11.2-q12 (involved in breast, Ovarian and cervical cancer)

Also however, we note that the family member is put on a "p" rather than "q" location.  This also has a profound meaning.   It just turn out that mutation on "q" location seems to have the worse prognosis and are more likely to be expressed  than those on "p" location.

The bad guy MYC is located 8q24 and is found on advanced forms of cancers (Ovarian, Breast, small cell, Esophageal and cervical but also in the Burkitt (ALL))
The nice MYCN, often a better prognosis indicator, is located on 2p24  but still can be involved in Neurobalstoma.

These are in fact speculation but check it out!

Another example
just go ahead and compare
breast cancer with FGFR1 located 8p11
and breast cancer with EGFR1 located 10q25
and call me if you find different!

PROOF OF CONCEPT NEEDED FOR PANCREATIC CANCER:

One of the complication or hurdle you encounter when you are dealing with abnormal genes
in pancreatic cancers is the the genes found in abnormal cancers are also found in benign conditions such as Adenoma or even pancreatitis.  Now if we assume that this is an Adenocarcinoma of the same origin embryonically as the colon (check that assumption out), we could apply the colon cancer model where
EARLY CANCER FOR ADENOCARCINOMA IS ANNOUNCED BY LOSS OR MUTATION IN CHROMOSOME 17:   IE GENES     (FOLLOWING THE COLON MODEL)
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-KRT20
-TEM 7
-MAP2K4
BAT-26
ALOX 12
TP53
BIRC5
NME1
ERBB2
GAS
TM4SF5

LATE CANCER,  LOSS OF CHROMOSOME 8 (FOLLOWING THE COLON MODEL)

CDH4
PSCA
MYC
 (FGFR1 AND BAG4 ARE HAVE A "p" LOCATION ON THE CHROMOSOSME)

TELOMERASES

ONCE AGAIN NATURE PLAYS IT SIMPLE FOR BIG THINGS!
ONE OF THE WAY NATURE CHECKS THE AGE OF CELLS  IS BY CHECKING THE LENGTH OF THEIR DNA SKIRT ATTACHED AT THE END OF THEIR CHROMOSOME.  ALL CELLS OF SAME TYPE START WITH A RELATIVELY SAME LENGTH OF SKIRT.  WITH ANY DIVISION, THE SKIRT IS CUT SHORTER.  IF THE SKIRT IS TOO SHORT TO EXPOSE THE END OF THE CHROMOSOME, THE CELL HAS LIVED LONG ENOUGH AND IT IS SENT FOR DESTRUCTION.  THE LENGTH OF THE SKIRT CAN BE PROLONGED BY SOME ENZYMES THOUGH TO FOOL THE CHECK SYSTEM.  THESE ENZYME ARE CALLED THE TELOMERASES.

CANCER CELLS DO NOT DIE BECAUSE THEY ACTIVATE THEIR  TEL-O-MERASE. AND EACH TIME THEY DIVIDE, THEIR TELOMERASE RESTORE THE LENGTH OR JUST GIVE THEM THE LONGEST SKIRT EVER TO BEAT THE SYSTEM!  RESEARCHERS ARE WORKING HARD TO SILENCE THE CANCER CELL TELOMERASES!  THE CRBCM IS LOOKING INTO THIS!