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Microbes That Cause Cancers

For ages 3 and up. You may also like Quick View. Submit Please enter a valid email address. Giantmicrobes are based on actual microbes, cells, organisms and other critters, only 1,, times actual size! Plush from all new materials. Each plush microbe includes a printed card with fun, educational and fascinating facts about the actual microbe or cell. Every product meets or exceeds U. Our bodies are made of billions of cells that are programmed to grow, divide, and die over time.

Cancer is a group of genetic disease caused by uncontrolled division of abnormal cells in the body. Prior to randomization individuals were screened for metastatic disease. Colon cancer and rectal cancer subjects were in separate but parallel studies and randomized into groups treated by resection alone or resection plus ASI.

Vaccines were begun in the ASI treatment group 4—5 weeks following surgery to allow for adequate immune recovery from surgery and anesthesia.


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A total of 24 colon and 17 rectal subjects composed the treatment group. With a median follow-up of 58 months, no benefits were seen in patients with rectal cancer who received ASI. The authors concluded that the study suggested that ASI may be beneficial to patients with colon cancer. In , Uyl-de Groot et al. The vaccine was processed within 48 h after surgery in order to have viable, metabolically active, autologous tumor cells. Analysis of prognostic benefit with a 5.

Unfortunately, no statistically significant prognostic benefits were achieved in Stage III patients [ ]. Grant et al [ 39 ] hypothesized that optimal chemotherapy with or without radiation followed by active immunization could eliminate microscopic residual disease and prolong survival. Immunization with GD3, a ganglioside expressed on the surface of most small cell lung cancers SCLC had not evoked a strong immune response.

Therefore BEC2, a large xenogenic protein which mimics GD3, was judged to be a good immunogenic candidate. This approach had proven successful in extending the lives of melanoma patients [ ]. The study population consisted of 15 patients with small cell lung cancer SCLC. All subjects had completed standard therapy and had achieved a partial or complete response.

Patients received a series of five intradermal immunizations consisting of 2. Blood was collected for serological analysis, and outcome was monitored. All patients developed anti-BEC2 antibodies, despite having received chemotherapy with or without thoracic radiation. Anti-GD3 antibodies were detected in five patients, including those with the longest relapse-free survival.

The median relapse-free survival for patients with extensive stage disease was The survival and relapse-free survival in this group of patients was substantially better than those observed in similar patients receiving standard therapy. A total of subjects were randomly assigned. Unfortunately, in this trial there was no improvement in survival, progression-free survival, or quality of life in subjects that were vaccinated. The effectiveness of vaccines for several cancers was examined in a series of investigations.

Tolerance against self-antigens was broken by genetically fusing ubiquitin with MHC I derivatives. Another approach coupled tumor-specific antibodies to functional IL This combination in addition to oral vaccination with plasmid-encoded tumor antigens significantly enhanced protection against carcinoma of the colon [ ], carcinoma of the lung [ ] and melanoma [ ]. Unstable cancer cells provided a challenge, however. Interestingly, this was overcome by targeting stable, proliferating endothelial cells of the tumor vasculature.

This novel approach effectively inhibited angiogenesis [ ]. In industrialized countries the incidence of H pylori has been steadily decreasing [ ]. The incidence of esophageal cancer EA , however, is increasing [ ]. Surprisingly, there is evidence that these two trends may be related. Several studies have determined that virulent strains of H pylori are found less commonly among patients with Barrett's esophagus and EA when compared with controls [ - ]. This led to studies that found positive associations among the increased incidence of obesity, GORD, Barrett's esophagus and EA [ ].

Recently, a nested case-control study was conducted by de Martel et al [ ] to assess the association between H. Of a total of , members of an integrated health care system who had participated in a multiphasic health checkup MHC during —, 52 patients developed EA during follow-up. Three randomly chosen control subjects from the MHC cohort were matched to each cancer subject, on the basis of age, gender, race, date and site of the MHC. Data on cigarette smoking, alcohol consumption, body mass index BMI , and education level were obtained. Interestingly, in patients with H. The authors found, however, that the absence of H.

An epidemiological study in Sweden sought to determine whether BMI was associated with esophageal malignancies compared to gastric adenocarcinoma and controls. In a nationwide, population-based case-control study by Lagergren et al [ ], between through , a total of patients with adenocarcinoma of the esophagus and patients with adenocarcinoma of the gastric cardia were enrolled.

These patients were compared with patients with incident esophageal squamous cell carcinoma and healthy controls. Odds ratios were determined from BMI and cancer case-control status and ratios estimated the relative risk for the two adenocarcinomas studied. Calculations used multivariate logistic regression with adjustment for potential confounding factors. The adjusted odds ratio was 7. The odds ratio for patients with cardia adenocarcinoma was 2.

