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--- home:diseases:cancer [06.12.2018] – [Microbial interaction and disease] sallieq
+++ home:diseases:cancer [09.14.2022] (current) – external edit 127.0.0.1
@@ Line 2: / Line 2: @@
 ======Cancer======
-According to a 2006 estimate, 18% of the global cancer burden is attributable to infectious agents, but almost every indication is that this figure is far too conservative.(({{pubmed>long:20930075}})) Researchers confined by the logic of Koch's postulates have looked for a single microbe causing a single disease. Evidence is accumulating, however, that it is communities of microbes that are responsible for cancer. According to the Marshall Pathogenesis, chronic microbes persist, in large part, by dysregulating the Vitamin D Receptor (VDR), a key nuclear receptor with a well-characterized role in both the innate immune response and metastasis suppression. Indeed one of the hallmarks of cancer is a disruption in the vitamin D endocrine system including high 1,25-D and slowed activity of the receptor. As they progressively multiply through a process known as successive infection, microbes elicit an inflammatory response, a response which has been shown to increase over time the risk of metastasis.
+According to a 2006 estimate, 18% of the global cancer burden is attributable to infectious agents, but almost every indication is that this figure is far too conservative.(({{pmid>long:20930075}})) Researchers confined by the logic of Koch's postulates have looked for a single microbe causing a single disease. Evidence suggests, however, that it is communities of microbes that are responsible for cancer. According to the Marshall Pathogenesis, chronic microbes persist, in large part, by dysregulating the Vitamin D Receptor (VDR), a key nuclear receptor with a well-characterized role in both the innate immune response and metastasis suppression. Indeed one of the hallmarks of cancer is a disruption in the vitamin D endocrine system including high 1,25-D and slowed activity of the receptor. As they progressively multiply through a process known as successive infection, microbes elicit an inflammatory response, a response which has been shown to increase over time the risk of metastasis.
 Several patients have worked with their doctors to treat their cancer with the Marshall Protocol. However, the MP appears to be most effective as a preventative measure.
+It may be particularly important for MP patients with cancer in the family to avoid caffeine as far as possible.
+"It is difficult to assess the practical significance of phagocytic suppression, but our previous work (unpublished) has shown that cancer cells can suppress phagocytosis in a similar manner. If this is the case, caffeine may be aiding in the suppression of immune response in the tumor microenvironment."  (({{pmid>long:27022462}}))
 =====Evidence of infectious cause=====
-According to D.L. Mager, “An overwhelming body of evidence has determined that relationships among certain bacteria and cancers exist.”(({{pubmed>long:14594792}}))  The growing number of examples of microbes associated with cancers include:
+According to D.L. Mager, “An overwhelming body of evidence has determined that relationships among certain bacteria and cancers exist.”(({{pmid>long:14594792}}))
+[[https://bmccancer.biomedcentral.com/track/pdf/10.1186/s12885-017-3234-4|Infections and cancer: the “fifty shades of immunity” hypothesis]]
+The growing number of examples of microbes associated with cancers include:
-  * **breast cancer** – Underscoring how cancer is a systemic disease, a 2006 study found that the gut bacteria //Helicobacter hepaticus// induces mammary adenocarcinoma in mice.(({{pubmed>long:16885333}}))
+  * **breast cancer** – Underscoring how cancer is a systemic disease, a 2006 study found that the gut bacteria //Helicobacter hepaticus// induces mammary adenocarcinoma in mice.(({{pmid>long:16885333}}))
   * **colon cancer** – //Streptococcus bovis// and //E. coli//
-  * **colorectal cancer** – A 2011 study of the colon microbiota in individuals with colon cancer versus those with a normal colonoscopy found a significant elevation of the //Bacteroides/Prevotella// population in cancer patients.(({{pubmed>long:21297998}})) Another study, this one performed in mice, showed that colitis (swelling of the large intestine) increases the risk of new colorectal tumors.(({{pubmed>long:22903521}}))
+  * **colorectal cancer** – A 2011 study of the colon microbiota in individuals with colon cancer versus those with a normal colonoscopy found a significant elevation of the //Bacteroides/Prevotella// population in cancer patients.(({{pmid>long:21297998}})) Another study, this one performed in mice, showed that colitis (swelling of the large intestine) increases the risk of new colorectal tumors.(({{pmid>long:22903521}}))
-  * **gastric cancer** – Chronic //H. pylori// infection is the major risk factor for gastric cancer.(({{pubmed>long:10710202}})) (({{pubmed>long:16103425}}))
+  * **gastric cancer** – Chronic //H. pylori// infection is the major risk factor for gastric cancer.(({{pmid>long:10710202}})) (({{pmid>long:16103425}}))
-  * **liver cancer** – It is "well established" that chronic infections with hepatitis B and C viruses (HBV, HCV) represent major risk factors for HCC.(({{pubmed>long:10710202}}))
+  * **liver cancer** – It is "well established" that chronic infections with hepatitis B and C viruses (HBV, HCV) represent major risk factors for HCC.(({{pmid>long:10710202}}))
-  * **lung cancer** – According to a 2011 meta-analysis, patients exposed to //C. pneumoniae// infection had a 48% greater risk for lung cancer risk, relative to those not exposed.(({{pubmed>long:21194924}}))
+  * **lung cancer** – According to a 2011 meta-analysis, patients exposed to //C. pneumoniae// infection had a 48% greater risk for lung cancer risk, relative to those not exposed.(({{pmid>long:21194924}}))
-  * **prostate cancer** – In a 2005 culture-based study, Cohen found that //Propionibacterium acnes// in 35% of prostate samples of 34 consecutive patients tested.(({{pubmed>long:15879794}}))
+  * **prostate cancer** – In a 2005 culture-based study, Cohen found that //Propionibacterium acnes// in 35% of prostate samples of 34 consecutive patients tested.(({{pmid>long:15879794}}))
+  * **Table of cancers** with associated agents. [[https://bmccancer.biomedcentral.com/track/pdf/10.1186/s12885-017-3234-4|Infections and Cancer]]
-With the recent advent of high throughput sequencing studies, we can expect additional insights into how diseases like cancer are associated with shifts in microbial communities.  (({{pubmed>long:27470177}}))
+With the recent advent of high throughput sequencing studies, we can expect additional insights into how diseases like cancer are associated with shifts in microbial communities.  (({{pmid>long:27470177}}))
+==== see also M P Study Site ====
+[[https://www.marshallprotocol.com/forum39/16259.html|Study shows mechanism for Microbiome to cause Cancer]]
+===== Innate immunity =====
+<blockquote>Macrophages are immune cells just like T and B cells, but differ in that they can eat cells that are not supposed to be in the body. In fact, they are the most prominent immune cell found in cancer, but unfortunately, most are often convinced to help cancer grow and spread. Cancer cells frequently stop macrophages from attacking them by expressing CD47, a "don't eat me" signal. Researchers now say that merely blocking inhibitory signals like CD47 is not always sufficient to convince macrophages to attack cancer. Instead, two signals are required. First, they need a signal to activate them—such as a toll-like receptor agonist. After that, a second signal—such as a CD47 inhibitor—can lower the threshold needed to wage battle on the cancer.</blockquote>
+"It turns out macrophages need to be primed before they can go to work, which explains why solid tumors may resist treatment with CD47 inhibitors alone,"   (({{pmid>long:30664738}}))
+Increasing evidence supports the occurrence of an intriguing link between tumor onset and development with the microenvironment in which cancer cells are embedded. In this context, a critical role of CD73, in calibrating the duration, magnitude and composition of adenosine signaling in cancer development and progression, has been identified.  (({{pmid>long:24958495}}))
+The Vitamin D3 analogue calcipotriol suppresses CpG-activated TLR9-MyD88 signalling in murine plasmacytoid dendritic cells (({{pmid>long:    29392742}}))
+{{tag>  }}
 =====Vitamin D metabolism=====
 <blockquote>We conclude that there is a deregulation of the Vitamin D signalling and metabolic pathways in breast cancer, favouring tumour progression. Thus, during mammary malignant transformation, tumour cells lose their ability to synthesize the active form of Vitamin D and respond to VDR-mediated Vitamin D effects, while increasing their ability to degrade this hormone.
