Complementary Therapies for Sarcomas

Traditional cancer therapies such as chemotherapy, radiation, and surgery have been employed in the treatment of sarcomas. It is true that in part, these therapies have in the past helped to reduce the presence of the disease,  but by in large, conventional therapies have  fallen short of  providing the same type of  outcomes  for sarcomas  that have been possible  for other  forms of  cancer.

Sarcomas have high rates of recurrence, suggesting that conventional therapies have been unable to change the ultimate course of  the disease.  The result is limited survival for many of those diagnosed with different  forms of  sarcoma.  It is also certain  in our understanding, categorization, and subsequent treatment of sarcoma is still in its early stages,  however,  our hope is  that as we learn  more about sarcoma cancers  and how they behave,  we may also  find better and more effective ways to treat these complex and seemingly resilient diseases.

Many patients and clinicians have begun to explore  adjunctive (“complementary”) therapies to assist more conventional treatments in the battle against sarcoma.  It is suggested  if  they are to be considered,  adjunctive therapies should be utilized only      after careful research has been conducted to ensure  such therapies do not interfere     with those prescribed by treating oncologists.

http://uterine-leiomyosarcoma.blogspot.com/

Uterine Leiomyosarcoma can be treated using an integrated approach to healing in     which multiple modalities are employed to support and activate the immune system. Traditional approaches by themselves have not proven effective for this rare type of cancer,  but a comprehensive alternative approach  will activate the immune system, improve well–being,  and sustain quality of life as the body does what it is designed              to do – go after and destroy cancer cells and prevent recurrence of the disease.

All of the information presented on this site has been said to be extracted from peer-reviewed, published studies by well-known academic centers or research institutions.    The founder of this group,  William “Bill” Peeples began his research into this subject    late 1996, when his wife, was diagnosed with endometrial stromal sarcoma, stage IV.   Bill’s wife was told that her cancer was inoperable and other treatments….  would be ineffective.

https://bpccancerprotocol.wordpress.com/the-cocktail-for-active-disease-part-one/

https://bpccancerprotocol.wordpress.com/cocktail-for-active-disease-part-two/

Bill began to research what other therapies might be available.  After initiation of               an alternative therapy, Bill’s wife’s cancer seemed to go into remission in early 1997.   Since then, his wife has remained healthy; however, Bill has continued his research           in an effort to assist other cancer patients including those with sarcomas. To find         other therapies that can assist them in achieving long-term survival.

There is additional info (not included below) re: dichloroacetate and  artemisinin … see:   www.pubmed.gov    

You’ll find additional information at:     www.cancerprotocol.com

 

Let me know if this comes through correctly….This should be the first line with green back ground…

The information about the basic cocktail can be found in the attachment.   There are 35,000 cancer references @ www.pubmed.gov  for the individual components which make up the cocktail.

 The low dose angiopreventative cocktail at the bottom of this page is for people who currently have: No Evidence of Disease  (NED)

William Li: Can we eat to starve cancer? | Video on TED.com

Omega-3 / Omega-6  Ratio and Cancer

http://www.youtube.com/watch?feature=player_detailpage&v=XaDt3AJQ98c#t=2312s

    

A Daring Treatment, a Little Girl’s Survival – New York Times

(click on inside of article) mediamulti video

antiangiogenic chemo:

Low-dose Metronomic Combined with Intermittent Bolus-dose Cyclophosphamide Is

Thrombospondin 1, a mediator of the antiangiogenic effects of low-dose metrono

The Anti-Angiogenic Basis of Metronomic Chemotherapy

cancer and copper:

made easy:

http://www.sciencedaily.com/releases/2004/02/040212080505.htm

Laboratory Study Explains Clinical Promise Of Anti-Angiogenesis Cancer Drug

Copper-Lowering Drug Stabilizes Advanced Cancer In Anti-angiogenesis Trial

Cancer Cells Forming Blood Vessels Send Their Copper To The Edge….

advanced:

X-ray fluorescence microscopy reveals large-scale relocalization and extracell    (edited by Judah Folkman)

