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Supplements, Research, AML Herbal Regimen

Peer reviewed journal papers preferred (PubMed) see: Google Scholar
Other Resources: NCCAM Clinical Trial Directory, Complimentary Medicine Search
Evidence Based CAM, Oregon State University, Sloan Kettering, Creighton University, NCCAM Herbs, HerbMed, Sigma-Aldrich

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

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.
    Paw paw and cancer: annonaceous acetogenins from discovery to commercial products.
    A novel mechanism for the control of clinical cancer: Inhibition of the production of adenosine triphosphate (ATP) with a standardized extract of paw paw.
    Identification of arctigenin as an antitumor agent having the ability to eliminate the tolerance of cancer cells to nutrient starvation
    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).
      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:
      Differentiation of human myeloid leukemia cells by plant redifferentiation-inducing hormones

ATP depleting agents help choose between apoptosis and necrosis:
      Intracellular adenosine triphosphate (ATP) concentration: a switch in the decision between apoptosis and necrosis.
      Apoptosis and necrosis: different execution of the same death.
      Control of apoptosis by the cellular ATP level.
      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)
Cellular Senescense http://www.ncbi.nlm.nih.gov/pubmed/17667954
      Cellular senescence: when bad things happen to good cells.
      Senescence, apoptosis or autophagy? When a damaged cell must decide its path--a mini-review.
      If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells.
      Cellular senescence, an unpopular yet trustworthy tumor suppressor mechanism
      Cellular senescence and cancer treatment
      Acquisition of oxidative DNA damage during senescence: the first step toward carcinogenesis?
      Pathways connecting telomeres and p53 in senescence, apoptosis, and cancer.
      Tumor cell senescence in cancer treatment.
      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)
      Differential effects of bcl-2 on cell death triggered under ATP-depleting conditions.
      DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosis.
      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)
telomere p53 http://www.ncbi.nlm.nih.gov/pubmed/11447765
      p53-dependent apoptosis pathways
      Telomere dysfunction suppresses spontaneous tumorigenesis in vivo by initiating p53-dependent cellular senescence
      The DNA damage signaling pathway connects oncogenic stress to cellular senescence
      Telomere dysfunction and tumour suppression: the senescence connection.
      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)
Telomerase And Senescense http://www.ncbi.nlm.nih.gov/pubmed/17570133
      Epigenetic and genetic mechanisms contribute to telomerase inhibition by EGCG.
      Telomerase inhibition, telomere shortening, and senescence of cancer cells by tea catechins.
      Blocking telomerase by dietary polyphenols is a major mechanism for limiting the growth of human cancer cells in vitro and in vivo
      Role of telomeres and telomerase in genomic instability, senescence and cancer
      Telomeres, stem cells, and hematology.

Questions re: using Green Tea during/after a transplant: engraftment inhibition? premature aging?
      Replicative senescence of hematopoietic stem cells during serial transplantation: does telomere shortening play a role?
      Telomerase is required to slow telomere shortening and extend replicative lifespan of HSCs during serial transplantation
      Telomeres, senescence, and hematopoietic stem cells.
      Epigenetic and genetic mechanisms contribute to telomerase inhibition by EGCG
      The role of telomere biology in bone marrow failure and other disorders.
      Age-related intrinsic changes in human bone-marrow-derived mesenchymal stem cells and their differentiation to osteoblasts

Do Stem Cells follow the same paths?
      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
      Apoptotic regulation in primitive hematopoietic precursors
      Primitive human hematopoietic precursors express Bcl-x but not Bcl-2.