My mentor pioneered metastatic inflammatory extravasation [J Biomec Eng
8/90 v112 p295+, Cell. 2010 Mar 19;140(6):883-99; Cell. 2006 Jan 27;124(2):263-6] A seminar on antitrypsin made me curious but I found it
causes metastasis [Mol Cell Proteomics. 2012 Nov;11(11):1320-39] causing me
to find articles suggesting trypsin may me antimetastatic [BMJ p240 27Jan
1906; Cancer Res. 2003 Oct 15;63(20):6575-8; Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S16-22] THe exception that may prove the rule is that pancreatic cancer seems to "hide" perhaps because trypsin is made in the pancreas.
From:
vjp2@BioStrategist.com
Newsgroups: sci.med:556777
Subject: Trypsin v metastasis?
Date: Tue, 2 Aug 2016 00:32:33 +0000 (UTC)
Message-ID: nnopn1$puh$
1@reader2.panix.com
My mentor pioneered metastatic inflammatory extravasation, so when I attended a talk on antitrypsin a few months ago, I began a jstor gedanken experiment which led me to wonder if trypsin can combat metastasis. Just a crazy thought: would it make sence to give any cancer survivors with a
serious (eg strep) cold trypsin, heparin, and retanoic acid along with any (mycin antibiotic; followed by a full body xray a month later. There's
another hunch I got about a strep/mycin/NMDAR pathway just anecdotally based
on folks I've know who got a bad cold just before their cancer showe dup.
I don't have any lab or funding, so I'm just guessing here.
Immunity, inflammation, and cancer. Grivennikov SI, Greten FR, Karin M. Cell. 2010 Mar 19;140(6):883-99. Inflammatory responses play decisive roles
at different stages of tumor development, including initiation, promotion, malignant conversion, invasion, and metastasis.
Macrophage diversity enhances tumor progression and metastasis. Qian BZ, Pollard JW. Cell. 2010 Apr 2;141(1):39-51. There is persuasive clinical and experimental evidence that macrophages promote cancer initiation and
malignant progression. During tumor initiation, they create an inflammatory environment that is mutagenic and promotes growth. As tumors progress to malignancy, macrophages stimulate angiogenesis, enhance tumor cell migration and invasion, and suppress antitumor immunity. At metastatic sites,
macrophages prepare the target tissue for arrival of tumor cells, and then a different subpopulation of macrophages promotes tumor cell extravasation, survival, and subsequent growth. Specialized subpopulations of macrophages
may represent important new therapeutic targets.
Condeelis J, Pollard JW. Macrophages: obligate partners for tumor cell migration, invasion, and metastasis. Cell. 2006 Jan 27;124(2):263-6. Macrophages within the tumor microenvironment facilitate angiogenesis and extracellular-matrix breakdown and remodeling and promote tumor cell
motility. Recent studies reveal that direct communication between macrophages and tumor cells leads to invasion and egress of tumor cells into the blood vessels (intravasation).
Nitric oxide synthase II suppresses the growth and metastasis of human cancer regardless of its up-regulation of protumor factors. Le X, Wei D,
Huang S, Lancaster JR Jr, Xie K. Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8758-63. Inducible nitric oxide (NO) synthase (NOS) II has been implicated in macrophage-mediated antitumor activity. However, use of the NOS II gene in cancer therapy is problematic because of the double-edged nature
of NO action. Herein we show that adenoviral vectors mediated effective NOS
II gene transfer into various human tumors. Production of NO significantly up-regulated multiple angiogenic molecules. However, the NO-producing tumor cells did not form tumors or metastases in ectopic or orthotopic xenograft
nude mouse models. The dramatic loss of malignancy was due to NO-mediated apoptosis.
A tumor-suppressive role for trypsin in human cancer progression.
Yamashita K, Mimori K, Inoue H, Mori M, Sidransky D. Cancer Res. 2003 Oct 15;63(20):6575-8. Our results support the notion that trypsin plays a tumor-suppressive role in human carcinoma.
Mixture of trypsin, chymotrypsin and papain reduces formation of metastases and extends survival time of C57Bl6 mice with syngeneic melanoma B16.
Wald M, Olejr T, Sebkov V, Zadinov M, Boubelk M, Pouckov P.
Cancer Chemother Pharmacol. 2001 Jul;47 Suppl:S16-22.
Our data suggest that serine and cysteine proteinases suppress B16
melanoma, and restrict its metastatic dissemination in C57B16 mice.
Trypsin In Cancer Author(s): F. W. Lambelle British Medical Journal,
Vol. 1, No. 2402 (Jan. 12, 1907), p. 113
Secretomic analysis identifies alpha-1 antitrypsin (A1AT) as a required protein in cancer cell migration, invasion, and pericellular fibronectin assembly for facilitating lung colonization of lung adenocarcinoma cells.
Chang YH, Lee SH, Liao IC, Huang SH, Cheng HC, Liao PC. Mol Cell
Proteomics. 2012 Nov;11(11):1320-39. Molecular and pathological confirmation demonstrated that altered expression of A1AT correlates with the metastatic potential of lung adenocarcinoma. The migration and invasion properties of CL1-5 cells were significantly diminished by reducing the expression and secretion of their A1AT proteins.
Angiogenesis inhibition and tumor regression caused by heparin or a
heparin fragment in the presence of cortisone. Folkman J, Langer R, Linhardt RJ, Haudenschild C, Taylor S. Science. 1983 Aug 19;221(4612):719-25.
Heparin or a heparin fragment administered with cortisone inhibited angiogenesis, caused regression of large tumor masses, and prevented metastases.
- = -
Vasos Panagiotopoulos, Columbia'81+, Reagan, Mozart, Pindus, BioStrategist
http://www.panix.com/~vjp2/vasos.htm
---{Nothing herein constitutes advice. Everything fully disclaimed.}---
[Homeland Security means private firearms not lazy obstructive guards]
[Urb sprawl confounds terror] [Phooey on GUI: Windows for subprime Bimbos]
--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)