Tag Archives: liver cancer

Is Your Cancer Curable or Just Treatable

Can Your Type of Cancer be Cured or Just Treated?

Because of the growing list on the Real Poisoning of America – Glycation, it’s become evident that I need to display a different post for the different types of damage that glycation induces. For all forms of cancer, I’ll reserve this notice for that purpose only. All reports Of CVDs and other heart disorders will be located on the Atherosclerosis page.  Dementias will be on a separate post as well with all other diseases and disorders inflammation is responsible for.

Listed below from PubMed or PMC or the FDA are reports of studies done on the effects of glycation and its influence in any cancer, which is a direct cause of glycation.

The whole premise behind these posts is to prove that the only way you can prevent these horrendous diseases, is to stop the glycation that is responsible for them and the only way you can stop the glycation is to stop feeding it. It’s really a simple solution, just not an easy one because of the addiction factor. However, YOU and only YOU have control over this and it all depends on what YOU put in you mouth when you eat.

I’ll admit that that can be hard when you have a whole industry trying to get you to eat more of what it is that glycates. This is because they are connected to another industry that feeds off of the unsuspected that buy into this ruse, all those whom the glycation affects, the public.

This report is dated Aug 9, 2016 and details AGEs role in lung cancer;

Hsia TC1,2, Yin MC3,4, Mong MC5.

Author information


Effects of carboxymethyllysine (CML) and pentosidine, two advanced glycation end-products (AGEs), upon invasion and migration in A549 and Calu-6 cells, two non-small cell lung cancer (NSCLC) cell lines were examined. CML or pentosidine at 1, 2, 4, 8 or 16 μmol/L were added into cells. Proliferation, invasion and migration were measured. CML or pentosidine at 4-16 μmol/L promoted invasion and migration in both cell lines, and increased the production of reactive oxygen species, tumor necrosis factor-α, interleukin-6 and transforming growth factor-β1. CML or pentosidine at 2-16 μmol/L up-regulated the protein expression of AGE receptor, p47(phox), intercellular adhesion molecule-1 and fibronectin in test NSCLC cells. Matrix metalloproteinase-2 protein expression in A549 and Calu-6 cells was increased by CML or pentosidine at 4-16 μmol/L. These two AGEs at 2-16 μmol/L enhanced nuclear factor κ-B (NF-κ B) p65 protein expression and p38 phosphorylation in A549 cells. However, CML or pentosidine at 4-16 μmol/L up-regulated NF-κB p65 and p-p38 protein expression in Calu-6 cells. These findings suggest that CML and pentosidine, by promoting the invasion, migration and production of associated factors, benefit NSCLC metastasis.

KEYWORDS:  CML; invasion; migration; non-small cell lung cancer; pentosidine

PMID: 27517907

PMCID: PMC5000686 DOI: 10.3390/ijms17081289 [PubMed – in process]  Free PMC Article

The following report submitted Sept 1, 2008 was concerned about RAGEs their correlation with cervical cancer;

  • Induction ofreceptor for advanced glycation end products by EBV latent membrane protein 1 and its correlation with angiogenesis and cervical lymph node metastasis in nasopharyngeal carcinoma.



The EBV oncoprotein, latent membrane protein 1 (LMP1), contributes to the metastasis of nasopharyngeal carcinoma (NPC) by inducing factors to promote tumor invasion and angiogenesis. The receptor for advanced glycation end products (RAGE) is associated with abnormal angiogenesis in diabetic microangiopathies. Moreover, some papers have suggested the association of RAGE overexpression with tumor metastasis; thus, the associations of RAGE with LMP1 and angiogenesis in NPC were examined.


Forty-two patients with NPC were evaluated for expressions of LMP1, RAGE, and S100 proteins and for microvessel counts by immunohistochemistry. Then, the RAGE induction by LMP1 was examined with Western blotting and luciferase reporter assay.


The microvessel counts were significantly higher in patients with high LMP1 expression or high RAGE expression compared with cases with low expressions (P=0.0049 and P<0.0001), respectively. Patients with advanced N classification were also significantly increased in these groups (P=0.0484 and P=0.0005). The expressions of LMP1 and RAGE proteins were clearly correlated in NPC tissues (P=0.0093). Transient transfection with LMP1 expression plasmid induced RAGE protein in Ad-AH cells. The expression of LMP1 transactivated the RAGE promoter as shown by luciferase reporter assay. Mutation of the reporter at nuclear factor-kappaB binding site (-671 to -663) abolished transactivation of the RAGE promoter by LMP1.


These results suggest that LMP1-induced RAGE enhances lymph node metastasis through the induction of angiogenesis in NPC. Nuclear factor-kappaB binding site (-671 to -663) is essential for transactivation of the RAGE promoter by LMP1.

As of today January 10, 2017 this news still has not been publicized, yet! No warnings about what causes glycation, only warnings against what doesn’t cause it.

One wouldn’t think that brain cancer would be affected by glycation, yet with clear evidence of it in the following report, dated Mar 2008;

  • HMGB1 as an autocrine stimulus in human T98G glioblastoma cells: role in cell growth and migration.


HMGB1 (high mobility group box 1 protein) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation and migration, mainly through RAGE (the receptor for advanced glycation end products); HMGB1-RAGE interactions have been found to be important in a number of cancers. We investigated whether HMGB1 is an autocrine factor in human glioma cells. Western blots showed HMGB1 and RAGE expression in human malignant glioma cell lines. HMGB1 induced a dose-dependent increase in cell proliferation, which was found to be RAGE-mediated and involved the MAPK/ERK pathway. Moreover, in a wounding model, it induced a significant increase in cell migration, and RAGE-dependent activation of Rac1 was crucial in giving the tumour cells a motile phenotype. The fact that blocking DNA replication with anti-mitotic agents did not reduce the distance migrated suggests the independence of the proliferative and migratory effects. We also found that glioma cells contain HMGB1 predominantly in the nucleus, and cannot secrete it constitutively or upon stimulation; however, necrotic glioma cells can release HMGB1 after it has translocated from the nucleus to cytosol. These findings provide the first evidence supporting the existence of HMGB1/RAGE signalling pathways in human glioblastoma cells, and suggest that HMGB1 may play an important role in the relationship between necrosis and malignancy in glioma tumours by acting as an autocrine factor that is capable of promoting the growth and migration of tumour cells.