Microorganisms and Cancer: Quest for a Therapy

Although a strong dose-dependent relation existed between BMI and esophageal adenocarcinoma, esophageal squamous-cell carcinoma was not associated with BMI. A modest but significant increase in intragastric acidity was also observed following the cure of H pylori infection which the authors postulated could contribute to gastroesophageal reflux disease GORD. The incidence of EA has increased rapidly over the last 30 years. During this period, the prevalence of Helicobacter pylori has decreased. Trends of increasing esophageal adenocarcinoma can be linked causally to increasing GORD which can be linked to an increasingly obese population.

There appeared to be no plausible biological mechanism of association between H pylori , obesity, and GORD until studies of ghrelin, however. Ghrelin was the first circulating hormone demonstrated to stimulate food intake in man. This peptide is produced in the stomach and regulates appetite, food intake, and body composition. The effects of ghrelin were examined in H pylori positive asymptomatic subjects by several investigators [ - ]. In a randomized double-blind cross-over study, by Wren et al.

Furthermore, visual analogue scores for appetite were greater during ghrelin compared to saline infusion. Ghrelin had no effect on gastric emptying, however. The authors concluded that endogenous ghrelin was a potentially important new regulator of the complex systems controlling food intake and body weight. Evidence is accumulating that ghrelin may explain the relative rarity of H. Findings from these studies and others support the notion that H. Studies have found that curing H pylori infection increased plasma ghrelin in healthy asymptomatic subjects which may lead to increased appetite, weight gain and contribute to the increasing obesity seen in Western populations where the prevalence of H pylori is low.

The Cancer Microbe - Alan Cantwell - Google Книги

This evidence supports the notion that decreasing incidence of H pylori infection may lead to increased levels of plasma ghrelin and that this hormone appears to be a factor in increasing obesity which elevates the risk of GORD which is positively associated with Barrett's esophagus and increased risk of esophageal adenocarcinoma. It appears that the absence of H. The implications for treatment of individuals with H.

They systematically reviewed the literature and estimated the expected annual incidence of esophageal or gastric cancer with and without eradication of H. The expected annual incidence of gastric cancer in patients with corpus atrophy with persistent infection was at least 5. Even for patients with accompanying reflux esophagitis or Barrett's esophagus, the incidence of gastric adenocarcinoma with persistent infection was higher than that of esophageal adenocarcinoma after eradication of infection.

The authors concluded, therefore, that if eradication of infection lowers the incidence of gastric cancer, it should be recommended for patients with corpus atrophy at all ages irrespective of the presence of reflux esophagitis or Barrett's esophagus, especially in populations having a high prevalence of gastric cancer [ ].

In summary, increased BMI has been linked with the elimination of H. As the sphincter mechanism at the esophagogastric junction is weakened by weight it is not surprising that obese individuals have a higher incidence of gastric reflux or GORD [ ]. The study by Lagergren [ ] provides evidence that these associations may be related as increasing body mass was associated with a stepwise increase in the risk of EA.

If eradication of H. Attenuated bacteria will enhance stimulation of the innate immune system yet increase the safety of a vaccine, [ ] therefore they may be ideal for the delivery of vaccines. Animal studies have shown that attenuated S. The identification of bacterial "carriers" for DNA vaccines that target cancer cells by site-specific colonization may allow the selective delivery of vaccine plasmids into tumor cells [ ]. Colonization of these species may be considered coincidental to favorable conditions provided by the tumor yet prove clinically useful.

Ultimately, however, the safety and efficacy of recombinant therapeutic agents expressed by plasmids must be conducted in appropriate animal models. Cancer is commonly defined as the uncontrolled growth of abnormal cells that have accumulated enough DNA damage to be freed from the normal restraints of the cell cycle. Several pathogenic bacteria, particularly those that can establish a persistent, infection, can promote or initiate abnormal cell growth by evading the immune system or suppressing apoptosis [ 54 , ].

Intracellular pathogens survive by evading the ability of the host to identify them as foreign. Other species or their toxins can alter host cell cycles or stimulate the production of inflammatory substances linked to DNA damage [ ]. The highly site-specific adherence of bacteria involves binding species-specific adhesions to the required cell surface receptors. The role of species that colonize tumors could be causal, coincidental or potentially protective.

If adhesion to the tumor in question is highly sensitive and specific it may be ideal not only in diagnosing the presence of a malignancy but also in delivering the appropriate therapy. The bacterial species associated with cancer etiology are diverse; however, the infections they cause share common characteristics [ 18 ].

Bacterial products in the treatment of cancer.

The time between acquiring the infection and cancer development is most often years or even decades as seen in cancers associated with H. Preventing or treating the infection may prevent the cancer in question. Notably, the vast majority of individuals infected with a cancer-causing species will not develop cancer [ 18 ]. Evidence suggests that certain individuals are more susceptible to infections linked to cancer development and that the incidence of certain cancers varies among populations.