-//**N. Lopes**, VDR Signalling Disrupted in Breast Cancer//(({{pubmed>long:20831823}}))
+//**N. Lopes**, VDR Signalling Disrupted in Breast Cancer//(({{pmid>long:20831823}}))
 </blockquote>
-According to the Marshall Pathogenesis, communities of microbes gain a survival advantage by reducing expression of the nuclear receptors that play important roles in the innate immune response, particularly the Vitamin D Receptor (VDR). Wang //et al.//'s analysis(({{pubmed>long:16002434}})) found that the VDR transcribes at least 913 genes including TLR2 and the antimicrobial peptides cathelicidin and the beta-defensins. When this metagenome reduces expression of the host VDR, in order to protect the microbiota against the endogenous antimicrobials, it also knocks out transcription of a key gene involved in cancer – MTSS1.
+According to the Marshall Pathogenesis, communities of microbes gain a survival advantage by reducing expression of the nuclear receptors that play important roles in the innate immune response, particularly the Vitamin D Receptor (VDR). Wang //et al.//'s analysis(({{pmid>long:16002434}})) found that the VDR transcribes at least 913 genes including TLR2 and the antimicrobial peptides cathelicidin and the beta-defensins. When this metagenome reduces expression of the host VDR, in order to protect the microbiota against the endogenous antimicrobials, it also knocks out transcription of a key gene involved in cancer – MTSS1.
-Wang's expression map found that the number one gene transcribed by an active VDR is CYP24A1 (also known as CYP24) and the number two is MTSS1, also known as tumor metastasis suppressor protein, which ends up as the "missing in metastasis" (MIM) protein. Several 2011 studies stated that the VDR acts to suppress tumors in skin.(({{pubmed>long:21276406}})) (({{pubmed>long:21519403}}))
+Wang's expression map found that the number one gene transcribed by an active VDR is CYP24A1 (also known as CYP24) and the number two is MTSS1, also known as tumor metastasis suppressor protein, which ends up as the "missing in metastasis" (MIM) protein. Several 2011 studies stated that the VDR acts to suppress tumors in skin.(({{pmid>long:21276406}})) (({{pmid>long:21519403}}))
-The slowed activity of the VDR in cancer patients has been widely noted. Several researchers have observed that the Vitamin D Receptor (VDR) becomes inactive in cancer patients at just the time when it should be most active.(({{pubmed>long:19133314}}))
+The slowed activity of the VDR in cancer patients has been widely noted. Several researchers have observed that the Vitamin D Receptor (VDR) becomes inactive in cancer patients at just the time when it should be most active.(({{pmid>long:19133314}}))
-  * Pospechova //et al.// found low expression and no transcriptional activity of VDR in used choriocarcinoma cell lines. "In conclusion, our results suggest an epigenetic repression of VDR gene expression and activity in choriocarcinoma cell lines, and a non-genomic effect of 1,25(OH)(2)D(3) in JEG-3 cells."(({{pubmed>long:19133314}}))
+  * Pospechova //et al.// found low expression and no transcriptional activity of VDR in used choriocarcinoma cell lines. "In conclusion, our results suggest an epigenetic repression of VDR gene expression and activity in choriocarcinoma cell lines, and a non-genomic effect of 1,25(OH)(2)D(3) in JEG-3 cells."(({{pmid>long:19133314}}))
-  * Lopes measured expression of the VDR, CYP27B1 and CYP24A1 of breast cancer by immunohistochemistry, finding  levels of VDR expression were diminished in invasive tumours (56.2%).(({{pubmed>long:20831823}}))
+  * Lopes measured expression of the VDR, CYP27B1 and CYP24A1 of breast cancer by immunohistochemistry, finding  levels of VDR expression were diminished in invasive tumours (56.2%).(({{pmid>long:20831823}}))
-  * High VDR expression in prostate tumors is associated with a reduced risk of lethal cancer, suggesting an important role of the vitamin D pathway in prostate cancer progression.(({{pubmed>long:21537045}}))
+  * High VDR expression in prostate tumors is associated with a reduced risk of lethal cancer, suggesting an important role of the vitamin D pathway in prostate cancer progression.(({{pmid>long:21537045}}))
@@ Line 45: / Line 72: @@
 Lower than normal levels of 25-D have been generally associated with chronic disease but the field of oncology offers a number of counterexamples:
-  * **risk of prostate cancer** – In a 2008 nested case-control study appearing in //Journal of the National Cancer Institute//, Ahn //et al.// found that patients with the lowest levels of 25-D also had the lowest risk of prostate cancer.(({{pubmed>long:18505967}}))
+  * **risk of prostate cancer** – In a 2008 nested case-control study appearing in //Journal of the National Cancer Institute//, Ahn //et al.// found that patients with the lowest levels of 25-D also had the lowest risk of prostate cancer.(({{pmid>long:18505967}}))
   * **risk of breast cancer** – In a 2011 study of nurses who were predominantly premenopausal, circulating 25-D levels were not significantly associated with breast cancer risk.
-  * **risk of pancreatic cancer** – Patients with the highest levels of 25-D were at greatest risk of pancreatic cancer.(({{pubmed>long:20562188}}))
+  * **risk of pancreatic cancer** – Patients with the highest levels of 25-D were at greatest risk of pancreatic cancer.(({{pmid>long:20562188}}))
-  * **some rarer cancers**(({{pubmed>long:20562188}})) – non-Hodgkin lymphoma or cancers of the endometrium, esophagus, stomach, kidney, ovary and pancreas
+  * **some rarer cancers**(({{pmid>long:20562188}})) – non-Hodgkin lymphoma or cancers of the endometrium, esophagus, stomach, kidney, ovary and pancreas
-  * **cancer mortality** – A 2010 longitudinal study found that both high and low concentrations of plasma 25(OH)D were associated with elevated risks of overall and cancer mortality, and low concentrations are associated with cardiovascular mortality.(({{pubmed>long:20720256}}))
+  * **cancer mortality** – A 2010 longitudinal study found that both high and low concentrations of plasma 25(OH)D were associated with elevated risks of overall and cancer mortality, and low concentrations are associated with cardiovascular mortality.(({{pmid>long:20720256}}))
+==== Are There Concerns About V.D Supplement ? ====
+There is a common misconception that vitamin D supplementation is safe at any reasonable level, or that if some is good, more may be better.