Even brain cancer is susceptible to glycation and its destructive effects. I can’t seem to find a cancer that isn’t affected by glycation.

The following study done in Sep 2013, and was concerned with the role of insulin and Insulin Growth Factor (IGF-1) signaling in cancer;


Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors in aging. GH/Insulin/insulin-like growth factor 1 (IGF-1) signaling molecules that have been linked to longevity include daf-2 and InR and their homologues in mammals, and inactivation of the corresponding genes increases lifespan in nematodes, fruit flies and mice. The life-prolonging effects of caloric restriction are likely related to decreasing IGF-1 levels. Evidence has emerged that antidiabetic drugs are promising candidates for both lifespan extension and prevention of cancer. Thus, antidiabetic drugs postpone spontaneous carcinogenesis in mice and rats, as well as chemical and radiation carcinogenesis in mice, rats and hamsters. Furthermore, metformin seems to decrease the risk for cancer in diabetic patients…

Research conducted during the last 15-20 years firmly established insulin, insulin-like and homologous signaling as key regulators of aging and longevity in organisms ranging from yeast to mammals.…disregulation of insulin signaling and carbohydrate homeostasis in diabetes produces numerous aging-like symptoms including increased risk of cancer and other age-related disease.

Three years after that study was completed and no word has reached the media to tell the public about this finding.

Published Oct 12, 2016, the following report acknowledges that diet plays a large role in the formation of AGEs the single most important factor in cancer, as AGEs are at the root of all cancers;


While the socioeconomic and environmental factors associated with cancer disparity have been well documented, the contribution of biological factors is an emerging field of research. Established disparity factors such as low income, poor diet, drinking alcohol, smoking, and a sedentary lifestyle may have molecular effects on the inherent biological makeup of the tumor itself, possibly altering cell signaling events and gene expression profiles to profoundly alter tumor development and progression. Our understanding of the molecular and biological consequences of poor lifestyle is lacking, but such information may significantly change how we approach goals to reduce cancer incidence and mortality rates within minority populations. In this review, we will summarize the biological, socioeconomic, and environmental associations between a group of reactive metabolites known as advanced glycation end-products (AGEs) and cancer health disparity. Due to their links with lifestyle and the activation of disease-associated pathways, AGEs may represent both a biological consequence and a bio-behavioral indicator of poor lifestyle which may be targeted within specific populations to reduce disparities in cancer incidence and mortality.

Published at the end of last year was this report on the effects of HMGB1 on most all lung diseases;


Lung diseases remain a serious problem for public health. The immune status of the body is considered to be the main influencing factor for the progression of lung diseases. HMGB1 (high-mobility group box 1) emerges as an important molecule of the body immune network. Accumulating data have demonstrated that HMGB1 is crucially implicated in lung diseases and acts as independent biomarker and therapeutic target for related lung diseases. This review provides an overview of updated understanding of HMGB1 structure, release styles, receptors and function. Furthermore, we discuss the potential role of HMGB1 in a variety of lung diseases. Further exploration of molecular mechanisms underlying the function of HMGB1 in lung diseases will provide novel preventive and therapeutic strategies for lung diseases.

The following report details the overexpression of glycation in ovarian cancer. It was submitted Oct 28, 2016;



Ovarian cancer is one of the important challenges in the field of gynecologic oncology because of some problems in understanding its etiology and pathogenesis. Receptor for advanced glycation end products (RAGE) is a multiligand trans-membranous receptor which is upregulated in some human cancers. Mechanisms of RAGE involvement in carcinogenesis of ovarian cancer are unknown.


This study aimed to investigate the expression of RAGE in ovarian cancers and its association with clinicopathological characteristics.


The RAGE expression level in ovarian cancer and corresponding noncancerous tissues were analyzed by real time quantitative RT-PCR and immunohistochemistry techniques.


Results indicated that RAGE gene was overexpressed in ovarian cancer tissue compared with adjacent noncancerous tissue (p < 0.001). A significant association between RAGE expression and tumor size (p = 0.04), depth of stromal invasion (p = 0.031), lymphovascular invasion (p = 0.041) and stage of cancer (p = 0.041) was observed. The receiver operating characteristic (ROC) analyses yielded the area under the curve (AUC) values of 0.86 for RAGE in discriminating ovarian cancer samples from non-cancer controls.


In conclusion overexpression of RAGE in ovarian cancer may be a useful biomarker to predict tumor progression.

What interests me is that nothing is said about what creates these RAGEs. For thirty years they’ve been examining the nature of glycation but have said nothing about what is responsible for the major portion of glycation, glucose consumption in the form of sugar and grains. I guess that’s not profitable.

What is profitable is finding more drugs to make people need more and more drugs. Evidenced here in this report dated Oct 23, 2014, yet nothing has been announced about this report, Did you hear about it?


