Insight into the molecular basis of Schistosoma haematobium-induced bladder cancer through urine proteomics

Bernardo, Carina; Cunha, Maria Claudia; Santos, Jorge; Costa, José Manuel Correia da; Brindley, Paul J.; Lopes, Carlos; Amado, Francisco; Ferreira, Rita; Vitorino, Rui; Santos, Lúcio Lara

doi:10.1007/s13277-016-4997-y

Cited by 23 publications

(17 citation statements)

References 42 publications

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“…Chromosomal damage and somatic mutations were frequently observed in these oncogenes in invasive squamous cell carcinomas of the bladder during UGS (Rosin et al, 1994). A recent proteomic analysis of urine samples from UGS patients additionally confirms the involvement of oxidative stress and immune responses in the development of S. haematobium -induced bladder cancer (Bernardo et al, 2016). …”

Section: Schistosomiasis and Cancermentioning

confidence: 84%

Parasite Infection, Carcinogenesis and Human Malignancy

et al. 2017

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Cancer may be induced by many environmental and physiological conditions. Infections with viruses, bacteria and parasites have been recognized for years to be associated with human carcinogenicity. Here we review current concepts of carcinogenicity and its associations with parasitic infections. The helminth diseases schistosomiasis, opisthorchiasis, and clonorchiasis are highly carcinogenic while the protozoan Trypanosoma cruzi, the causing agent of Chagas disease, has a dual role in the development of cancer, including both carcinogenic and anticancer properties. Although malaria per se does not appear to be causative in carcinogenesis, it is strongly associated with the occurrence of endemic Burkitt lymphoma in areas holoendemic for malaria. The initiation of Plasmodium falciparum related endemic Burkitt lymphoma requires additional transforming events induced by the Epstein-Barr virus. Observations suggest that Strongyloides stercoralis may be a relevant co-factor in HTLV-1-related T cell lymphomas. This review provides an overview of the mechanisms of parasitic infection-induced carcinogenicity.

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Section: Schistosomiasis and Cancermentioning

confidence: 84%

Parasite Infection, Carcinogenesis and Human Malignancy

et al. 2017

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“…Proteomic analysis can help to identify biological processes that could be of importance in carcinogenesis [28]. Schistosoma haematobium was associated with bladder cancer using proteomic profiling [29]. Products of the nematode, Anisakis pegreffii, were shown to upregulate heat shock protein 70 (Hsp70) with a corresponding decrease in apoptosis [30].…”

Section: Microbiome (Tab 1)mentioning

confidence: 99%

Microbiome and morbid obesity increase pathogenic stimulus diversity

Brücher

Jamall

2019

4open

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The microbiome, the relationship between environmental factors, a high-fat diet, morbid obesity, and host response have been associated with cancer, only a small fraction of which (<10%) are genetically triggered. This nongenetic association is underpinned by a worldwide increase in morbid obesity, which is associated with both insulin resistance and chronic inflammation. The connection of the microbiome and morbid obesity is reinforced by an approximate shift of about 47% in the estimated total number of bacteria and an increase from 38,000,000,000,000 in a reference man to 56,000,000,000,000 in morbid obesity leading to a disruption of the microbial ecology within the gut. Humans contain 6,000,000,000 microbes and more than 90% of the cells of the human body are microorganisms. Changes in the microflora of the gut are associated with the polarization of ion channels by butyrate, thereby influencing cell growth. The decrease in the relative proportion of Bacteroidetes together with a change in the fermentation of carbohydrates by bacteria is observed in morbid obesity. The disruption of homeostasis of the microflora in the obese changes signaling and crosstalk of several pathways, resulting in inflammation while suppressing apoptosis. The interactions between the microbiome and morbid obesity are important to understand signaling and crosstalk in the context of the progression of the six-step sequence of carcinogenesis. This disruption of homeostasis increases remodeling of the extracellular matrix and fibrosis followed by the none-resolvable precancerous niche as the internal pathogenic stimuli continue. The chronic stress explains why under such circumstances there is a greater proclivity for normal cells to undergo the transition to cancer cells.

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“…On the other hand, both EMT and Shh signaling are induced by TGF-β in bladder cancer [162]. Recently proteome profiling of urine samples from bladder cancer patients associated with Schistosoma haematobium infection [163] revealed further strong evidence of the proposed multi-sequence carcinogenesis process [17,18].…”

Section: In Vitro and In Vivo Evidencementioning

confidence: 99%

Somatic Mutation Theory - Why it's Wrong for Most Cancers

Brücher¹,

Jamall

2016

Cell Physiol Biochem

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Hysteron proteron reverses both temporal and logical order and this syllogism occurs in carcinogenesis and the somatic mutation theory (SMT): the first (somatic mutation) occurs only after the second (onset of cancer) and, therefore, observed somatic mutations in most cancers appear well after the early cues of carcinogenesis are in place. It is no accident that mutations are increasingly being questioned as the causal event in the origin of the vast majority of cancers as clinical data show little support for this theory when compared against the metrics of patient outcomes. Ever since the discovery of the double helical structure of DNA, virtually all chronic diseases came to be viewed as causally linked to one degree or another to mutations, even though we now know that genes are not simply blueprints, but rather an assemblage of alphabets that can, under non-genetic influences, be used to assemble a business letter or a work of Shakespearean literature. A minority of all cancers is indeed caused by mutations but the SMT has been applied to all cancers, and even to chemical carcinogenesis, in the absence of hard evidence of causality. Herein, we review the 100 year story of SMT and aspects that show why genes are not just blueprints, how radiation and mutation are associated in a more nuanced view, the proposed risk of cancer and bad luck, and the in vitro and in vivo evidence for a new cancer paradigm. This paradigm is scientifically applicable for the majority of non-heritable cancers and consists of a six-step sequence for the origin of cancer. This new cancer paradigm proclaims that somatic mutations are epiphenomena or later events occurring after carcinogenesis is already underway. This serves not just as a plausible alternative to SMT and explains the origin of the majority of cancers, but also provides opportunities for early interventions and prevention of the onset of cancer as a disease.

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Insight into the molecular basis of Schistosoma haematobium-induced bladder cancer through urine proteomics

Cited by 23 publications

References 42 publications

Parasite Infection, Carcinogenesis and Human Malignancy

Parasite Infection, Carcinogenesis and Human Malignancy

Microbiome and morbid obesity increase pathogenic stimulus diversity

Somatic Mutation Theory - Why it's Wrong for Most Cancers

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