For example, gallbladder cancer is 3 times higher in females as in males in all populations [ 26 ]. Lung cancer is highest in populations that smoke however, only a small proportion of smokers develop lung cancer [ 42 ]. Although colon cancer is the 3 rd highest cancer in the United States, individuals with IBD have a far greater risk of colorectal cancer than individuals without IBD [ 56 - 58 ]. A screening test for oral cancer based on salivary counts of bacterial species is appealing.

Currently saliva is meeting the demand for inexpensive, non-invasive, and easy-to-use diagnostic aids for oral and systemic diseases, and for assessing risk behaviors such as tobacco and alcohol use. Although the colonization of certain bacterial species may be coincidental to favorable conditions provided by OSCC, increased numbers of certain salivary species may be clinically useful if shown to be a signature of oral cancer and if sensitivity and specificity are improved.

Successful treatment for cancers was reported by Dr. Coley and others one hundred years ago. His approach of using killed bacterial vaccines was surprisingly effective in some patients even in the latest stages of cancer. Coley believed that the human immune system had the power to cure cancers if properly stimulated. Today, some investigators agree and have designed new treatments that stimulate the immune system to recognize and target the lesion. Recent reports suggest that attenuated bacterial vaccines can safely and effectively deliver plasmids encoding tumor self antigens.

These studies have reported successful treatment of certain cancers and prevention of recurrences [ 39 , , ]. Cancer vaccines although promising, present significant challenges. These include identification of highly effective bacterial strains and their attenuations, addressing safety issues and the problem of overcoming the peripheral T cell tolerance against tumor self-antigens [ ]. Further, the response to vaccines will likely vary among individuals.

It appears that colonization by certain bacteria may reduce the risk of cancer in some populations. The epidemiological trends of esophageal adenocarcinoma and Helicobacter pylori infection have stimulated research into whether these may be coincidental or due to an inverse association. Intriguing results suggest there is an association represented by a complex continuum that begins with curing infections of virulent strains of H.

The absence of H. High ghrelin levels appear to be associated with increased incidence of obesity. Obesity is reported to be a contributing factor in GORD. If these relationships can be proven, then the colonization of this species and its seemingly negative association with EA may be more clearly understood.

In summary, recent research has uncovered a great deal of information regarding the bacterial mechanisms used to cause, colonize or cure cancer, however, many questions remain. For example, do the bacteria in question initiate, promote, or merely show affinity for the neoplasm? Conversely does cancer weaken the host which facilitates acquiring the infection? Can the highly site specific colonization of certain bacteria for a tumor be clinically useful in diagnosis or treatment? Could attenuated bacteria be used in vaccines to safely and effectively deliver therapeutic agents?

The continued exploration of these questions will bring research ever closer to the prevention, early diagnosis and truly effective treatment of this scourge of mankind. My sincere thanks to Dr.

Additional Information

Richard Pharo for his valuable input on the editing of this manuscript and to Susan Orlando and Daniel McCloskey for their generous assistance in obtaining publications and organizing references. National Center for Biotechnology Information , U. Journal List J Transl Med v. Published online Mar Author information Article notes Copyright and License information Disclaimer. Received Jan 19; Accepted Mar This article has been cited by other articles in PMC. Abstract Research has found that certain bacteria are associated with human cancers.

Introduction An overwhelming body of evidence has determined that relationships among certain bacteria and cancers exist. Salmonella typhi and gallbladder cancer Worldwide annual incidence of gallbladder cancer GC is 17 million cases with high incidence rates in certain populations. Chlamydophila pneumoniae and lung cancer Lung cancer is the leading cause of cancer death in the United States and many countries in the Western world.

Streptococcus bovis and colorectal cancer Colorectal cancer CRC is a common malignancy in developed countries and is the 3rd most common cancer in the United States [ 38 ]. Genetic predisposition to cancer-causing infections Research has shown that some populations are genetically predisposed to the infections that are associated with cancer and indeed have a higher risk of the cancer in question. Supervised clustering analysis based on EGFR gene mutations elucidated a subgroup including all EGFR gene mutated tumors, which showed significantly shorter disease-free survival To analyze the genetic alterations of primary lung adenocarcinoma in a high-throughput way, Shibata et al.

Bacterial site-specific colonization Bacterial adherence is thought to be the first important step in colonization. Bacteria associated with a coincidental or diagnostic role Each year nearly 30, Americans are diagnosed with oral cancer [ 73 , 74 ]. Bacteria and the prevention or treatment of cancer Evidence is mounting that certain species of bacteria or their toxins may indeed have a protective or curative role in some cancers. Tumors and coley's toxins Spontaneous tumor regression has followed severe bacterial, fungal, viral and protozoal infections.