A hypoxic tumor microenvironment is characteristic of many cancer types, including one of the most lethal, pancreatic cancer. We recently demonstrated that the receptor for advanced glycation end products (RAGE) has an important role in promoting the development of pancreatic cancer and attenuating the response to chemotherapy. We now demonstrate that binding of RAGE to oncogenic KRAS facilitates hypoxia-inducible factor 1 (HIF1)α activation and promotes pancreatic tumor growth under hypoxic conditions. Hypoxia induces NF-κB-dependent and HIF1α-independent RAGE expression in pancreatic tumor cells. Moreover, the interaction between RAGE and mutant KRAS increases under hypoxia, which in turn sustains KRAS signaling pathways (RAF-MEK-ERK and PI3K-AKT), facilitating stabilization and transcriptional activity of HIF1α. Knock down of RAGE in vitro inhibits KRAS signaling, promotes HIF1α degradation, and increases hypoxia-induced pancreatic tumor cell death. RAGE-deficient mice have impaired oncogenic KRAS-driven pancreatic tumor growth with significant downregulation of the HIF1α signaling pathway. Our results provide a novel mechanistic link between NF-κB, KRAS, and HIF1α, three potent molecular pathways in the cellular response to hypoxia during pancreatic tumor development and suggest alternatives for preventive and therapeutic strategies.

Obviously the continuing need to examine the damage instead of warning about the glycating substance proves to be more lucrative than realizing the actual cure, removing the glycating substances from the diet. Too be removal involves conquering an addiction. That wouldn’t be too bad if this addiction wasn’t inflicted on us. But it was, making this addiction damn near impossible to conquer.

This is evidenced by this study dated July 18, 2016 and shows the influence of HMGB1 and M2 like macrophages;


Hypoxia is a hallmark of cancer that is strongly associated with invasion, metastasis, resistance to therapy and poor clinical outcome. Tumour hypoxia affects immune responses and promotes the accumulation of macrophages in the tumour microenvironment. However, the signals linking tumour hypoxia to tumour-associated macrophage recruitment and tumour promotion are incompletely understood. Here we show that the damage-associated molecular pattern High-Mobility Group Box 1 protein (HMGB1) is released by melanoma tumour cells as a consequence of hypoxia and promotes M2-like tumour-associated macrophage accumulation and an IL-10 rich milieu within the tumour. Furthermore, we demonstrate that HMGB1 drives IL-10 production in M2-like macrophages by selectively signalling through the Receptor for Advanced Glycation End products (RAGE). Finally, we show that HMGB1 has an important role in murine B16 melanoma growth and metastasis, whereas in humans its serum concentration is significantly increased in metastatic melanoma. Collectively, our findings identify a mechanism by which hypoxia affects tumour growth and metastasis in melanoma and depict HMGB1 as a potential therapeutic target.

Stomach cancer is influenced as well by glycation as explained in this report submitted Oct 1, 2015;


Micrometastasis is the major cause of treatment failure in gastric cancer (GC). Because epithelial-to-mesenchymal transition (EMT) is considered to develop prior to macroscopic metastasis, EMT-promoting factors may affect micrometastasis. This study aimed to evaluate the role of extracellular high-mobility group box-1 (HMGB1) in EMT and the treatment effect of combined targeting of HMGB1 and interleukin-8 (IL-8) at early-stage GC progression through interrupting EMT promotion. Extracellular HMGB1 was induced by human recombinant HMGB1 and pCMV-SPORT6-HMGB1 plasmid transfection. EMT activation was evaluated by immunoblotting, immunofluorescence and immunohistochemistry. Increased migration/invasion activities were evaluated by in vitro transwell migration/invasion assay using all histological types of human GC cell lines (N87, MKN28 SNU-1 and KATOIII), N87-xenograft BALB/c nude mice and human paired serum-tissue GC samples. HMGB1-induced soluble factors were measured by chemiluminescent immunoassay. Inhibition effects of tumor growth and EMT activation by combined targeting of HMGB1 and IL-8 were evaluated in N87-xenograft nude mice. Serum HMGB1 increases along the GC carcinogenesis and reaches maximum before macroscopic metastasis. Overexpressed extracellular HMGB1 promoted EMT activation and increased cell motility/invasiveness through ligation to receptor for advanced glycation end products. HMGB1-induced IL-8 overexpression contributed the HMGB1-induced EMT in GC in vitro and in vivo. Blocking HMGB1 caused significant reduction of tumor growth, and addition of human recombinant IL-8 rescues this antitumor effects. Our results imply the role of HMGB1 in EMT through IL-8 mediation, and a potential mechanism of GC micrometastasis. Our observations suggest combination strategy of HMGB1 and IL-8 as a promising diagnostic and therapeutic target to control GC micrometastasis.

More evidence of Glycation in Breast cancer is in this report from Dec 23, 2016;

Nass N1, Ignatov A2, Andreas L3, Weißenborn C2, Kalinski T3, Sel S4.

Author information


Advanced glycation end products (AGEs) accumulate as a result of high concentrations of reactive aldehydes, oxidative stress, and insufficient degradation of glycated proteins. AGEs are therefore accepted biomarkers for aging, diabetes, and several degenerative diseases. Due to the Warburg effect and increased oxidative stress, cancer cells frequently accumulate significant amounts of AGEs. As the accumulation of AGEs may reflect the metabolic state and receptor signaling, we evaluated the potential prognostic and predictive value of this biomarker. We used immunohistochemistry to determine the AGE Nε-carboxymethyl lysine (CML) in 213 mammary carcinoma samples and Western blotting to detect AGEs in cell cultures. Whereas no significant correlation between hormone receptor status and CML was observed in cell lines, CML accumulation in tumors was positively correlated with the presence of estrogen receptor alpha, the postmenopausal state, and age. A negative correlation was found for grade III carcinomas and triple-negative cases.

Again, this form of cancer can be curable if you remove the glycating factor. I have yet to find a cancer that can’t be cured by taking away the glycating factor, glucose. Why then is glucose still a recommended food, as in carbohydrates such as “whole grains”?

