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Showing posts with label gemcitabine. Show all posts
Showing posts with label gemcitabine. Show all posts
Tuesday, February 5, 2013
NEW DEVELOPMENTS
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Sunday, January 27, 2013
UPDATE ON TREATMENTS OF PERIPHERAL T CELL LYMPHOMA
3 AGGRESSIVE TYPES:
==================
1. PTLC- NOS
2. AITL: AngioImmunoblastic
3ALCL (Anaplastic large cell (ALK +) 6% AND alk NEGATIVE
CD30 , t(2,5)(p23,q25)
---------------------------------------------------------------------------------
1 Peripheral T cell lymphoma not otherwise specified
-PET
-Gene Profiling
treat it with EPOCH (CHOEP) or Etoposide based regimen followed by transplant
consider Romidepsin (upfront in Europe)
followed by Gemcitabine, Navelbine (Doxil)
Europeans give ACVBP +/- Romidepsin (Vindesin not available in the US)
refractory disease" FDA has released 3 drugs, their role and position is being evaluated"
=============
Romidepsin
Pralatrexate
CD30 positive - BRENTUXIMAB VEDOITIN
----------------------------------------------------------------------------------------------
2. some T cell lymphoma are clearly Indolent i.e Mycosis Fungoides (MF)
-------------------------------------------------------------------------------
3. Anaplastic Large cell Lymphoma
ALK negative
for Europeans ACVBP followed by transplant
USA, same paradigm as in PTCL NOS
FOR ALK POSITIVE -- CHOP ALONE IS THE BEST NO TRANSPLANT (NO ETOPOSIDE NEEDED) (THE GERMAN STUDY WAS RETROSPECTIVE )
CRIZOTINIB
PRALATREXATE AND ROMIDEPSIN HAVE BEEN USED IN CLINICAL TRIAL
---------------------------------------------------------------------------------------------------------
4. ANGIOIMMUNOBLASTIC
STEROIDS
SOME CLAIM CYCLOSPORINE (PARTICULARLY WHEN HEMOLYTIC ANEMIA)
IN EUROPE CHOP-ROMIDEPSIN
IN USA, GEMZAR
FOR THOSE WITH A COMPONENT OF CD20 POSITIVE, RITUXAN +STEROID
WHATEVER YOU DO, DON'T GIVE ADRIAMYCIN!
3 AGGRESSIVE TYPES:
==================
1. PTLC- NOS
2. AITL: AngioImmunoblastic
3ALCL (Anaplastic large cell (ALK +) 6% AND alk NEGATIVE
CD30 , t(2,5)(p23,q25)
---------------------------------------------------------------------------------
1 Peripheral T cell lymphoma not otherwise specified
-PET
-Gene Profiling
treat it with EPOCH (CHOEP) or Etoposide based regimen followed by transplant
consider Romidepsin (upfront in Europe)
followed by Gemcitabine, Navelbine (Doxil)
Europeans give ACVBP +/- Romidepsin (Vindesin not available in the US)
refractory disease" FDA has released 3 drugs, their role and position is being evaluated"
=============
Romidepsin
Pralatrexate
CD30 positive - BRENTUXIMAB VEDOITIN
----------------------------------------------------------------------------------------------
2. some T cell lymphoma are clearly Indolent i.e Mycosis Fungoides (MF)
-------------------------------------------------------------------------------
3. Anaplastic Large cell Lymphoma
ALK negative
for Europeans ACVBP followed by transplant
USA, same paradigm as in PTCL NOS
FOR ALK POSITIVE -- CHOP ALONE IS THE BEST NO TRANSPLANT (NO ETOPOSIDE NEEDED) (THE GERMAN STUDY WAS RETROSPECTIVE )
CRIZOTINIB
PRALATREXATE AND ROMIDEPSIN HAVE BEEN USED IN CLINICAL TRIAL
---------------------------------------------------------------------------------------------------------
4. ANGIOIMMUNOBLASTIC
STEROIDS
SOME CLAIM CYCLOSPORINE (PARTICULARLY WHEN HEMOLYTIC ANEMIA)
IN EUROPE CHOP-ROMIDEPSIN
IN USA, GEMZAR
FOR THOSE WITH A COMPONENT OF CD20 POSITIVE, RITUXAN +STEROID
WHATEVER YOU DO, DON'T GIVE ADRIAMYCIN!
Sunday, November 25, 2012
SEARCHING FOR A CANCER CURE
At CRBCM we believe that CPRIT is our necessary path to Victory over Cancer.
We also know we will not get its help this time around, not because we do not deserve the help but frankly because it is distracted. Science is an objective thing. It is a race. You have the right move, the right stuff, you win, no matter where you come from. It is the Olympics without steroids.