+  * It is clear that vitamin D intakes and serum 25(OH)D must be very high—perhaps 200-400 ng/mL—to cause the classic toxicity of marked hypercalcemia and kidney and liver damage.
+  *
+  * However, emerging observational data suggest that adverse outcomes may occur at much lower levels, such as in the 50-75 ng/mL range. These suspected adverse outcomes appear to include increases in all-cause mortality and increases in the rate of heart disease and some cancers.
+The Vitamin D3 analogue calcipotriol suppresses CpG-activated TLR9-MyD88 signalling in murine plasmacytoid dendritic cells (({{pmid>long:29392742}}))
+Vitamin D receptor-mediated skewed differentiation of macrophages initiates myelofibrosis and subsequent osteosclerosis. (({{pmid>long:30718230}}))
+  a Cochrane meta-analysis that included 18 randomized clinical trials comparing vitamin D administration versus no intervention in healthy population found no difference regarding cancer incidence.  In randomised controlled trials, relative risks for all cause mortality were 0.89 (0.80 to 0.99) for vitamin D3 supplementation and 1.04 (0.97 to 1.11) for vitamin D2 supplementation. The effects observed for vitamin D3 supplementation remained unchanged when grouped by various characteristics. However, for vitamin D2 supplementation, increased risks of mortality were observed in studies with lower intervention doses and shorter average intervention periods.  (({{pmid>long:    24690623}}))
-<html>
-<!--
 ====1,25-dihydroxyvitamin D ====
-Mawer //et al.// reported that 1,25-D is such a sensitive indicator of the immune response that it can even be used to determine prognosis in breast cancer with bone metastasis.(({{pubmed>long:8989244}})) As the level of 1,25-D falls, the level of the innate immune system's ability to mount an immune response also falls, and the prognosis becomes less favorable. This seems to indicate that it might be possible to use the level of 1,25-D as one means of suggesting whether or not breast cancer treatment is effective if doctors know how to interpet the results. But, one should note that the patients in the above study had bone metastasis.
+Mawer //et al.// reported that 1,25-D is such a sensitive indicator of the immune response that it can even be used to determine prognosis in breast cancer with bone metastasis.(({{pmid>long:8989244}})) As the level of 1,25-D falls, the level of the innate immune system's ability to mount an immune response also falls, and the prognosis becomes less favorable. This seems to indicate that it might be possible to use the level of 1,25-D as one means of suggesting whether or not breast cancer treatment is effective if doctors know how to interpet the results. But, one should note that the patients in the above study had bone metastasis.
--->
-</html>
-===== Single species vs. communities of microbes =====
+[[https://autoimmunityresearch.org/hormones.pdf|Hormonal changes result from change in 1,25 dihydroxyvitamin-D]]
-Alicia H. Chang and Julie Parsonnet of Stanford University writes that a transmissible cause of cancer was suspected as early as the 16th century. It was not until the late 20th century definitively identified a bacterial cause of at least some types of cancer to most researchers' satisfaction.(({{pubmed>long:20930075}})) Identifying the full range of microbes which cause cancer, however, has been more challenging. To date, there have been a handful of cases that fulfill Koch's postulates (e.g., //H. pylori// and gastric cancer) where a single microbe is known to cause a single type of cancer. Consistent with Koch, researchers have tended to work in this vein, for example, looking at the 500+ species that inhabit the colon in the hopes of pinpointing the one and only bacterial species responsible for colorectal cancer.(({{pubmed>long:20930075}}))
+==== Other Immune Suppressants ====
-A number of types of chronic infection have been observed to be associated with cancers in some studies, but without an identified specific bacterial pathogen. Examples are chronic ulcers and osteomyelitis sinus tracts (squamous cell carcinoma), chronic urinary tract infections (UTIs) (bladder cancer), and chronic prostatitis (prostate cancer).(({{pubmed>long:20930075}}))
+Women with hereditary cancer predispositions should put their smartphones, tablets, and laptops into air-plane mode at all times when not in use.   (({{pmid>long:    29456806}}))
+Glioblastomas and malignant gliomas are the most common primary malignant brain tumors, with an annual incidence of 5.26 per 100,000 population. These tumors are typically associated with a dismal prognosis and poor quality of life. Only radiation exposure and certain genetic syndromes are well-defined risk factors for malignant glioma.   (({{pmid>long:    24193082}}))
+This compound has antiproliferative and antimigratory effects in squamous cell carcinoma, glioblastoma, and breast cancer cell lines (({{pmid>long:    31025400}}))
+Several researchers have highlighted a possible link between glioma and human cytomegalovirus (HCMV).  (({{pmid>long:30888562}}))
+[[https://sacramento.cbslocal.com/2019/03/25/ripon-cell-tower-school-removal-cancer/|Cell tower removed after 4 students get cancers]]
+[[https://prepforthat.com/portland-blocking-5g-networks-over-health-risks/|Officials Attempt To Block 5G Network Installation Over Health Risks]]
+===== Microbial involvement =====
+==== Single species vs. communities of microbes ====
+Alicia H. Chang and Julie Parsonnet of Stanford University writes that a transmissible cause of cancer was suspected as early as the 16th century. It was not until the late 20th century definitively identified a bacterial cause of at least some types of cancer to most researchers' satisfaction.(({{pmid>long:20930075}})) Identifying the full range of microbes which cause cancer, however, has been more challenging. To date, there have been a handful of cases that fulfill Koch's postulates (e.g., //H. pylori// and gastric cancer) where a single microbe is known to cause a single type of cancer. Consistent with Koch, researchers have tended to work in this vein, for example, looking at the 500+ species that inhabit the colon in the hopes of pinpointing the one and only bacterial species responsible for colorectal cancer.(({{pmid>long:20930075}}))
+A number of types of chronic infection have been observed to be associated with cancers in some studies, but without an identified specific bacterial pathogen. Examples are chronic ulcers and osteomylitis, sinus tracts (squamous cell carcinoma), chronic urinary tract infections (UTIs) (bladder cancer), and chronic prostatitis (prostate cancer).(({{pmid>long:20930075}}))
 The Marshall Pathogenesis is at complete odds with Koch's postulates, suggesting that it is not one species but entire communities of microbes that are responsible for many cancers. The process by which a person accumulates microbes responsible for disease is known as “successive infection.” In successive infection, an infectious cascade of pathogens progressively slow the immune response and allow for subsequent infections to proliferate, resulting in dysbiosis (microbial imbalances). According to this model, a single microbe may not need to be present in all cases of disease in order to be implicated in it.
@@ Line 69: / Line 132: @@
-===== Slow-growing microbes elicit inflammation =====
+==== Slow-growing microbes elicit inflammation ====
 <blockquote>In almost all examples of bacterial inflammation and human cancer, the implicated bacteria reside in the host for many years and create an environment of persistent inflammation. Specific bacteria that have been shown to cause chronic inflammation and an increased risk of cancer include //Helicobacter pylori// (gastric adenocarcinoma) and //Salmonella enterica serovar Typhimurium// or //Paratyphi// (biliary cancer).
