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Two papers examine the influence of different stem cell characteristics on tumorigenesis in an organ-specific and age-associated manner, continuing the debate on the influence of intrinsic and extrinsic factors on cancer risk.

Doc number: 22

Two papers examine the role of cell competition in tumorigenesis.

Patient Education Significance & Background: The process of carcinogenesis is very complex and not yet fully understood. What we do know is that exposure to certain chemicals and/or substances called carcinogens can initiate DNA damage inside cells that then alters the genes that control the cell division cycle. Proto-oncogenes and tumor suppressor genes can be adversely affected. Sometimes, exposure to these cancer-causing substances occurs unknowingly and/or by accident. However more commonly, these substances enter our bodies through purposeful lifestyle behaviors and choices in a recurring fashion. Preventative strategies that focus on increasing public awareness through education, health fairs, and volunteerism as well as professional advocacy are essential for the health, safety, and well-being of our fellow human beings. Most lay people have very little understanding of the linkages and the consequences of what they allow inside their bodies that can possibly lead up to cancer development. Purpose: This presentation will briefly describe the role of specific carcinogens in the process of carcinogenesis, specifically regarding altering proto-oncogenes and tumor suppressor genes and with other pertinent hallmarks of cancer. Scientific explanations on why a cancer might not respond to therapy, relapse, and progress despite treatment or even change completely to another form will be explained. Interventions: This presentation will share valuable and reliable resources of information for the oncology nurse to utilize while performing health promotion and cancer prevention strategies geared for the public's benefit and to increase awareness. Patients are usually more open to receiving heath information from oncology nurses compared to most other health care providers. Results: There are approximately 63 to 122 substances known to cause human cancer with hundreds more thought to be probable causes according to most recent reports from the National Toxicology Program (NTP) and the International Agency for Research on Cancer (IARC) respectively. Many of these substances exist in our environment, our food supply, and in things we consume or ingest; and many are legal for purchase in the Unites States. In contrast, other known substances are available that can offer some protection by blocking and/or repairing these altered genes. Discussion: Although cancer development cannot be completely avoided, purposeful adjustments to our lifestyle choices can have a potentially significant beneficial impact, safeguard our bodies from these DNA alterations, and ultimately lessen the risk of cancer in most individuals.

The gut microbiota and liver cancer have a complex interaction. However, the role of gut microbiome in liver tumor initiation remains unknown. Herein, liver cancer was induced using hydrodynamic transfection of oncogenes to explore liver tumorigenesis in mice. Gut microbiota depletion promoted liver tumorigenesis but not progression. Elevated sterol regulatory element-binding protein 2 (SREBP2) was observed in mice with gut flora disequilibrium. Pharmacological inhibition of SREBP2 or Srebf2 RNA interference attenuated mouse liver cancer initiation under gut flora disequilibrium. Furthermore, gut microbiota depletion impaired gut tryptophan metabolism to activate aryl hydrocarbon receptor (AhR). AhR agonist Ficz inhibited SREBP2 posttranslationally and reversed the tumorigenesis in mice. And, AhR knockout mice recapitulated the accelerated liver tumorigenesis. Supplementation with Lactobacillus reuteri, which produces tryptophan metabolites, inhibited SREBP2 expression and tumorigenesis in mice with gut flora disequilibrium. Thus, gut flora disequilibrium promotes liver cancer initiation by modulating tryptophan metabolism and up-regulating SREBP2.

The human microbiota is symbiotic with the host and can create a variety of metabolites. Under normal conditions, microbial metabolites can regulate host immune function and eliminate abnormal cells in a timely manner. However, when metabolite production is abnormal, the host immune system might be unable to identify and get rid of tumor cells at the early stage of carcinogenesis, which results in tumor development. The mechanisms by which intestinal microbial metabolites, including short-chain fatty acids (SCFAs), microbial tryptophan catabolites (MTCs), polyamines (PAs), hydrogen sulfide, and secondary bile acids, are involved in tumorigenesis and development by regulating immune responses are summarized in this review. SCFAs and MTCs can prevent cancer by altering the expression of enzymes and epigenetic modifications in both immune cells and intestinal epithelial cells. MTCs can also stimulate immune cell receptors to inhibit the growth and metastasis of the host cancer. SCFAs, MTCs, bacterial hydrogen sulfide and secondary bile acids can control mucosal immunity to influence the occurrence and growth of tumors. Additionally, SCFAs, MTCs, PAs and bacterial hydrogen sulfide can also affect the anti-tumor immune response in tumor therapy by regulating the function of immune cells. Microbial metabolites have a good application prospect in the clinical diagnosis and treatment of tumors, and our review provides a good basis for related research.