It amazes me how many studies they find to say the same thing over and over again. Yet they keep doing it, day after day after day, in an unending cycle dependence. This report on the effects of RAGEs on esophageal and lung cancers;


The receptor for advanced glycation end products (RAGE) interacts with several ligands and is involved in various human diseases. Several splicing forms of the RAGE gene have been characterized, and two general mechanisms are usually responsible for the generation of soluble receptors. However, variants distribution and respective roles in different tumors are not clear. We analyzed RAGE and hRAGEsec mRNA expression in esophageal and lung cancer by RT-polymerase chain reaction. The Agilent clipper 1000 Bioanalyzer using lab-on-a-chip technology was applied to size and quantify the polymerase chain reaction products. Western blotting was performed to measure total soluble RAGE protein levels. The results showed that RAGE and its splice variants increased in esophageal cancers and decreased in lung cancers. We conclude that RAGE presents as a major isoform; soluble RAGE may also play certain roles in esophageal cancer and lung cancer.

How many reports does the FDA or the USDA need to tell them that what they’re recommending for everyone to eat, is doing them more harm than good, far more.

This report dated June 15, 2007 shows the effects if AGEs on chondrosarcoma, a bone cancer;



Chondrosarcoma, the second most frequent primary malignant bone tumor, is classified into 3 grades according to histologic criteria of malignancy. However, a low-grade lesion can be difficult to distinguish from a benign enchondroma, whereas some histologically low-grade lesions may carry a poor prognosis. The receptor for advanced glycation endproducts (RAGE) and its ligand, high-mobility group box-1 (HMGB1), was quantified in enchondromas and chondrosarcomas to determine whether these markers were associated with histological malignancy and prognosis.


Enchondromas (n = 20) and typical chondrosarcomas (n = 39) were evaluated for RAGE, endogenous secretory RAGE (esRAGE, a splice variant form), and HMGB1 protein expression by immunohistochemistry including laser confocal microscopy. The content of esRAGE in resected specimens was measured with an enzyme-linked immunosorbent assay. Associations of these molecules with histology and clinical behavior of tumors were analyzed.


Expression of esRAGE and HMGB1 was observed in all specimens. The numbers of cells positive for esRAGE and HMGB1 expression were positively associated with histologic grade. Expression of esRAGE was significantly higher in chondrosarcomas than in enchondromas (P < .001). Tissue esRAGE content was also significantly higher in grade 1 and 2 chondrosarcomas than enchondromas (P = .0255 and P = .008, respectively). High expression of esRAGE in grade 1 chondrosarcoma was associated with subsequent recurrence (P = .0013), lung metastasis (P = .0071), and poor survival (P < .001).


Assessment of esRAGE expression should aid in diagnostic and prognostic determinations in chondrosarcoma.

This report dated Nov 23, 2016 shows the effects that glycation and  AGEs have on ovarian cancer, prostate cancer,

  1. Introduction

Reactive oxygen species (ROS), generated as consequence of oxidative metabolism, activate signal transduction pathways, which contribute to cellular homeostasis [1]. Metabolically active cells, neutrophils, and macrophages from the immune system produce high levels of ROS.

  1. The Function of HMGB Proteins and Other Redox Sensors during Oxidative Stress in Ovarian Cancer

OS has been proposed as a cause of ovarian cancer. HMGB1 is considered a biomarker for ovarian cancer [3839] and increased levels of interleukin-8 protein (IL-8) and HMGB1 correlate with poor prognosis in prostate and ovarian cancer cells [125].

  1. Oxidative Stress in Prostate Cancer and the Function of HMGB Proteins and Other Redox Sensors

The human prostate anatomy displays a zonal architecture, corresponding to central, periurethral transition, peripheral zone, and anterior fibromuscular stroma. The majority of prostate carcinomas are derived from the peripheral zone, while benign prostatic hyperplasia arises from the transition zone [129].

Finally, several research lines outline the direct importance of HMGB proteins in prostate cancer and their implications in therapy. Increased HMGB2 expression [177], HMGB1 expression [41], or coexpression of RAGE and HMGB1 [178179] has been associated with prostate cancer progression and has been correlated to poor patient outcome.

  1. Conclusions and Perspectives

ROS overproduction and imbalance are a primary cause of malignancy in the onset of cancer. Cells have evolved multiple strategies in response to ROS production and HMGB proteins play a major role in many molecular mechanisms participating in these responses. In the nucleus, HMGB proteins affect DNA repair, transcription, and chromosomal stability; in cytoplasm they determine key decisions that finally lead towards autophagy or apoptosis; as extracellular signals they produce changes that affect the microenvironment of the tumour and attract cells from the immune system. In turn, the inflammatory onset can increase ROS production and therefore enhances the response. HMGB1 and HMGB2 are expressed at the highest levels in immune cells and, besides, they have been related to cancers, which are hormone-responsive, such as ovarian and prostate cancers. Since HMGB proteins have many different functions and are necessary in healthy cells, an improved strategy to modulate their role in cancer progression could be to act through other proteins interacting specifically with them. The identification of HMGB partners, which could be univocally associated with specific cancerous processes or with mechanism of cisplatin resistance, is a field of interest for ongoing translational cancer research. Interactome strategies are outstanding for the development of these research lines.

A search for cervical cancer and glycation returned 602 studies in the PMC index and started with this study;

We investigated the significance of high- mobility group box1 (HMGB1) and T-cell-mediated immunity and prognostic value in cervical cancer… HMGB1 expression may activate Tregs or facilitate Th2 polarization to promote immune evasion of cervical cancer. Elevated HMGB1 protein in cervical carcinoma samples was associated with a high recurrence of HPV infection in univariate analysis… Data collected here demonstrated that the expression of HMGB1 in cervical lesions increased with tumor progression.

