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beachlifeisfun

11/18/15 10:32 AM

#45265 RE: Pyrrhonian #45263

I notice that most of your references are rather dated...the area has advanced substantially since the publishing of most of these works...

One of the more recent ones (2011) you cite does stand out:

Conclusion
Intradermal vaccination resulted in superior anti-tumor T cell induction when compared to intranodal vaccination. No advantage of additional IL-2 treatment could be demonstrated.



http://clincancerres.aacrjournals.org/content/early/2011/07/19/1078-0432.CCR-11-1261.full.pdf

Note that I do not consider the 2015 review that you cite as recent, since it is simply review of past work.

By the way, can you tell me whether DC-Vax-L uses naturally occurring DC or are they monocyte derived?

From the same article that you cited:

the overall survival of patients treated with pDCs was greatly increased in comparison to matched controls treated with standard chemotherapy.

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TheFollower

11/18/15 10:42 AM

#45269 RE: Pyrrhonian #45263

Pyr's Article:
Clin Cancer Res. 2003 Nov 1

Beach's:
Clin Cancer Res. 2011 Mar 15;
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CaptainObvious

11/18/15 10:51 AM

#45270 RE: Pyrrhonian #45263

You very well know that the maturity level of the DC is claimed by NWBO as the secret sauce. The immaturity stage in the study you cite could be completely different.

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gnawkz

11/18/15 7:22 PM

#45292 RE: Pyrrhonian #45263

Hey Pyrr, questions:

1. Are the DCs for DCVax-L not already matured when injected into the body? I thought only DCVax-D is partially matured upon injection.

2. Is there a difference between partial maturity and immaturity? Previous communications from the company indicate there is a substantial difference. Have you found research to suggest otherwise?

3. The immaturity referenced in the case studies that you've shared, are those immature DCs or already on their pathway to maturation?

4. Is the type of cancer important here? GBM vs Melanoma?

5. Is the size of the tumor an important factor here? The studies you've shared are for Melanoma, a type of cancer that can grow to be of a substantial size. For GBM, since space is limited, it cannot grow beyond a certain size. Is it logical to correlate the size of the tumor with the effectiveness of the immunosuppressive environment? (Larger tumor = stronger immunosuppressive environment.)

6. In addition, if the size of the tumor is minimal, would the number of DCs needed to migrate to the lymph node be smaller for there to be a clinical benefit?

Thanks in advance for the research.