FOOD FOR THOUGHT

* A trial has shown that Doxepin rinse may reduce pains from oral Radiation induced Mucositis.

*Radiation post lumpectomy does improve survival even in the elderly
*Memantine 20 mg daily did alleviate loss of cognitive functions post whole brain Radiation
* Now that Tamoxifen can be given for 10 Years, people are still suggesting that switching at 5 years to Letrozole in postmenopausal women, is better but may be we need another clinical trial?  It is reported that switching to Letrozole lead a a 48% drop of Recurrence and 24% drop in chance of death!

*Should maintenance alpha interferon be given in Esophageal and gastric cancer with Non-mutated Interferon receptors? or cancer with over expressed NF-kB.
does overexpression of FOS predict response to Interleukin or Interferon.

*It is wrong to stop inhibitor to VEGF IN CANCER TREATMENT UNTIL DISEASE PROGRESSION, AND INSTEAD OF STOPPING, REPLACE IT BY AN MTOR INHIBITOR, THIS WILL ADD AN OPTION TO COLON CANCERS!
ESMO DID SHOW THAT UPFRONT COMBINATION OF AVASTIN AND MTOR FAILED TO IMPROVE RESULTS (renal cancers) BUT GIVING MTOR AFTER AVASTIN FAILURE IS STILL BELIEVED TO BE BETTER (PROOF OF CONCEPT.  DOES THE ESCAPE MECHANISMS TO AVASTIN OFFER AN OPPORTUNITY TO MTOR INHIBITOR FOR ACTION OR ACTIVITY? WHAT ARE THE PREDICTORS TO MTOR INHIBITORS 'ACTION?  IS TISSUE HYPOXIA SECONDARY TO ENDOTHELIAL DISTURBANCES RESULTING FROM AVASTIN A PREDISPOSITION TO MTOR INHIBITOR ACTION?

*SHOULD WE GO AHEAD AND USE NAB-PACLITAXEL AND GEMZAR IN ADJUVANT SETTING NOW?(PANCREATIC CANCER)

*ADDING ERLOTINIB TO AVASTIN AS MAINTENANCE THERAPY AFTER FIRST LINE CHEMOTHERAPY OFFERED BETTER PROGRESSION FREE SURVIVAL (1 MONTH BETTER) IN A PHASE III TRIAL PRESENTED AT ASCO 2012! (COLON CANCER)

LOX Lysyl-Oxidase

This gene found in gastric and bladder cancer is prognostic.  Its amplification allows the cell to deal with austere conditions in Metastatic conditions.  It seems to be amplifying under the impetus of HIF (Hypoxia induced factor). Its amplification appears more reactive than driving the resulting dowstream reaction.It can affect the structure of laminin and collagen through its formation of Aldehyde.
It can push proliferation by acting as a co-factor at nuclear level.
It can affect AKT (Protein Kinase B).
Recently, a study in Sarcoma using a Doxorubicin isoform was set in motion. Expression of LOX should be included in the analysis since Hypoxia was a component of the treatment.
LOX would not be a principal target in a treatment strategy since it addresses mostly metastasis, it either an adjunct treatment, or will have a role in Maintenance therapy.

Hypothesis for Cancer Research: Mucinous Cancer

One of the bad types of gastroenterologic cancers such as Gastric and Colon cancers is the one known as Mucinous Cancer.  Basically, this cancer produces a Mucin assumed to be a viscous liquid surrounding the cell.  This tumor spreads early and deeply. At the time it is found, most of the time, the cancer is in advanced stage.  Researchers have explained this phenomenon by stating that this Mucin contains many ingredients suppressive to immunity (including Cytokines), and soluble Molecules (such as Prostaglandin E2) that may down regulate local immunity against the cancer.  It may also have those metalloproteases that we discussed in our earlier post for research suggestions on Oct, 14, 2012
Prostaglandins in general respond to anti inflammatory agents.
CAN WE MEASURE THE LEVEL OF TISSUE PROSTAGLANDINS IN MUCINOUS CANCERS AS A PREDICTOR OF ANTI-INFLAMMATORY (ASPIRIN) MAINTENANCE THERAPY POST PRIMARY TREATMENT TO DECREASE RATE OF METASTASIS IN COLON AND GASTRIC CANCERS?

CAN ANTI-MUCIN (AFTER WE KNOW THE REAL CONTENT FOR SPECIFIC CANCER TISSUE) PROVIDE AN INCREASE OF ANTIBODY BINDING TO CANCER CELLS?

TREG CELLS are cells involved in tolerance of our own cells.  They work to stop us from killing our own cells.  ARE THEY INCREASED IN CANCERS TO DECREASE CELLULAR IMMUNITY AGAINST CANCERS?

CANCER CELLS SEEMS TO HAVE A SELF GROWTH HORMONE WHICH IS SECRETED IN ITS IMMEDIATE SURROUNDING.  THIS HORMONE ACTS THROUGH RECEPTORS ON THE EXTERNAL MEMBRANE OF THE CELL.  THE PROFILE OF RECEPTORS ON CANCER MEMBRANES IS DEFINITELY DIFFERENT FROM THE NORMAL CELL.  WHY CAN'T WE PRACTICE "PROFILING" BY INVENTORYING ALL THE RECEPTORS (OR CRITICAL RECEPTORS)?
RECEPTORS ARE MADE BY GENES MOSTLY, WE CAN CONTROL THESE THROUGH OUR KNOWLEDGE OF GENETICS.  IF WE KNOW RECEPTORS EXCLUSIVE TO CANCER CELLS,
CAN WE DEVELOP ANTIBODY TO THESE RECEPTORS?