I wanted to see the relationship between glycation and bladder cancer. My search returned 616 studies, with the first one dated Feb 25, 2015;

Bladder cancer is the 4th most common cancer among men in the U.S. and more than half of patients experience recurrences within 5 years after initial diagnosis.

Oct 29, 1993;

  • Expression of receptors foradvanced glycosylation end products on renal cell carcinoma cells in vitro.


Proteins that have been modified by long-term expose to glucose accumulate advanced glycosylation end products (AGEs) as a function of protein age. In these studies, we have examined the interaction of AGE-protein with renal cell carcinoma cells (RCC) in vitro, using AGE-modified bovine serum albumin (AGE-BSA) as a probe. AGE-BSA showed tendency to induce in vitro cell growth of RCC cells and promoted the production of interleukin-6 (IL-6), an in vitro autocrine growth factor. Reverse transcriptase-polymerase chain reaction analysis revealed that RCC cells used here express mRNA for a receptor for AGEs (RAGE). These results suggested that AGEs taken up through RAGE on RCC cells might play a role in promoting the growth of RCC cells.

This was discovered in the summer of 1993 or prior, yet nothing was ever announced by the FDA or the USDA that there might be a preventative diet to protect against cancer. Did you hear anything about sugar or carbohydrates causing this kind of damage? I didn’t. Yet the evidence is clear as day from a study done over 20 years ago. Still, nobody announced these revelations as they were being discovered. This report submitted Dec 2012;

  • Functional amyloid formation byStreptococcus mutans

In summary, there is a growing realization that amyloid formation is a directed, widespread, functional process that contributes to the biology of numerous micro-organisms, with particular relevance for adhesion and biofilm formation. We have now demonstrated amyloid formation by the cariogenic pathogen S. mutans, which is not surprising considering its biofilm niche. In addition to the contribution of amyloids to virulence by facilitating the adhesion, biofilm formation and invasion of pathogens, microbial amyloids have been postulated to contribute to systemic diseases, including Alzheimer’s and Parkinson’s, possibly by seeding amyloid formation in the brain (Broxmeyer, 2002Díaz-Corrales et al., 2004MacDonald, 2006Miklossy et al., 2006).

Copied from PMC on Liver cancer;

According to the database from GLOBOCAN 2012, liver cancer has the fifth highest incidence rate and is the second most life-threatening cancer in the world. There were an estimated 14.1 million new cases and 8.2 million cancer deaths worldwide in 2012, among which there were 782,500 new patients and 745,500 deaths caused by liver cancer [1].

HMGB1 has been demonstrated as a critical role in a number of cancers, including colorectal [10], breast [11,12], lung [13,14,15,16], prostate [17], cervical [18], skin [19], kidney [20,21], gastric [22,23,24,25,26], pancreatic [27,28,29], osteosarcoma [30] and leukemia [31].

Recently, HMGB1 has been recognized as a pro-angiogenesis factor leading to the generation of vascular endothelial growth factor (VEGF) in colon cancer [54,55], while RAGE was identified as the requirement for cell angiogenesis in HCC [56].

Autophagy and apoptosis are recognized as both the programmed cell deaths. In HCC, the release of HMGB1 from nuclei to cytoplasm was reported as an inducer for cell autophagic cell death, which may be associated with ROS and/or Beclin-1.

In summary, HMGB1 plays a pivotal role in oncogenesis and progression in HCC which may be a potential target for therapies and is worthy of further study.

This free report appeared in PubMed 3/1/2016, it expresses the role AGEs and RAGE play in Colorectal  cancer;



Advanced glycation end products (AGEs) and their receptor RAGE emerge as important pathogenic contributors in colorectal carcinogenesis. However, their relationship to the detoxification enzyme Glyoxalase (GLO)-I and Adiponectin receptors (AdipoR1, AdipoR2) in colorectal carcinoma (CRC) is currently understudied. In the present study, we investigated the expression levels of the above molecules in CRC compared to adjacent non-tumoral tissue and their potential correlation with clinicopathological characteristics and patients’ survival.


We analyzed the immunohistochemical expression of AGE, RAGE, GLO-1, AdipoR1 and AdipoR2 in 133 primary CRC cases, focusing on GLO-I. The tumour MSI status was further assessed in mucinous carcinomas. Western immunoblotting was employed for validation of immunohistochemical data in normal and tumoral tissues as well in three CRC cell lines. An independent set of 55 patients was also used to validate the results of univariate survival analysis regarding GLO-I.


CRC tissue showed higher intensity of both AGE and RAGE expression compared with normal colonic mucosa which was negative for GLO-I in most cases (78 %). Western immunoblotting confirmed AGE, RAGE and GLO-I overexpression in tumoral tissue. GLO-I expression was directly related to RAGE and inversely related to AGE immunolabeling. There was a trend towards higher expression of all markers (except for RAGE) in the subgroup of mucinous carcinomas which, although of borderline significance, seemed to be more prominent for AdipoR1 and AGE. Additionally, AGE, AdipoR1 and Adipo R2 expression was related to tumor grade, whereas GLO-1 and AdipoR1 to T-category. In survival analysis, AdipoR2 and GLO-I overexpression predicted shortened survival in the entire cohort and in early stage cases, an effect which for GLO-I was reproduced in the validation cohort. Moreover, GLO-I emerged as an independent prognosticator of adverse significance in the patients’ cohort.


We herein provide novel evidence regarding the possible interactions between the components of AGE-RAGE axis, GLO-I and adiponectin receptors in CRC. AGE and AdipoR1 are possibly involved in colorectal carcinogenesis, whereas AdipoR2 and GLO-I emerged as novel independent prognostic biomarkers of adverse significance for patients with early disease stage. Further studies are warranted to extend our observations and investigate their potential therapeutic significance.