-//**Alicia H. Chang**// (({{pubmed>long:20930075}}))</blockquote>
+//**Alicia H. Chang**// (({{pmid>long:20930075}}))</blockquote>
 Chang offers several examples of why chronic microbes are key to cancer:
-  * **//Helicobacter pylori// and gastric cancer** –  A meta-analysis of 12 nested case-control studies found that there was a two times greater risk of gastric cancer for patients who had //H. pylori//. When serology was tested at least a decade before diagnosis, when the stomach might have been less disrupted by the progression to cancer, the relative risk was even greater: 4.9 times.(({{pubmed>long:11511555}})) In a cohort study in Japan that evaluated both intestinal-type and diffuse-type cancers, only //H. pylori//-infected subjects developed stomach cancer, making the risk ratio infinite.(({{pubmed>long:18765120}}))
+  * **//Helicobacter pylori// and gastric cancer** –  A meta-analysis of 12 nested case-control studies found that there was a two times greater risk of gastric cancer for patients who had //H. pylori//. When serology was tested at least a decade before diagnosis, when the stomach might have been less disrupted by the progression to cancer, the relative risk was even greater: 4.9 times.(({{pmid>long:11511555}})) In a cohort study in Japan that evaluated both intestinal-type and diffuse-type cancers, only //H. pylori//-infected subjects developed stomach cancer, making the risk ratio infinite.(({{pmid>long:18765120}}))
-  * **//Chlamydia trachomatis// and cervical cancer** – //Chlamydia trachomatis// is an obligate, intracellular, Gram-negative bacterium that can be transmitted sexually. Similar to the //H. pylori// serology studies of gastric cancer, the risk of cervical cancer with //C. trachomatis// infection is greater with increasing time from serum sampling to cancer diagnosis.(({{pubmed>long:10585579}}))
+  * **//Chlamydia trachomatis// and cervical cancer** – //Chlamydia trachomatis// is an obligate, intracellular, Gram-negative bacterium that can be transmitted sexually. Similar to the //H. pylori// serology studies of gastric cancer, the risk of cervical cancer with //C. trachomatis// infection is greater with increasing time from serum sampling to cancer diagnosis.(({{pmid>long:10585579}}))
-  * **Colonic microflora and colon cancer** –  The best evidence supporting the inflammation theory in colorectal cancer is seen in the augmented risk of patients with inflammatory bowel diseases, i.e., ulcerative colitis and Crohn's disease. The cumulative incidence of colon cancer in IBD is as high as 18% at 30 years postdiagnosis.(({{pubmed>long:11247898}})) Epidemiologic studies show that the severity and duration of inflammation in IBD dictate cancer risk.(({{pubmed>long:14762782}}))
+  * **Colonic microflora and colon cancer** –  The best evidence supporting the inflammation theory in colorectal cancer is seen in the augmented risk of patients with inflammatory bowel diseases, i.e., ulcerative colitis and Crohn's disease. The cumulative incidence of colon cancer in IBD is as high as 18% at 30 years postdiagnosis.(({{pmid>long:11247898}})) Epidemiologic studies show that the severity and duration of inflammation in IBD dictate cancer risk.(({{pmid>long:14762782}}))
-  * **//Neisseria gonorrhoeae// and bladder cancer** – Two case-control studies reported increased associated risk of 110% and 140%.(({{pubmed>long:1985779}})) (({{pubmed>long:6191422}})) For comparison, syphilis, which does not cause urethritis, was also examined in one of the studies, and no association was found
+  * **//Neisseria gonorrhoeae// and bladder cancer** – Two case-control studies reported increased associated risk of 110% and 140%.(({{pmid>long:1985779}})) (({{pmid>long:6191422}})) For comparison, syphilis, which does not cause urethritis, was also examined in one of the studies, and no association was found
-  * **Nonspecific urinary tract infections** – The irritation caused by chronic urinary tract infections and chronic indwelling catheters has been implicated in bladder cancer in spinal cord injury patients.(({{pubmed>long:7557751}}))
+  * **Nonspecific urinary tract infections** – The irritation caused by chronic urinary tract infections and chronic indwelling catheters has been implicated in bladder cancer in spinal cord injury patients.(({{pmid>long:7557751}}))
-  * **//Borrelia burgdorferi// and MALT lymphoma of the skin** – Studies from Scotland and Italy have reported an association between //B. burgdorferi// and primary cutaneous B-cell lymphoma (PCBCL), a type of MALT lymphoma. However, studies in the United States, Asia, and parts of Europe have found little evidence of B. burgdorferi in PCBCL patients. As Chang suggests, perhaps the variable prevalence of infection in PCBCL is explained by the different prevalences of Borrelia strains across the world or by differences in techniques used for detection of infection.(({{pubmed>long:20930075}}))
+  * **//Borrelia burgdorferi// and MALT lymphoma of the skin** – Studies from Scotland and Italy have reported an association between //B. burgdorferi// and primary cutaneous B-cell lymphoma (PCBCL), a type of MALT lymphoma. However, studies in the United States, Asia, and parts of Europe have found little evidence of B. burgdorferi in PCBCL patients. As Chang suggests, perhaps the variable prevalence of infection in PCBCL is explained by the different prevalences of Borrelia strains across the world or by differences in techniques used for detection of infection.(({{pmid>long:20930075}}))
-===== Inflammation induces cancer =====
+==== Inflammation induces cancer ====
-According to Chang,(({{pubmed>long:20930075}})) Virchow first described the irritation hypothesis of carcinogenesis in the 19th century concluding that chronic irritation stimulated the cancer cells to grow. The inflammatory process is characterized by damage caused by the host's immune response to the infection rather than by the infecting organism itself. Over 100 years since Virchow's discoveries, the “chronic irritation hypothesis” remains a widely supported mechanism for carcinogenesis by infectious agents. Today the relationship between inflammation, innate immunity and cancer is widely accepted.(({{pubmed>long:21088404}}))
+According to Chang,(({{pmid>long:20930075}})) Virchow first described the irritation hypothesis of carcinogenesis in the 19th century concluding that chronic irritation stimulated the cancer cells to grow. The inflammatory process is characterized by damage caused by the host's immune response to the infection rather than by the infecting organism itself. Over 100 years since Virchow's discoveries, the “chronic irritation hypothesis” remains a widely supported mechanism for carcinogenesis by infectious agents. Today the relationship between inflammation, innate immunity and cancer is widely accepted.(({{pmid>long:21088404}}))
 During a normal response to infection, inflammation is created as a means for the host to combat invading pathogens. Inflammation is first initiated by the recruitment of phagocytes to the site of infection. The phagocytes recruited to the site of infection also secrete proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), and chemokines that attract more phagocytes and other cells of the immune system to the site of infection to amplify the inflammatory response. These cells respond through physiological processes mediated by the cellular enzymes NADPH oxidase, superoxide dismutase (SOD), myeloperoxidase, and nitric oxide synthase (NOS).