We at CRBCM have understood one thing, in the race for the cure, harnessing the force and laws of nature has an unparalleled advantage. Forcing a cell to die can be done by telling and convincing it to die. Or blasting it and crossing our fingers and hoping it will die. Chemotherapy did this mostly the second way but its success was partial. Chemotherapy only works when it manages to finally talk the language. Indeed, some chemotherapy manages to reach the syllables of the cellular language of death.
Sorting through the maze of messages, 2 powerful set of syllables come out:
1. That if it fails to repair broken DNA and therefore does not perform GENE REPAIR, this fact will automatically activate your P53 leading to an automatic stop of the cell into its cycle division. There is no loophole to this principle unless the P53 is abnormal. Knowing this is powerful. Now we understand why Cisplatin (and to some extent Gemcitabine) is a powerful drug because it disrupts the DNA structure. We also understand that cells with rapid repair of DNA, will brush it off, literally.
2.with further proof of principle, we believe that there is a second automatic message or syllables.
Destruction of Microfilaments (and therefore secondarily Microtubules in general) during cell division, leads to an automatic release of Caspase from the Mitochondria no matter what (and this is what includes the BCL-2 protection). It is in this law that resides the strength of Taxanes. Medication that works even in resistant diseases such as Melanoma where Abraxane has a role. Taxanes' limitations appear to be in the type of microtubules attacked. Medication that attacks Microfilament of the type involved in cell divison, where the Centromere is attached, appears to send a more determinant trigger to Caspase release. This is where our interest comes in the Anti-kinesin. We believe and predict that an effective anti-kinesin drug in combination with Taxane and Cisplatin/gemzar based combination, will harness best this law. They will prove to be effective in cure because they will be effective in both treatment and maintenance settings. This is also why the combination of Gemzar and Taxol has proven to be the strongest non platinum combination.
Following this principle, we believe now at CRBCM, that target therapy not following the laws of nature will have only 20-30% response rate, meaning effective in only the cells that lack loophole mechanisms. (this also means because of phenotype heterogeneity, 70-85% of cells have potentially intrinsic loophole to any signal transduction target stimulation or blockage).
Lets keep our eyes on the ball, do not invest in stuff they are throwing at you! More to come...
At CRBCM we believe that CPRIT is our necessary path to Victory over Cancer.
We also know we will not get its help this time around, not because we do not deserve the help but frankly because it is distracted. Science is an objective thing. It is a race. You have the right move, the right stuff, you win, no matter where you come from. It is the Olympics without steroids.
We at CRBCM have understood one thing, in the race for the cure, harnessing the force and laws of nature has an unparalleled advantage. Forcing a cell to die can be done by telling and convincing it to die. Or blasting it and crossing our fingers and hoping it will die. Chemotherapy did this mostly the second way but its success was partial. Chemotherapy only works when it manages to finally talk the language. Indeed, some chemotherapy manages to reach the syllables of the cellular language of death.
Sorting through the maze of messages, 2 powerful set of syllables come out:
1. That if it fails to repair broken DNA and therefore does not perform GENE REPAIR, this fact will automatically activate your P53 leading to an automatic stop of the cell into its cycle division. There is no loophole to this principle unless the P53 is abnormal. Knowing this is powerful. Now we understand why Cisplatin (and to some extent Gemcitabine) is a powerful drug because it disrupts the DNA structure. We also understand that cells with rapid repair of DNA, will brush it off, literally.
2.with further proof of principle, we believe that there is a second automatic message or syllables.
Destruction of Microfilaments (and therefore secondarily Microtubules in general) during cell division, leads to an automatic release of Caspase from the Mitochondria no matter what (and this is what includes the BCL-2 protection). It is in this law that resides the strength of Taxanes. Medication that works even in resistant diseases such as Melanoma where Abraxane has a role. Taxanes' limitations appear to be in the type of microtubules attacked. Medication that attacks Microfilament of the type involved in cell divison, where the Centromere is attached, appears to send a more determinant trigger to Caspase release. This is where our interest comes in the Anti-kinesin. We believe and predict that an effective anti-kinesin drug in combination with Taxane and Cisplatin/gemzar based combination, will harness best this law. They will prove to be effective in cure because they will be effective in both treatment and maintenance settings. This is also why the combination of Gemzar and Taxol has proven to be the strongest non platinum combination.
Following this principle, we believe now at CRBCM, that target therapy not following the laws of nature will have only 20-30% response rate, meaning effective in only the cells that lack loophole mechanisms. (this also means because of phenotype heterogeneity, 70-85% of cells have potentially intrinsic loophole to any signal transduction target stimulation or blockage).
Lets keep our eyes on the ball, do not invest in stuff they are throwing at you! More to come...
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