Are these enough reports to prove how directly influence diabetes? After reading this can you see the logic in controlling your diabetes by controlling your carb intake? Where are the warnings from the FDA and the USDA? Don’t they care about what they’re recommending? Don’t they understand because of their recommendations, they sending millions of Moms and Dads, sisters and brothers, husbands and wives to their slow, expensive, painful deaths?

These are free reports that are available to everyone. All you have to do is search for them at the National Library of Medicine in the National Institute of Health. There are literally 100s of thousands of reports on the effects of glycation that remain hidden in the PubMed and PMC databases except to the few who look through them.  The only ones looking through this database are the drug companies looking for more ways to make money. Nobody is looking to warn anyone of the dangers of this food.

My question is why? The answer I get is, “there’s no money in it”. That’s is why I said in my first book, it would be a shame if profits and money weren’t the primary motivating factors in our society, but they are, and we have to live with it. That’s why I choose not to buy into it. It’s the same choice you have.

Carbs and Cancer go together like love and marriage.

How Carbs Influence Cancer

Cancer is responsible for over 8,200,000 deaths every year.

Cancer comes in so many different forms , it makes it very difficult to nail down any one solution for all the different types of cancer. However, playing a major influence in half of the different types of cancer, listed below, is one common thread that permeates our diets everywhere – glucose. It’s woven of three strands – wheat, sugar and grain based foods (flour and sugar). These basic staples that we were all encouraged to eat massive quantities of, is actually what’s killing us. The worst aspect of this whole problem is that we were told to eat them. We were told that they should be the largest portion of our meals and that we eat them on a daily basis. We were told to do this because, (we were told) that it was healthy for us. Why was the truth was never shared? I don’t know. But we do know now, just how dangerous this food staple really is. Cancer is like the carriage to the carbs’ horse. Carbs lead the way and the cancer follows.

I mentioned in Carbs! The Newly Discovered Death Sentence that this is not healthy food, and I intend to prove it, starting with  this page.

Because of the lack of studies done of the effects of wheat in the diet and cancer, it’s not always easy to piece the information together. Many of the studies that were done years ago have been suppressed from public knowledge and are not easy to obtain now. Dr Davis and Dr Perlmutter have already located many of these studies and they can be found in their books, Wheat Belly and Grain Brain. I spent only enough time to decipher sugar and wheat’s influence in half of the various types of cancer listed below. If the CPSC is considering warnings for chemicals that cause cancer, (which they are in California) why isn’t anyone considering warnings for the consumption of these food staples, sugar and flour?

Suffice it to say, there is enough evidence here to prove that this food source should come with the same warning that everything that causes cancer has to bear, like cigarettes, and now, processed meats and fast foods, and chemicals in California. (California’s attorney general, Bill Lockyer, filed suit in August against McDonald’s; Burger King; Frito-Lay, owned by PepsiCo; and six other food companies, saying that they should be forced to put labels on all fries and potato chips sold in California. The proposed warning might say something to this effect: “This product contains a chemical known to the state of California to cause cancer.”)

It’s interesting that California is going after fast food companies for the “cancer causing French fries” when it’s the bread that has as much if not more influence on cancer as trans-fats. I’ll admit, French fries play a definite role in cancer, but if they’d only look at the studies that show how sugar and wheat cause cancer, diabetes, HBP, cardio-vascular disease, digestive disorders, etc they’d soon have labels on everything that flour and sugar were used in. The full list is viewable on the page mentioned above.

This page is going to show how this food actually contributes to the environmental factors that are at the root cause of many cancers.

Cancer – There are over 100 different known cancers that affect humans.[2] causing 8.2 million deaths as of 2012 The great majority of cancers, some 90–95% of cases, are due to environmental factors. The remaining 5–10% are due to inherited genetics.[5] Environmental, as used by cancer researchers, means any cause that is not inherited genetically, such as lifestyle, economic and behavioral factors, and not merely pollution.[28] Common environmental factors that contribute to cancer death include tobacco (25–30%), diet and obesity (30–35%), infections (15–20%), radiation (both ionizing and non-ionizing, up to 10%), stress, lack of physical activity, and environmental pollutants.[5] Diet, physical inactivity, and obesity are related to up to 30–35% of cancer deaths.[5][39  The largest influence in obesity is wheat, sugar and grain based foods.