-The result is the release of reactive oxygen and nitrogen oxide species (ROS and RNOS) to kill potential pathogens. The free radicals and secondary products derived from them, such as secondary amines, HNO2, N2O3, and peroxynitrite, may damage DNA, proteins, and cell membranes and indirectly induce cell repair. Areas of tissue injury and inflammation trigger regenerative cell division from tissue and marrow-derived stem cells. Increased cell division may lead to point mutations, deletions, or translocations as damaged DNA escapes the repair system; the aberrant DNA is then propagated by subsequent cell division. This can result in disordered cell differentiation and, ultimately, oncogenesis. Hence, chronic inflammation, caused by microbes, instigates a cycle of cell damage, repair, and compensatory proliferation that promotes the development of cancer cells.(({{pubmed>long:21088404}}))
+The result is the release of reactive oxygen and nitrogen oxide species (ROS and RNOS) to kill potential pathogens. The free radicals and secondary products derived from them, such as secondary amines, HNO2, N2O3, and peroxynitrite, may damage DNA, proteins, and cell membranes and indirectly induce cell repair. Areas of tissue injury and inflammation trigger regenerative cell division from tissue and marrow-derived stem cells. Increased cell division may lead to point mutations, deletions, or translocations as damaged DNA escapes the repair system; the aberrant DNA is then propagated by subsequent cell division. This can result in disordered cell differentiation and, ultimately, oncogenesis. Hence, chronic inflammation, caused by microbes, instigates a cycle of cell damage, repair, and compensatory proliferation that promotes the development of cancer cells.
+<blockquote>
+Advanced stage follicular lymphoma (FL) is incurable by conventional therapies......  until  intranodal injections of low-dose rituximab (5 mg), immature autologous dendritic cells, and granulocyte-macrophage colony-stimulating factor at the same lymphoma node.(({{pmid>long:25293773}}))</blockquote>
-===== Microbial interaction and disease =====
+==== Microbial interaction and disease ====
-According to some sporadic reports, cancer regresses following spontaneous bacterial infection.(({{pubmed>long:15663328}})) Competition between an ever-changing mix of microbes, and the variable attention the immune system pays to any one component of that mix, may explain the waxing and waning of different cancerous states.
+According to some sporadic reports, cancer regresses following spontaneous bacterial infection.(({{pmid>long:15663328}})) Competition between an ever-changing mix of microbes, and the variable attention the immune system pays to any one component of that mix, may explain the waxing and waning of different cancerous states.
-Natural killer cells "are cytotoxic lymphocytes specialized in early defense against virus-infected and transformed cells."(({{pubmed>long:28236750}}))   "are able to recognize and trigger cell death in tumors by detecting receptor expression abnormalities in transformed cells"(({{pubmed>long:27115170}}))
+Natural killer cells "are cytotoxic lymphocytes specialized in early defense against virus-infected and transformed cells." (({{pmid>long:28236750}})) and  "are able to recognize and trigger cell death in tumors by detecting receptor expression abnormalities in transformed cells". (({{pmid>long:27115170}}))
-For example, //H. pylori// can cause gastric cancer or MALT lymphoma in some individuals. In contrast, exposure to //H. pylori// appears to reduce the risk of esophageal cancer in others. //Salmonella typhi// infection has been associated with the development of gallbladder cancer; however //S. typhi// has been associated with positive outcomes for melanoma, colon and bladder cancers.(({{pubmed>long:16566840}}))
+For example, //H. pylori// can cause gastric cancer or MALT lymphoma in some individuals. In contrast, exposure to //H. pylori// appears to reduce the risk of esophageal cancer in others. //Salmonella typhi// infection has been associated with the development of gallbladder cancer; however //S. typhi// has been associated with positive outcomes for melanoma, colon and bladder cancers.(({{pmid>long:16566840}}))
 Further, the live bacterium, Bacillus Calmette-Guérin (BCG) (see [[#vaccines|below]]), touted by some as a cancer vaccine, may also "work" by changing the path of successive infection, thus leading to immune disease (and cancers). After such an insult, the immune system focuses on //Mycobacterium bovis// (main component of BCG) and away from the chronic pathogens fueling the inflammation or cancer.
-A similar dynamic is clear when it comes to autoimmune disease: lupus has been shown to inhibit the development of malaria (//Plasmodium falciparum//).(({{pubmed>long:19657771}}))
+A similar dynamic is clear when it comes to autoimmune disease: lupus has been shown to inhibit the development of malaria (//Plasmodium falciparum//).(({{pmid>long:19657771}}))
-===== Metastatic communities parallel biofilm =====
+==== Metastatic communities parallel biofilm ====
 Some have suggested provocatively that communities of metastatic cancerous cells closely resemble communities of microbes known as biofilm.
@@ Line 113: / Line 179: @@
 <blockquote>We suggest that the quorum-sensing-controlled bacterial biofilm formation process closely parallels the steps in metastatic colonization. Cells migrate toward/on target surfaces (organ-specific homing), show cell-cell and cell-matrix interactions (tumor cell-stromal cell crosstalk), remain subclinical until they can mount an effective attack (dormancy), form complex structures with channels for nutrient flow (vascularized lesions), and contain resistant cells which can cause disease recurrence (persistors). Using ovarian cancer as an example, we present data supporting the connection between metastatic colonization and quorum sensing and discuss the implications for understanding and controlling metastasis formation.
-//**Jonathan Hickson** et al.// (({{pubmed>long:18516689}}))</blockquote>
+//**Jonathan Hickson** et al.// (({{pmid>long:18516689}}))</blockquote>
@@ Line 125: / Line 191: @@
 {{section>:home:alternate:genetic_predisposition#cancer&noheader&firstseconly}}
+ <blockquote>These findings suggest that pro-tumorigenic entotic engulfment activity is associated with mutant p53 expression, and the two combined are a key factor in genomic instability (({{pmid>long:30076358}}))</blockquote>
-====Tobacco====
+==== Tobacco ====
 {{section>:home:special:smoking#smoking_tobacco&noheader&firstseconly}}
-=====Marshall Protocol as a treatment for cancer?=====
+==== Stress derived from interaction of particular personalities ====
+in particular [[https://duckduckgo.com/?q=energy+vampires&t=ffnt&atb=v117-1&ia=about|the empathic personality and the 'energy vampire']]
+from https://mpkb.org/home/social/talking#dealing_with_antagonism
+<blockquote>Sadly, some people in your life may not want you to get well. For example, sometimes a partner or close friend can not tolerate change. Consciously or unconsciously they may undermine your efforts. It will be up to you to quietly persist, knowing that your recovery can only lead to a better outcome for both of you.
+In an extreme case, there may be someone who is literally toxic, even socio-pathic. “Learn to value yourself, Learn to say No!” and if necessary, Remove yourself from the influence of any such person.</blockquote>
+===== Marshall Protocol as a treatment for cancer? =====
 The MP uses olmesartan to activate the VDR, a nuclear receptor which is downregulated in cancer. While the MP appears to be a sensible preventive, it is not suitable for treating active metastasis.
@@ Line 138: / Line 223: @@
 //**Trevor Marshall, PhD**//
 </blockquote>
+==== Research ====
+This result provides a new idea on the anti-tumor mechanism of olmesartan, which may be used as a novel therapeutic target of cervical cancer.  (({{pmid>long:28304186}}))
+Research has shown that the renin-angiotensin system is implicated in a wide range of biological processes and diseases.  [[https://oatext.com/pdf/ICST-4-231.pdf|
+Renin-angiotensin system and cancer]]
 ====Safety of olmesartan====
@@ Line 143: / Line 237: @@
-A 2010 meta-analysis of randomized controlled trials administering ARBs, the class of drugs (which olmesartan belongs to), concluded the the drugs were associated with a small increase in the incidence of cancer.(({{pubmed>long:20542468}})) This publication was widely rebuked, as one can see from the number of comments in PubMed referring to [[http://www.ncbi.nlm.nih.gov/pubmed/20542468|this article]].