Copper Control as an Antiangiogenic Anticancer Therapy: Lessons from Treating

Tetrathiomolybdate Inhibits Angiogenesis and Metastasis Through Suppression  

  Tetrathiomolybdate promotes tumor necrosis and pr events distant metastases by

Copper-dependent activation of hypoxia-inducible f…[Blood. 2005] – PubMed Re

Warburg effect:

As described by Warburg more than 50 years ago, tumour cells maintain a high glycolytic rate even in conditions of adequate oxygen supply. However, most of tumours are subjected to hypoxic conditions due to the abnormal vasculature that supply them with oxygen and nutrients. Thus, glycolysis is essential for tumour survival and spread. A key step in controlling glycolytic rate is the conversion of fructose-6-P to fructose-1,6-P(2) by 6-phosphofructo-1-kinase (PFK-1). The activity of PFK-1 is allosterically controlled by fructose-2,6-P(2), the product of the enzymatic activity of a dual kinase/phosphatase family of enzymes (PFKFB1-4) that are increased in a significant number of tumour types.. Thus, targeting PFKFB enzymes, either directly or through inhibition of HIF-1, appears as a promising approach for the treatment of certain tumours. In turn, these enzymes are induced by hypoxia through the activation of the HIF-1 complex (hypoxia-inducible complex-1), a transcriptional activator that controls the expression of most of hypoxia-regulated genes. HIF-1 complex is overexpressed in a variety of tumours and its expression appears to correlate with poor prognosis and responses to chemo or radiotherapy

PMID: 17661163 [PubMed – indexed for MEDLINE

Energy Boost: The Warburg Effect Returns in a New Theory of Cancer — Garber 9

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How Vitamin C Stops Cancer   ()   HIF-1 inhibition hyperlinked article

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N-acetyl-cysteine promotes angiostatin production and vascular collapse in an orthotopic model of breast cancer.

Agarwal AMuñoz-Nájar UKlueh UShih SCClaffey KP.

Department of Physiology, University of Connecticut Health Center, Farmington, Connecticut 06030-3501, USA.

The antioxidant N-acetyl-cysteine (NAC) has been shown to be chemopreventive in clinical studies, and in recent studies, has shown promise in preventing tumor progression. Although the effects of NAC on tumorigenesis have been associated with decreased angiogenesis, the mechanism of the anti-angiogenic activity has not been determined. In the following study, we describe a novel mechanism whereby NAC therapy blocks MDA-MB-435 breast carcinoma cell proliferation and metastasis in an in v iv o tumorigenic model. Athymic nude mice bearing MDA-MB-435 xenografts were treated with systemic NAC daily for 8 weeks. NAC treatment resulted in endothelial cell apoptosis and reduction of microvascular density within the core of the tumor leading to significant tumor cell apoptosis/necrosis. Angiostatin accumulated in tumors from NAC-treated but not control animals. Additional studies using a vascular endothelial growth factor-dependent chicken chorioallantoic membrane angiogenic assay recapitulated NAC-induced endothelial apoptosis and coordinate production of angiostatin, a potent endothelial apoptotic factor. In vitro studies showed angiostatin was formed in endothelial cultures in a vascular endothelial growth factor- and NAC-dependent manner, a process that requires endothelial cell surface plasminogen activation. These results suggest that systemic NAC therapy promotes anti-angiogenesis through angiostatin production, resulting in endothelial apoptosis and vascular collapse in the tumor.

PMID: 15111315 [PubMed – indexed for MEDLINE]

PMCID: PMC1615662

Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports.

Nebeling LCMiraldi FShurin SBLerner E .

Nutrition Department, Case Western Reserve University, School of Medicine, Cleveland, Ohio, USA.