We’re only going to look at a few of the 100s of different kinds of cancer.
Of the 12 listed below, we’ll look at 6 of those in detail further below;
  1. Lung cancer – 1.56 million deaths annually, as of 2012
  2. Pancreatic cancer – 330,000 deaths globally
  3. Colorectal (colon) cancer – 610,000 deaths (Inflammatory bowel disease – 51,000 deaths in 2013 due to inflammatory bowel disease (largest influence to colorectal cancer) alone.)
  4. Breast cancer – 18.2% of all cancer deaths for men and women together or 283,920 deaths
  5. Liver cancer – In 2013, 300,000 deaths from liver cancer were due to hepatitis B, hepatitis C, or alcohol
  6. Thyroid cancer – in 2010, 36,000 deaths globally up from 24,000 in 1990.[35]Obesity may be associated with a higher incidence of thyroid cancer, but this relationship remains the subject of much debate.[36] 
  7. Ovarian cancer – estimated 15,000 deaths in 2008
  8. Cervical cancer – 266,000 deaths
  9. Prostate Cancer – In 2010 it resulted in 256,000 deaths up from 156,000 deaths in 1990.[155]
  10. Bladder cancer – is the 9th leading cause of cancer with 430,000 new cases[3]
  11. Kidney cancer –17,870 deaths in the US and the UK alone in 2012, with 208,000 new cases each year
  12. Endometrial cancer – caused 76,000 deaths
Let’s take a closer look at some of these types of cancer;
  • Lung cancer – 1.56 million deaths annually, as of 2012, is the most common cause of cancer in the US. The most common cause of lung cancer is smoking which warnings are required on cigarette packs.
  • Breast cancergallery-thumbnails– 18.2% of all cancer deaths for men and women together or 283,920 deaths is the second most common cause of cancer related deaths in women. Risk factors for developing breast cancer include: female sex, obesity, lack of physical exercise, drinking alcohol, hormone replacement therapy during menopauseionizing radiation, early age at first menstruation, having children late or not at all, older age, and family history.[2][4 There is a relationship between diet and breast cancer, including an increased risk with a high fat diet,[44] alcohol intake,[45] and obesity,[46] related to higher cholesterol levels.[47] In breast adipose tissue, overexpression of leptin leads to increased cell proliferation and cancer.[69] Dietary iodine deficiency may also play a role. [48] Don’t forget what increases leptin levels in the system more than anything else. What would happen to breast cancer if you removed wheat, sugar and grains from the diet? Would that decrease the expression leptin and put a hamper of the spread of cancer? A high fat diet, in this case would be a diet that creates a lot of fat. Carbs create fat. Eating fat doesn’t. I’ve never seen a warning about obesity and breast cancer, or that eating grain based foods can cause obesity. There should be.
  • Prostate Cancer – In 2010 it resulted in 256,000 deaths up from 156,000 deaths in 1990.[155]  is the leading cause of cancer death in males worldwide.   The data on the relationship between diet and prostate cancer is poor.[87] In light of this the rate of prostate cancer is linked to the consumption of the Western diet.[87] There is little if any evidence to support an association between trans fat, saturated fat and carbohydrate intake and risk of prostate cancer.[87][88] Evidence regarding the role of omega-3 fatty acids in preventing prostate cancer does not suggest that they reduce the risk of prostate cancer, although additional research is needed.[87][89] Vitamin supplements appear to have no effect and some may increase the risk.[9][87] High calcium intake has been linked to advanced prostate cancer.[90] Consuming fish may lower prostate cancer deaths but does not appear to affect its occurrence.[91] Some evidence supports lower rates of prostate cancer with a vegetarian diet.[92] There is some tentative evidence for foods containing lycopene and selenium.[93] Diets rich in cruciferous vegetables, soy, beans and other legumes may be associated with a lower risk of prostate cancer, especially more advanced cancers.[94]  Men who get regular exercise may have a slightly lower risk, especially vigorous activity and the risk of advanced prostate cancer.[94]
  • Colorectal cancer – 610,000 deaths (Inflammatory bowel disease – 51,000 deaths in 2013 due to inflammatory bowel disease (largest influence to colorectal cancer) alone.) IBD is a complex disease which arises as a result of the interaction of environmental and genetic factors. It is increasingly thought that alterations to enteral (probiotics?) bacteria can contribute to inflammatory gut diseases[20][21]IBD affected individuals have been found to have 30-50 percent reduced biodiversity of commensalism bacteria such as a decrease in Firmicutes (namely lachnosperacieae and Bacteroidetes), what I believe are pro-biotics (but I can’t find a definitive answer to that). Further evidence of the role of gut flora in the cause of inflammatory bowel disease is that IBD affected individuals are more likely to have been prescribed antibiotics in the 2-5 year period before their diagnosis than unaffected individuals.[22]The enteral bacteria can be altered by environmental factors, such as Concentrated milk fats (a common ingredient of processed foods and confectionery) or oral medications such as antibiotics and oral iron preparations.[23] This tells me that those who are taking headache medication (NSAIDs) often, are themselves open for colorectal cancer and one thing we know about wheat and grain consumption is that it causes headaches, forcing one to use NSAIDs for pain relief.
  • Liver cancer – In 2013, 300,000 deaths from liver cancer were due to hepatitis B, hepatitis C, or alcohol. Liver cancer, also known as hepatic cancer, is a cancer that originates in the liver. Liver tumors are discovered on medical imaging equipment (often by accident) or present themselves symptomatically as an abdominal mass, abdominal painyellow skin, nausea or liver dysfunction. The leading cause of liver cancer is cirrhosis due to either hepatitis B, hepatitis C, or alcohol.[1] Cirrhosis is most commonly caused by alcoholhepatitis Bhepatitis C, and non-alcoholic fatty liver disease.[1][2] Non-alcoholic fatty liver disease(NAFLD) is one of the causes of fatty liver, occurring when fat is deposited (steatosis) in the liver due to causes other than excessive alcohol use. NAFLD is related to insulin resistance and the metabolic syndrome and may respond to treatments originally developed for other insulin-resistant states (e.g.diabetes mellitus type 2) such as weight loss, metformin, and thiazolidinediones.[4] We know that carbohydrate consumption in the form of wheat and grains cause insulin resistance. Doesn’t it make sense then, that the consumption of wheat and grains has a major influence in liver cancer?
  • Kidney cancer – Factors that increase the risk of kidney cancer include smoking, which can double the risk of the disease; regular use of NSAIDs such as ibuprofen and naproxen, which may increase the risk by 51%[9] or may not;[10] obesity; faulty genes; a family history of kidney cancer; having kidney disease that needs dialysis; being infected with hepatitis C; and previous treatment for testicular cancer or cervical cancer. There are also other possible risk factors such as kidney stones [11] and high blood pressure, which are being investigated.[12] 17,870 deaths in the US and the UK alone in 2012, with 208,000 new cases each year
  • Bladder cancer – is the 9th leading cause of cancer with 430,000 new cases[3] and 165,000 deaths occurring in 2012.[4]  Urothelial carcinoma is a prototypical example of a malignancy arising from environmental carcinogenic influences. By far the important cause is cigarette smoking, which contributes to approximately half of the disease burden. Chemical exposures such as those sustained by workers in the petroleum industry, the manufacture of paints and pigments (prototypically aniline dyes), and agrochemicals are known to predispose to urothelial cancer. Interestingly, risk is lowered by increased liquid consumption, presumably as a consequence of increased urine production and thus less “dwell time” on the urothelial surface. Conversely, risk is increased among long-haul truck drivers and others in whom long urine dwell-times are encountered. As with most epithelial cancers, physical irritation has been associated with increased risk of malignant transformation of the urothelium. Thus, urothelial carcinomas are more common in the context of chronic urinary stone disease, chronic catheterization (as in patients with paraplegia or multiple sclerosis), and chronic infections. Some particular examples are listed below:

