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Supplements, Research, AML Herbal Regimen

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Apoptosis, Review, Epigenetics, ROS Therapy, Blood-Brain, Cell Paths, Synergisms
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Cellular Demise - Many Ways To Go:

5/25/2009

This page all started from a discussion I was having with my friend Jeff. about the role ATP depletion plays in triggering apoptosis and/or eliminating chemo resistance. I believe ATP depletion plays a supporting, not necessarily primary role in cancer treatment. I've been suggesting that constant usage of ATP depleting supplements inhibits apoptosis. This is an attempt to organize some of the reasons, methods, and tools I use to achieve cancer cell destinations.

New research on Jasmonates (plant hormones) show that they deplete ATP and direct towards necrosis instead of apoptosis. I haven't been able to obtain jasmonates, however something I do have is PawPaw which contains the most potent (ATP depleting) annonaceous acetogenins. I also use Burdock and Dong Quai to push cancer cells over the nutrient starvation edge.

http://www.ncbi.nlm.nih.gov/pubmed/18598079
    Paw paw and cancer: annonaceous acetogenins from discovery to commercial products.
http://www.pawpawresearch.com/pawpaw-trials1.pdf
    A novel mechanism for the control of clinical cancer: Inhibition of the production of adenosine triphosphate (ATP) with a standardized extract of paw paw.
http://www.ncbi.nlm.nih.gov/pubmed/16452235
    Identification of arctigenin as an antitumor agent having the ability to eliminate the tolerance of cancer cells to nutrient starvation
http://www.ncbi.nlm.nih.gov/pubmed/16288865
    Angelmarin, a novel anti-cancer agent able to eliminate the tolerance of cancer cells to nutrient starvation

These days (see dosage log) I am coordinating these tools (PawPaw, Burdock, Dong Quai)
    ...with ROS therapy agents (Green Tea, Curcumin, FeverFew, Garlic, Quercetin, Ellagic Acid, etc.)
    ...Differentiation Therapy agents (Rieshi Mushrooms, Curcumin, etc.)
    ...and Immune Modulating agents (Rieshi, Shitake, Maitake, Una da Gato, etc.)

It is fascinating how all these tools synergize, modulating cellular metabolism to
    ...help "decide" between differentiation, and apoptosis
    ...redirect cell death from apoptosis towards necrosis
    ...or push towards senescence (hopefully eventual phagocytosis)
    ...and promote or block autophagy (option or distraction).

http://www.ncbi.nlm.nih.gov/pubmed/19351640
Programmed cell death and cancer

While it might be more elegant to shift gears
onto the apoptosis exit ...sometimes our only
option might be to pop the clutch in 4th,
kill the engine, and get towed off.

Antioxidents help choose between apoptosis and differentiation:

http://www.ncbi.nlm.nih.gov/pubmed/12685824
Differentiation of human myeloid leukemia cells by plant redifferentiation-inducing hormones

ATP depleting agents help choose between apoptosis and necrosis:

http://www.ncbi.nlm.nih.gov/pubmed/9126928
      Intracellular adenosine triphosphate (ATP) concentration: a switch in the decision between apoptosis and necrosis.
http://www.ncbi.nlm.nih.gov/pubmed/10989658
      Apoptosis and necrosis: different execution of the same death.
http://www.ncbi.nlm.nih.gov/pubmed/8549813
      Control of apoptosis by the cellular ATP level.
http://www.ncbi.nlm.nih.gov/pubmed/10567915
      Aponecrosis: morphological and biochemical exploration of a syncretic process of cell death sharing apoptosis and necrosis.

Senescense - another "fork in the road" (with risks?) (immune modulation ...end with phagocytosis)

http://www.ncbi.nlm.nih.gov/pubmed/17667954
      Cellular senescence: when bad things happen to good cells.
http://www.ncbi.nlm.nih.gov/pubmed/18451641
      Senescence, apoptosis or autophagy? When a damaged cell must decide its path--a mini-review.
http://www.ncbi.nlm.nih.gov/pubmed/11991684
      If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells.
http://www.ncbi.nlm.nih.gov/pubmed/14611669
      Cellular senescence, an unpopular yet trustworthy tumor suppressor mechanism
http://www.ncbi.nlm.nih.gov/pubmed/17027159
      Cellular senescence and cancer treatment
http://www.ncbi.nlm.nih.gov/pubmed/18056954
      Acquisition of oxidative DNA damage during senescence: the first step toward carcinogenesis?
http://www.ncbi.nlm.nih.gov/pubmed/15865944
      Pathways connecting telomeres and p53 in senescence, apoptosis, and cancer.
http://www.ncbi.nlm.nih.gov/pubmed/12782571
      Tumor cell senescence in cancer treatment.
http://www.ncbi.nlm.nih.gov/pubmed/7097159
      Phagocytosis of senescent neutrophils by human monocyte-derived macrophages and rabbit inflammatory macrophages