OBJECTIVE: Establish dietary-induced ketosis in pediatric oncology patients to determine if a ketogenic state would decrease glucose availability to certain tumors, thereby potentially impairing tumor metabolism without adversely affecting the patient’s overall nutritional status. DESIGN: Case report. SETTING: University Hospitals of Cleveland. SUBJECTS: Two female pediatric patients with advanced stage malignant Astrocytoma tumors. INTERVENTIONS: Patients were followed as outpatients for 8 weeks. Ketosis was maintained by consuming a 60% medium chain triglyceride oil-based diet. MAIN OUTCOME MEASURES: Tumor glucose metabolism was assessed by Positron Emission Tomography (PET), comparing [Fluorine-18] 2-deoxy-2-fluoro-D-glucose (FDG) uptake at the tumor site before and following the trial period. RESULTS: Within 7 days of initiating the ketogenic diet, blood glucose levels declined to low-normal levels and blood ketones were elevated twenty to thirty fold. Results of PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects. One patient exhibited significant clinical improvements in mood and new skill development during the study. She continued the ketogenic diet for an additional twelve months, remaining free of disease progression. CONCLUSION: While this diet does not replace conventional antineoplastic treatments, these preliminary r=2 0esults suggest a potential for clinical application which merits further research.

PMID: 7790697 [PubMed – indexed for MEDLINE]

Targeting energy metabolism in brain cancer: review and hypothesis.

Seyfried TNMukherjee P.

Biology Department, Boston College, Chestnut Hill, MA 02467, USA. thomas.seyfried@bc.edu

Malignant brain tumors are a significant health problem in children and adults and are often3D2 0unmanageable. As a metabolic disorder involving the dysregulation of glycolysis and respiration, malignant brain cancer is potentially manageable through changes in metabolic environment. A radically different approach to brain cancer management is proposed that combines metabolic control analysis with the evolutionarily conserved capacity of normal cells to survive extreme shifts in physiological environment. In contrast to malignant brain tumors that are largely dependent on glycolysis for energy, normal neurons and glia readily transition to ketone bodies (beta-hydroxybutyrate) for energy in vivo when glucose levels are reduced. The bioenergetic transition from glucose to ketone bodies metabolically targets brain tumors through integrated anti-inflammatory, anti-angiogenic, and pro-apoptotic mechanisms. The approach focuses more on the genomic flexibility of normal cells than on the genomic defects of tumor cells and is supported from recent studies in orthotopic mouse brain tumor models and in human pediatric astrocytoma treated with dietary energy restriction and the ketogenic diet.

PMID: 16242042 [PubMed]

PMCID: PMC1276814

Clinical Trials (PDQ®) – National Cancer Institute  (Atkins trial through NCI at Albert Einstein Medical College)

SHS North America — KetoCal                 (Ketogenic formulation for those with cachexia)

LOW DOSE ANGIOPREVENTATIVE COCKTAIL

1  500mg Acetyl-l-carnitine* SW 1000 100 caps

1  600 mg Alpha lipoic acid* SWU190 120 caps

1  325 mg. Aspirin

1  B 100 complex multi-vitamin with 500mg of C

1  900 mg Curcumin Complex * SWH084 60 caps

1  600 mg Green Tea Extract

1  250 mg Korean Ginseng * SW426 300 caps

2   3 mg Melantonin* SW502 120 caps

1  500 mg Milk Thistle * D7SW966 100 caps

1  600 mg N-acetylcysteine* SW854 100 caps

1 1000 mg Omega three fish oil

1 30 mg Resveratrol Complex * SWU248 60 caps

1 100 mcg Selenium* SW545 300 caps

1 550 mg Shark liver oil* SWU107 60 SFG

1 1,000 IU Vitamin D-3 * SW1030 250 caps

1 50 mg Zinc Gluconate* SW205 100 caps

*Swanson Health Products 1(800) 437-4148 (low cost)

Bill Peeples (954) 424-8424

*** Do not take Angio-preventative Cocktail …. While healing…. (from surgery, fracture or other trauma) While pregnant. 

For more information: 
< /A> “search archives” www.sciencedaily.com
www.pubmed.gov
www.cancerprotocol.com Bill Peeples (954)424-8424 
whpeeples@aol.com

This Blog Post is dedicates to the memory of my friends sister:

Jennifer Lochtefeld  Born on Nov. 13, 1973

Passed away at 8:03 a.m. on June 9, 2015

at The James Cancer Center in Columbus, Ohio.

 

 

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