Replies to post #200801 on Avid Bioservices Inc (CDMO)

[Carboat]

Not just the general investment community unable to put pieces together , neither can: the bio media scientists and doctors, the hedge funds that specialize in bio, their PhD researchers, the bio median and journals with their scientists ...good thing we have penny stock board members here.

[biopharm]

Harold Dvorak : Peregrine Pharmaceuticals KOL : Cancer starts with Inflammation : Part II

...chronic inflammation fuels cancer.

Lots of information along this chain of posts with Harold Dvorak and the small quote above is all part of the mix: Cancer from inflammation, MDSC's..etc from a tumor that is like that wound that never heals. Its only a matter of time before we have some bigger message being covered in dept, in exactly what has been discovered along the Notch Signaling pathway that builds up, that is bad and eventually leads to cancer.

A wound that fails to heal properly is where it all begins.

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Tumors: Wounds That Do Not Heal—Redux

Harold F. Dvorak*

This Article

doi: 10.1158/2326-6066.CIR-14-0209 Cancer Immunol Res
January 2015 3; 1



- Author Affiliations

The Center for Vascular Biology Research and the Departments of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.

?*Corresponding Author:
Harold F. Dvorak, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, RN227C, Boston, MA 02215. Phone: [phone]; Fax: [phone]; E-mail: [e-mail]

Abstract

Similarities between tumors and the inflammatory response associated with wound healing have been recognized for more than 150 years and continue to intrigue. Some years ago, based on our then recent discovery of vascular permeability factor (VPF)/VEGF, I suggested that tumors behaved as wounds that do not heal. More particularly, I proposed that tumors co-opted the wound-healing response to induce the stroma they required for maintenance and growth. Work over the past few decades has supported this hypothesis and has put it on a firmer molecular basis. In outline, VPF/VEGF initiates a sequence of events in both tumors and wounds that includes the following: increased vascular permeability; extravasation of plasma, fibrinogen and other plasma proteins; activation of the clotting system outside the vascular system; deposition of an extravascular fibrin gel that serves as a provisional stroma and a favorable matrix for cell migration; induction of angiogenesis and arterio-venogenesis; subsequent degradation of fibrin and its replacement by “granulation tissue” (highly vascular connective tissue); and, finally, vascular resorption and collagen synthesis, resulting in the formation of dense fibrous connective tissue (called “scar tissue” in wounds and “desmoplasia” in cancer). A similar sequence of events also takes place in a variety of important inflammatory diseases that involve cellular immunity. Cancer Immunol Res; 3(1); 1–11. ©2015 AACR.

http://cancerimmunolres.aacrjournals.org/content/3/1/1.full?ijkey=uOMFhATZNzdzs&keytype=ref&siteid=aacrjnls

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Myeloid-Derived Suppressor Cells: Linking Inflammation and Cancer

April 15, 2009

The concept that chronic inflammation contributes to tumor initiation and progression was proposed by the German pathologist Rudolf Virchow over 140 years ago (1). Although his hypothesis was overlooked for many years, abundant epidemiological data show a strong correlation between inflammation and cancer incidence. For example, mesothelioma, lung, prostate, bladder, pancreatic, cervical, esophageal, melanoma, and head and neck cancers are frequently associated with long-term inflammation, whereas gall bladder, liver, ovarian, colorectal, and bladder cancers are associated with specific infectious agents (2, 3, 4). Additional evidence linking inflammation and cancer comes from studies demonstrating that long-term users of nonsteroidal anti-inflammatory drugs, including aspirin, are at a significantly lower risk of developing colorectal (5), lung, stomach, esophageal (6),and breast (4) cancers. There is also experimental data supporting a causative relationship between chronic inflammation and cancer onset and progression. For example, blocking inflammatory mediators or signaling pathways regulating inflammation reduces tumor incidence and delays tumor growth, while heightened levels of proinflammatory mediators or adoptive transfer of inflammatory cells increases tumor development (4). These findings have renewed interest in Virchow’s hypothesis and have led to studies aimed at clarifying the mechanisms responsible for the association.

http://www.jimmunol.org/content/182/8/4499.full

I think its been long enough that many have known what leads to cancer and whether we pinpoint MDSC's or inflammation, how long is it before the world knows that PS Targeting is the absolute #1 solution that is safe and synergistic with all of the greedy BP pipelines.

Digging deeper and just may be coincidence, but I found a nice little picture example of "inflammation" and the most common effects from a "biolegend" website...I know, it can't be "the family" but lots of stranger things have happened.

http://www.biolegend.com/media_assets/basic_immunology/Inflammation.jpg