Bcl-2 protein imbalance prevents apoptosis/necrosis/senescense (making Green Tea (EGCG) especially helpful)

http://www.ncbi.nlm.nih.gov/pubmed/11120600
      Differential effects of bcl-2 on cell death triggered under ATP-depleting conditions.
http://www.ncbi.nlm.nih.gov/pubmed/17565509
      DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosis.
http://www.ncbi.nlm.nih.gov/pubmed/14678963
      Cancer prevention by tea polyphenols is linked to their direct inhibition of antiapoptotic Bcl-2-family proteins

p53 necessary for BOTH apoptosis and senescense pathways (thank you Quercetin)

http://www.ncbi.nlm.nih.gov/pubmed/11447765
      p53-dependent apoptosis pathways
http://www.ncbi.nlm.nih.gov/pubmed/17396137
      Telomere dysfunction suppresses spontaneous tumorigenesis in vivo by initiating p53-dependent cellular senescence
http://www.ncbi.nlm.nih.gov/pubmed/17671427
      The DNA damage signaling pathway connects oncogenic stress to cellular senescence
http://www.ncbi.nlm.nih.gov/pubmed/18500246
      Telomere dysfunction and tumour suppression: the senescence connection.
http://www.ncbi.nlm.nih.gov/pubmed/15735102
      Ellagic acid potentiates the effect of quercetin on p21waf1/cip1, p53, and MAP-kinases without affecting intracellular generation of reactive oxygen species in vitro.

Telomerase can prevent senescense signaling (but again - thank you Green Tea)

http://www.ncbi.nlm.nih.gov/pubmed/17570133
      Epigenetic and genetic mechanisms contribute to telomerase inhibition by EGCG.
http://www.ncbi.nlm.nih.gov/pubmed/9712707
      Telomerase inhibition, telomere shortening, and senescence of cancer cells by tea catechins.
http://www.ncbi.nlm.nih.gov/pubmed/12591733
      Blocking telomerase by dietary polyphenols is a major mechanism for limiting the growth of human cancer cells in vitro and in vivo
http://www.ncbi.nlm.nih.gov/pubmed/17767195
      Role of telomeres and telomerase in genomic instability, senescence and cancer
http://www.ncbi.nlm.nih.gov/pubmed/18263784
      Telomeres, stem cells, and hematology.

Questions re: using Green Tea during/after a transplant: engraftment inhibition? premature aging?

http://www.ncbi.nlm.nih.gov/pubmed/12032768
      Replicative senescence of hematopoietic stem cells during serial transplantation: does telomere shortening play a role?
http://www.ncbi.nlm.nih.gov/pubmed/12663456
      Telomerase is required to slow telomere shortening and extend replicative lifespan of HSCs during serial transplantation
http://www.ncbi.nlm.nih.gov/pubmed/17960423
      Telomeres, senescence, and hematopoietic stem cells.
http://www.ncbi.nlm.nih.gov/pubmed/17570133
      Epigenetic and genetic mechanisms contribute to telomerase inhibition by EGCG
http://www.ncbi.nlm.nih.gov/pubmed/18160098
      The role of telomere biology in bone marrow failure and other disorders.
http://www.ncbi.nlm.nih.gov/pubmed/18248663
      Age-related intrinsic changes in human bone-marrow-derived mesenchymal stem cells and their differentiation to osteoblasts

Do Stem Cells follow the same paths?

http://www.ncbi.nlm.nih.gov/pubmed/10969785
      Human acute myeloid leukemia CD34+/CD38- progenitor cells have decreased sensitivity to chemotherapy and Fas-induced apoptosis, reduced immunogenicity, and impaired dendritic cell transformation capacities
http://www.ncbi.nlm.nih.gov/pubmed/9731062
      Apoptotic regulation in primitive hematopoietic precursors
http://www.ncbi.nlm.nih.gov/pubmed/7542499
      Primitive human hematopoietic precursors express Bcl-x but not Bcl-2.

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