+A 2010 meta-analysis of randomized controlled trials administering ARBs, the class of drugs (which olmesartan belongs to), concluded the the drugs were associated with a small increase in the incidence of cancer.(({{pmid>long:20542468}})) This publication was widely rebuked, as one can see from the number of comments in PubMed referring to [[https://www.ncbi.nlm.nih.gov/pubmed/20542468|this article]].
-In the wake of the study, physicians [[http://www.theheart.org/article/1091359.do|contended]] that it is extremely unlikely that ARBs are associated with an increased risk of cancer, with one physician saying he has data that, if added to the analysis, would wipe out any cancer signal. (See also [[http://www.medscape.com/viewarticle/724008|statement by Dr. Henry Black attesting to the safety of Benicar]]. Registration required.) Overall, they say, the media splash this paper has made could cause irreparable damage to the reputation of ARBs, which they consider vital tools in their armamentarium, and may unfortunately prompt many patients to stop taking the medicines, putting themselves at increased risk of cardiovascular and renal events.
+In the wake of the study, physicians [[https://www.theheart.org/article/1091359.do|contended]] that it is extremely unlikely that ARBs are associated with an increased risk of cancer, with one physician saying he has data that, if added to the analysis, would wipe out any cancer signal. (See also [[https://www.medscape.com/viewarticle/724008|statement by Dr. Henry Black attesting to the safety of Benicar]]. Registration required.) Overall, they say, the media splash this paper has made could cause irreparable damage to the reputation of ARBs, which they consider vital tools in their armamentarium, and may unfortunately prompt many patients to stop taking the medicines, putting themselves at increased risk of cardiovascular and renal events.
 Note also that the primary ARBs being evaluated, candesartan and telmisartan, have significantly different actions than olmesartan. According to the //in silico// emulations of Dr. Marshall, they are VDR antagonists.
+==== Risk ====
+<blockquote>analyses found no evidence that cancer risk increased with increasing duration of ARB exposure (RR increase per year=0.99)
+CONCLUSION:  In this large nationwide cohort, use of ARBs was not significantly associated with increased risk of incident cancer overall or of lung cancer.  (({{pmid>long:21482967}}))</blockquote>
 =====Other treatments=====
-====Vitamin D========
-<mainarticle> [[home:pathogenesis:vitamind:cancer|Vitamin D and cancer]] </article>
-{{section>:home:pathogenesis:vitamind:cancer#vitamin_D_and_cancer&noheader&firstseconly}}
+[[https://cancerres.aacrjournals.org/content/69/6/2260.short|Bicarbonate Increases Tumor pH and Inhibits Spontaneous Metastases]]
 ====Chemotherapy and radiation====
-Chemotherapy is aggressively immunosuppressive, and will allow a patient's bacterial load to return, by shutting down your immune system. For example, hepatitis infections(({{pubmed>long:21472116}})) as is pneumocystis pneumonia have been known to become reactivated during chemotherapy.(({{pubmed>long:17458875}}))
+Chemotherapy is aggressively immunosuppressive, and will allow a patient's bacterial load to return, by shutting down your immune system. For example, hepatitis infections(({{pmid>long:21472116}})); also pneumocystis pneumonia have been known to become reactivated during chemotherapy.(({{pmid>long:17458875}}))
+==== Treatment for acute active Cancers====
+[[https://www.nature.com/articles/nrc3298|Evolutionary dynamics of carcinogenesis and why targeted therapy does not work]]
+[[https://cancerres.aacrjournals.org/content/69/11/4894.short|Adaptive Therapy]]
+==== Toll-like receptor 9 (TLR9) agonists ====
+The activity and safety of these novel anticancer agents are being explored in a wide range of tumor types as part of a variety of therapeutic strategies with the goal of harnessing the immune response to fight cancer.  (({{pmid>long:18176597}}))
+Activation of Toll-Like Receptor 9 by DNA from Different Bacterial Species   (({{pmid>long:16428738}}))
 ====Vaccines====
-Some physicians have recommended the Bacillus Calmette-Guérin (BCG) vaccine as a treatment for cancer. There is no evidence to support such an intervention. BCG is live bacterium, //Mycobacterium bovis//, and has been fingered as having directly caused sarcoidosis, for example.(({{pubmed>long:12734491}})) (({{pubmed>long:2602688}}))
+Some physicians have recommended the Bacillus Calmette-Guérin (BCG) vaccine as a treatment for cancer. There is no evidence to support such an intervention. BCG is live bacterium, //Mycobacterium bovis//, and has been fingered as having directly caused sarcoidosis, for example.(({{pmid>long:12734491}})) (({{pmid>long:2602688}}))
@@ Line 171: / Line 281: @@
 //**Gene**, MarshallProtocol.com//</blockquote>
+==== Vitamins ====
+=== Vitamin D ===
+<mainarticle> [[home:pathogenesis:vitamind:cancer|Vitamin D and cancer]] </article>
+{{section>:home:pathogenesis:vitamind:cancer#vitamin_D_and_cancer&noheader&firstseconly}}
+=== Vitamin E ===
+Vitamin E supplementation and the risk of heart failure in women.
+(({{pmid>long:    22438520}}))
+Supplementation with vitamin E did not result in any significant improvements in prognostic or functional indexes of heart failure or in the quality of life of patients with advanced heart failure.(({{pmid>long:    11157316}}))
+Canolol was found to counteract the fibrotic effects of vitamin E + CoQ10 on cardiac fibrosis in the context of a high-fat diet enriched with RSO. This effect occurred through a restoration of cardiac Ag2R-1b mRNA expression and decreased ischemia.(({{pmid>long:    29456586}}))
+=== Foods ===
+[[https://www.ncbi.nlm.nih.gov/pubmed/29660776|Pawpaw]]  contains acetogenins that can inhibit the growth of cancer cells. (({{pmid>long:29660776}}))
+The 95% ethanol extract of the ripe fruit showed strong high inhibitory effect against various microorganisms. (({{pmid>long:30557901}}))
 ====Gene therapy====
-Researchers trialling gene therapies against cancer have been unsuccessful to date. Such initiatives have yet to take into account the types of intracellular microbes implicated by the Marshall Pathogenesis. One, a Duke University program, to tailor cancer treatments to certain cancers [[http://nyti.ms/q2fXgK|has ended in disaster and lawsuits]].
+Researchers trialling gene therapies against cancer have been unsuccessful to date. Such initiatives have yet to take into account the types of intracellular microbes implicated by the Marshall Pathogenesis. One, a Duke University program, to tailor cancer treatments to certain cancers [[https://nyti.ms/q2fXgK|has ended in disaster and lawsuits]].
@@ Line 182: / Line 316: @@
 Cancer kills when it is "invasive," spreading from primary sites to other sites and proliferating there. The only sure way to know the disease is cancer is to allow it to progress to a point where there is no question one has a proliferative disease. Clearly, this is not a tenable option as at a certain point, it is impossible to intervene. However, the risk of a false positive is also great. Chemotherapy will destroy the immune system, allowing microbes to multiply and leading to greater chronic inflammation when chemotherapy is discontinued. These two considerations have to be balanced, and it is a matter of debate whether many oncologists fully appreciate this balance. It is worth noting that false positives increase the apparent "success rate" of oncology, and there is therefore limited incentive to minimize them.