The one factor that intrigues me the most is the influence of agrochemicals, in the disease. Some of the most treated foods in our diet are wheat, corn, soy and grain based foods. They genetically modify these foods to withstand the rigors of agrochemicals like herbicides and insecticides, both of which contribute to bladder cancer. What is the one food that we were all told to eat the most of? Grains. If this one food were taken out of the diet, would that affect the numbers of people dying from bladder cancer? I think so. (I’m sure Monsanto doesn’t think so.)

Risk factors for pancreatic adenocarcinoma include:[2][3][4][32]

  1. Age, gender, and race; the risk of developing pancreatic cancer increases with age. Most cases occur after age 65,[4] while cases before age 40 are uncommon. The disease is slightly more common in men than women, and in the United States is over 1.5 times more common in African Americans, though incidence in Africa is low.[4]
  2. Cigarette smoking is the best-established avoidable risk factor for pancreatic cancer, approximately doubling risk among long-term smokers, the risk increasing with the number of cigarettes smoked and the years of smoking. The risk declines slowly after smoking cessation, taking some 20 years to return to almost that of non-smokers.[33]
  3. Obesity; a BMI greater than 35 increases relative risk by about half.[3]
  4. Family history; 5–10% of pancreatic cancer cases have an inherited component, where people have a family history of pancreatic cancer.[2] The risk escalates greatly if more than one first-degree relative had the disease, and more modestly if they developed it before the age of 50.[6] Most of the genes involved have not been identified.[2][34] Hereditary pancreatitis gives a greatly increased lifetime risk of pancreatic cancer of 30–40% to the age of 70.[5] Screening for early pancreatic cancer may be offered to individuals with hereditary pancreatitis on a research basis.[35] Some people may choose to have their pancreas surgically removed to prevent cancer developing in the future.[5]
    1. Pancreatic cancer has been associated with the following other rare hereditary syndromes: Peutz–Jeghers syndrome due to mutations in the STK11 tumor suppressor gene (very rare, but a very strong risk factor); dysplastic nevus syndrome (or familial atypical multiple mole and melanoma syndrome, FAMMM-PC) due to mutations in the CDKN2A tumor suppressor gene; autosomal recessiveataxia-telangiectasia and autosomal dominantly inherited mutations in the BRCA2gene and PALB2 gene; hereditary non-polyposis colon cancer (Lynch syndrome); and familial adenomatous polyposis. Pan NETs have been associated with multiple endocrine neoplasia type 1 (MEN1) and von Hippel Lindau syndromes.[2][5][6]
  5. Chronic pancreatitis appears to almost triple risk, and as with diabetes, new-onset pancreatitis may be a symptom of a tumor.[5] The risk of pancreatic cancer in individuals with familial pancreatitis is particularly high.[5][34]
  6. Diabetes mellitus is a risk factor for pancreatic cancer and (as noted in the Signs and symptoms section) new-onset diabetes may also be an early sign of the disease. People who have been diagnosed with Type 2 diabetes for longer than ten years may have a 50% increased risk, as compared with non-diabetics.[5]
  7. Specific types of food (as distinct from obesity) have not been clearly shown to increase the risk of pancreatic cancer.[2] Dietary factors for which there is some evidence of slightly increased risk include processed meatred meat, and meat cooked at very high temperatures (e.g. by frying, broiling or barbecuing).[36][37]

Highlighted areas are all wheat and grain caused conditions that would not exist if this food weren’t in our diet.

If 90 – 95% of all cases of cancer are due to lifestyle and behavioral factors, what does that say about our eating habits? Our eating habits are the most influential factor in anyone’s lifestyle. The old adage, “you are what you eat”, is more valid here, than anywhere else.

Our individual diets are what separate us from each other more than almost anything else, as that’s what distinguishes us from each other. In every diet, there exists one common thread throughout the world, and that’s grains, wheat in the western hemisphere and rice in the eastern hemisphere. They’re in every diet of every ethnicity. This is the one common thread that affects everyone on the planet. It does so simply because it’s in every diet on the planet, in some fashion or another.

As evidenced above, there are 6 types of cancer on this page, alone, in which wheat and grains play a part. If you eat food that causes cancer and you’ll more than likely, contract cancer.

What if this one factor was removed from the equation of cancer? What if wheat and grains were removed from our diets? What would happen if you took out that one factor in the equation of cancer, out of the equation? Would you still come still come up with the same result?

I contend that it would change the whole equation enough that the end result of cancer would inevitably be changed. This begs the question, if we removed wheat and grains from the diet, would that be a start for a cure for cancer?

I understand why a warning label is on every pack of cigarettes, one should be, we know that smoking causes lung cancer. If they put out warnings for something that may cause cancer, like processed meats and ‘fast foods’, why can’t they put out a warning for something that clearly causes cancer, sugar and wheat based products?

Hopefully, the day will come soon.

Next, we’ll take a closer look at cardiovascular diseases and grains influence there.

A thousand thanks to Wikipedia, I would have never been able to compile this without their help. 85% of this page came directly from Wkikpedia.