Helicobacter pylori and esophageal adenocarcinoma In industrialized countries the incidence of H pylori has been steadily decreasing [ ]. Promising carriers of DNA vaccines Attenuated bacteria will enhance stimulation of the innate immune system yet increase the safety of a vaccine, [ ] therefore they may be ideal for the delivery of vaccines. Conclusion Cancer is commonly defined as the uncontrolled growth of abnormal cells that have accumulated enough DNA damage to be freed from the normal restraints of the cell cycle.

Competing interests The author s declare that they have no competing interests. Acknowledgements My sincere thanks to Dr. Cancer Epidemiol Biomarkers Prev. Genotypic variability of hepatitis viruses associated with chronic infection and the development of hepatocellular carcinoma. J Am Dent Assoc. Helicobacter infection , chronic inflammation, and the development of malignancy. Regression of gastric high grade mucosa associated lymphoid tissue MALT lymphoma after Helicobacter pylori eradication.

Infection, immunity, and cancer. Arch Pathol Lab Med. Epidemiology of typhoid carriers among blood donors and patients with biliary, gastrointestinal and other related diseases.


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How bacteria could cause cancer: Typhoid carriers among patients with gallstones are at increased risk for carcinoma of the gallbladder. Carcinoma of the gallbladder — is it a sequel of typhoid? Carcinogenic properties of proteins with pro-inflammatory activity from Streptococcus infantarius formerly S.

Association of Streptococcus bovis bacteremia with colonic neoplasia and extracolonic malignancy. Promotion of intestinal carcinogenesis by Streptococcus bovis. The triad of Streptococcus bovis bacteremia, colonic pathology, and liver disease. Chlamydia pneumoniae infection and risk of lung cancer. An association between chronic infection with Chlamydia pneumoniae and lung cancer.

A prospective 2-year study. Chlamydia pneumoniae infection and the risk of female early-onset lung cancer. Infections as a major preventable cause of human cancer. Chronic Chlamydophila pneumoniae infection in lung cancer, a risk factor: A bacterial toxin that controls cell cycle progression as a deoxyribonuclease I-like protein. Tumor-associated macrophages express lymphatic endothelial growth factors and are related to peritumoral lymphangiogenesis.

Increased oxidative DNA damage in Helicobacter pylori infected human gastric mucosa. Prostaglandin E2 increases growth and motility of colorectal carcinoma cells. Inducible nitric oxide synthase, nitrotyrosine and apoptosis in Helicobacter pylori gastritis: Epidemiology and molecular pathology of gallbladder cancer.

CA Cancer J Clin. Geographical distribution and risk factors. Cancer mortality in chronic typhoid and paratyphoid carriers. Association between hepatobiliary cancer and typhoid carrier state. Genetic epidemiology of cholesterol cholelithiasis among Chilean Hispanics, Amerindians, and Maoris. Risk factors for gallbladder cancer. An international collaborative case-control study. Increasing gall-bladder cancer mortality rate during the last decade in Chile, a high-risk area. Epidemiology of gallbladder cancer and trends in cholecystectomy rates in Scotland, — Chlamydia pneumoniae and chronic lung diseases.

Scand J Infect Dis. Chlamydia pneumoniae as a respiratory pathogen. Prior lung disease and risk of lung cancer in a large prospective study. Commensal bacteria, redox stress, and colorectal cancer: Cancer of the colon. Colon Cancer Alliance Colorectal cancer: These species have been noticed as something associated with some colon cancer tissue samples, but this new work shows that things are a lot deeper than that.

When rodents are transplanted with xenograft tumor tissues of this type, antibiotic treatment metronidazole actually slows tumor progression. And just as in that case, this strongly suggests that any patients with this sort of tumor should be tried out on antibiotic therapy; there would seem to be little to lose and potentially much to gain. So, can these bacteria be called bio-markers for these cancers? These bacterial infections may have a potential use assuming they are first validated as biomarkers of susceptibility, or used in some other way in developing a prognosis.

The connection with peptic ulcers and H. It is interesting, but not surprising to read about the connection with Fusobacterium. Regardless the scope of this work is compelling and historically antibacterial treatment for peptic ulcers is efficacious. It would be great to see human trials on this course for colorectal cancers. There is another interesting one here. It may suggest that chronic inflammation in GI would lead to cancer? Recurrent infection progressively disables host protection against intestinal inflammation.

Yang WH, et al. Or is it news because Dana-Farber, Broad, Harvard, Barcelona, Yale now notice this 7 years since it was first reported? It seems entirely reasonable to me, as a non-biologist, that inflammation could increase the risk of cancer. Anything that increases mitosis rates is going to increase defective mitosis rates and the mutations that lead to cancer. It is worth noting that metronidazole becomes activated by intracellular reduction, which occurs more readily in bacterial cells than human cells. Once reduced, the compound indiscriminately damages DNA.