+Papillary carcinomas are a special histological type of breast cancer, and have a relatively good outcome. (({{pmid>long:22025283}}))
 ====Screenings not as effective as touted ====
-  * **mammograms for breast cancer** – According to a 2009 //BMJ// analysis, the best evidence suggests that for every 2,000 women who are screened over 10 years, only one stands to have her life saved by the mammogram program, whereas the risk of getting an unnecessary breast cancer diagnosis is 10 times that. Gøtzsche has written a [[http://www.ncbi.nlm.nih.gov/pubmed?term=Breast%20screening%20G%C3%B8tzsche%20bmj|number of papers]] about the mismatch between mammograms' reputation and their track record for saved lives. For more, read the  [[http://www.reuters.com/article/idUSTRE62N00A20100324|Reuters article]] or the [[http://www.latimes.com/health/boostershots/la-heb-mammogram-breast-cancer-20111024,0,7621737.story|article in the L.A. Times]].
+  * **mammograms for breast cancer** – According to a 2009 //BMJ// analysis, the best evidence suggests that for every 2,000 women who are screened over 10 years, only one stands to have her life saved by the mammogram program, whereas the risk of getting an unnecessary breast cancer diagnosis is 10 times that. Gøtzsche has written a [[https://www.ncbi.nlm.nih.gov/pubmed?term=Breast%20screening%20G%C3%B8tzsche%20bmj|number of papers]] about the mismatch between mammograms' reputation and their track record for saved lives. For more, read the  [[https://www.reuters.com/article/idUSTRE62N00A20100324|Reuters article]] or the [[https://www.latimes.com/health/boostershots/la-heb-mammogram-breast-cancer-20111024,0,7621737.story|article in the L.A. Times]].
-  * **prostate cancer** – According to a [[http://www.nytimes.com/2011/10/07/health/07prostate.html|recommendation]] by the United States Preventive Services Task Force, healthy men should no longer receive a P.S.A. blood test to screen for prostate cancer because the test does not save lives over all and often leads to more tests and treatments that needlessly cause pain, impotence and incontinence in many. It is interesting to note, however, that in some individuals, levels of prostate specific antigen (PSA) rise shortly after acquisition of gonorrhea, nongonococcal urethritis, chlamydial infection, and trichomoniasis, suggesting prostatic inflammation.(({{pubmed>long:16600802}}))
+  * **prostate cancer** – According to a [[https://www.nytimes.com/2011/10/07/health/07prostate.html|recommendation]] by the United States Preventive Services Task Force, healthy men should no longer receive a P.S.A. blood test to screen for prostate cancer because the test does not save lives over all and often leads to more tests and treatments that needlessly cause pain, impotence and incontinence in many. It is interesting to note, however, that in some individuals, levels of prostate specific antigen (PSA) rise shortly after acquisition of gonorrhea, nongonococcal urethritis, chlamydial infection, and trichomoniasis, suggesting prostatic inflammation.(({{pmid>long:16600802}}))
@@ Line 205: / Line 341: @@
 =====Animal models=====
-To date, animal models have had limited success to emulate cancers, particularly because the immune systems of even close relatives of humans are significantly different. For example, the infamous [[http://en.wikipedia.org/wiki/TGN1412|TeGenero study]] was initially trialled without a problem in apes. When it was introduced into the humans, it was a disaster.
+To date, animal models have had limited success to emulate cancers, particularly because the immune systems of even close relatives of humans are significantly different. For example, the infamous [[https://en.wikipedia.org/wiki/TGN1412|TeGenero study]] was initially trialled without a problem in apes. When it was introduced into the humans, it was a disaster.
@@ Line 222: / Line 358: @@
 sarcoidosis, bladder cancer
-Read the [[http://bacteriality.com/2008/07/18/interview24/|interview]]
+Read the [[https://bacteriality.com/2008/07/18/interview24/|interview]]
 <html></div></div>
@@ Line 243: / Line 379: @@
 //**Debra**, MarshallProtocol.com//
 </blockquote>
@@ Line 257: / Line 391: @@
 </blockquote>
-<blockquote> I found breast cancer in 1990, had a lumpectomy and follow up mastectomy with lymph node removal, as the cancer had begun to spread there. Similarly spreading, but in different organs, killed my mother at a slightly later stage of life. She had not sought treatment until too late. I have no doubt that prompt surgery and follow up radiotherapy and tamoxifen saved my life.  At that period there were no alternatives or understanding of the microbiome.
+<blockquote>__Proliferating breast cancer__
+I found breast cancer in 1990, had a lumpectomy and follow up mastectomy with lymph node removal, as the cancer had begun to spread there. Similarly spreading, but in different organs, killed my mother at a slightly later stage of life. She had not sought treatment until too late. I have no doubt that prompt surgery and follow up radiotherapy and tamoxifen saved my life.  At that period there were no alternatives or understanding of the microbiome.
 Interestingly, I also developed a pre-cancerous site on my skin.  This was removed in day surgery.  Something appeared years later, about the size of a 5 cent piece close to the scar of the first. I was not alarmed, but watched it for any sign of change and reported to my doctor who was prescribing my Olmesartan according to the Marshall Protocol. She duly sent me to the skin specialist, who adopted a wait and see approach. (//There would have been complications in skin surgery on that arm because of the lymphoedema developed due to air travel after the lymph node removal//). After a couple of visits he took fine detail pictures of the changing blemish. One of these days I would like to go back and ask for these pictures, as a year later, the cancer had completely gone.
@@ Line 265: / Line 400: @@
 //**Sallie Q**, MarshallProtocol.com//
 </blockquote>
+===== Recent research =====
+Senescent cells contribute to both age-related degeneration and hyperplastic pathologies, including cancer. (({{pmid>long:31138644}}))
+Paclitaxel Reduces Tumor Growth by Reprogramming Tumor-Associated Macrophages to an M1 Profile in a TLR4-Dependent Manner.  (({{pmid>long:30104241}}))
+{{section>:home:pathogenesis:innate_immunity#recent_research_into_valuable_proteins&noheader}}
+Discovery of novel nonsteroidal VDR agonists with novel diarylmethane skeleton for the treatment of breast cancer. (({{pmid>long:30579121}}))
+Olmesartan and Bay11-7082 inhibit the MCF-7 cells growth indicating RAS and NF-kappaB pathway blockade lead to cytotoxicity and apoptosis induction against tumour cells. So ARBs and NF-kappaB pathway inhibitors could be considered as anticancer drugs in future.  (({{pmid>long:26138656}}))
+In this large population-based gastro-oesophageal cancer cohort, we found moderately reduced cancer-specific mortality among ARB users. However, confirmation in further independent epidemiological studies with sufficient staging information is required.  (({{pmid>long:29105106}}))
+miR-205 mediates the inhibition of cervical cancer cell proliferation using olmesartan.  (({{pmid>long:28304186}}))
+Therapeutic potentials of SCFA receptors [section 7 in   (({{pmid>long:27113407}})) ]
+Recent progress in understanding the role of GPR41, GPR43 and GPR109A in health and disease demonstrate that these receptors do not just regulate inflammation and cancer in intestine, but also influence other gastrointestinal functions, allergies, adipogenesis, central nervous system and cardiovascular health.
+ review current evidence on the role of the human microbiota in four cancer types (colorectal cancer, head and neck cancer, pancreatic cancer, and lung cancer) proposed as affected by both the oral and gut microbiota (({{pmid>long:28822617}}))
+ results suggest that the six lactic acid bacteria mixture from kefir has strong effects on natural immunity and tumor cell cytotoxicity(({{pmid>long:29584690}}))
+ Using metabolomics, we investigated the metabolic influence that microbial biofilms have on colon tissues and the related occurrence of cancer.(({{pmid>long:25959674}}))
+Vitamin D and immune cells stimulate bone marrow disease (({{pmid>long:30718230}}))
+ a 10% increase in the proportion of ultra-processed foods in the diet was associated with a significant increase of greater than 10% in risks of overall and breast cancer.  (({{pmid>long:29444771}}))
+In this large prospective study, (101 257 participants aged 18 and over, mean age 42.2, SD 14.4; median follow-up time 5.1 years)  the consumption of sugary drinks was positively associated with the risk of overall cancer and breast cancer. 100% fruit juices were also positively associated with the risk of overall cancer. These results need replication in other large scale prospective studies. They suggest that sugary drinks, which are widely consumed in Western countries, might represent a modifiable risk factor for cancer prevention. [[https://www.bmj.com/content/366/bmj.l2408|BMJ 2019;366:l2408]]
 =====Read more=====
-  * [[http://www.youtube.com/watch?v=s-uCeh7BGBY|Inflammation, metabolism, aging and cancer: Dangerous Liaisons]] – Distinguished Prof. Michael Karin 2010 Harvey Prize Laureate delivered this lecture at the Technion Rappaport Faculty of Medicine on March 14, 2011. Prof. Karin received the Harvey prize in recognition of his pioneering research that has led to the deciphering of the molecular mechanisms by which mammalian cells respond to inflammatory cytokines, environmental stress and various pathogens.
+  * [[https://www.youtube.com/watch?v=s-uCeh7BGBY|Inflammation, metabolism, aging and cancer: Dangerous Liaisons]] – Distinguished Prof. Michael Karin 2010 Harvey Prize Laureate delivered this lecture at the Technion Rappaport Faculty of Medicine on March 14, 2011. Prof. Karin received the Harvey prize in recognition of his pioneering research that has led to the deciphering of the molecular mechanisms by which mammalian cells respond to inflammatory cytokines, environmental stress and various pathogens.
-  * [[http://www.oatext.com/pdf/ICST-4-231.pdf|2017 review of RAS system observations suggesting cancer stem cells may be a novel therapeutic target]]
+  * [[https://www.oatext.com/pdf/ICST-4-231.pdf|2017 review of RAS system observations suggesting cancer stem cells may be a novel therapeutic target]]
-  * [[http://www.reuters.com/article/2012/01/07/us-argentina-fernandez-idUSTRE8060CB20120107|Argentina's Fernandez sent home, never had cancer]] – Argentine President Cristina Fernandez never had cancer despite being diagnosed with the disease last month and having her thyroid gland removed.
+  * [[https://cancerres.aacrjournals.org/content/79/13_Supplement/5282.short|2019 focusing on how senescence occurs in epithelial cells, the cells that line the surfaces of the organs and structures in the body and the type of cells in which most cancers arise]]
+  *  Bicarbonate of soda may even contribute to cancer prevention.(({{pmid>long:28083722}}))
+  * [[https://www.reuters.com/article/2012/01/07/us-argentina-fernandez-idUSTRE8060CB20120107|Argentina's Fernandez sent home, never had cancer]] – Argentine President Cristina Fernandez never had cancer despite being diagnosed with the disease last month and having her thyroid gland removed.
   * [[https://en.wikipedia.org/wiki/List_of_unproven_and_disproven_cancer_treatments|Wiki list of unproven & disproven treatments]]
-  * [[http://www.foodsmatter.com/es/health_risks/articles/goldsworthy-biological-effects-04-12.pdf|biological effects]]
+  * [[https://www.amjmed.com/article/S0002-9343(15)00509-4/pdf|Questions About Vitamin D for Primary Care Practice: Input From an NIH Conference]]
-  * [[http://bioinitiative.org/report/wp-content/uploads/pdfs/sec01_2012_summary_for_public.pdf|Bioinitiative Report]]
+  * [[https://www.foodsmatter.com/es/health_risks/articles/goldsworthy-biological-effects-04-12.pdf|biological effects of non-ionising electromagnetic fields]]
+  * [[https://bioinitiative.org/report/wp-content/uploads/pdfs/sec01_2012_summary_for_public.pdf|Bioinitiative Report]]
 "The most serious  health  endpoints  that  have  been  reported  to  be  associated  with  extremely  low  frequency  (ELF)  and/or
@@ Line 290: / Line 464: @@
-New Evidence Links Virus to Brain Cancer - http://www.med.wisc.edu/news-events/news/new-evidence-links-virus-to-brain-cancer/32922
+  (({{pmid>long:000}}))
+  (({{pmid>long:000}}))
+New Evidence Links Virus to Brain Cancer - https://www.med.wisc.edu/news-events/news/new-evidence-links-virus-to-brain-cancer/32922
@@ Line 324: / Line 502: @@
-well-established tumor-promoting function of chronic inflammation (Karin and Greten, 2005)(({{pubmed>long:16175180}}))
+well-established tumor-promoting function of chronic inflammation (Karin and Greten, 2005)(({{pmid>long:16175180}}))
 types of cancer versus one
@@ Line 347: / Line 525: @@
 The relationship between cancer and inflammation is controversial. (IMO) A good review of the issues is available from
-[[http://www.joimr.org/phorum/read.php?f=2&i=50&t=50|JOIMR]]
+[[https://www.joimr.org/phorum/read.php?f=2&i=50&t=50|JOIMR]]
 Additionally, two of the markers used in Flow Cytometry (used as the 'gold standard' for breast cancer) bcl2 and CD10, are both elevated in the inflammatory diseases, leading to misdiagnosis in a lot of cases, probably in a majority of cases. These misdiagnoses also bias the epidemiological studies.
@@ Line 384: / Line 562: @@
 "There's a lot of research going on at the moment in general to find additional breast cancer genes. What we're saying here is that research is likely to be successful," Begg said.
-~Andrew Stern, [[http://www.reuters.com/article/healthNews/idUSN0848849720080108|Reuters]]
+~Andrew Stern, [[https://www.reuters.com/article/healthNews/idUSN0848849720080108|Reuters]]
 </blockquote>
@@ Line 392: / Line 570: @@
 Almost half of all cancer survivers have ill health in later years.
-http://www.sciencedaily.com/releases/2011/10/111010104047.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fhealth_medicine%2Fmental_health+%28ScienceDaily%3A+Health+%26+Medicine+News+--+Mental+Health+Research%29
+https://www.sciencedaily.com/releases/2011/10/111010104047.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fhealth_medicine%2Fmental_health+%28ScienceDaily%3A+Health+%26+Medicine+News+--+Mental+Health+Research%29
 </blockquote>
@@ Line 432: / Line 610: @@
-http://www.forbes.com/sites/melaniehaiken/2012/05/10/can-getting-sick-give-you-cancer-new-research-says-sometimes-yes/
+https://www.forbes.com/sites/melaniehaiken/2012/05/10/can-getting-sick-give-you-cancer-new-research-says-sometimes-yes/

home/diseases/cancer.1528776781.txt.gz · Last modified: 06.12.2018 by sallieq