1,721,108 research outputs found
Cancer screenings, diagnostic technology evolution, and cancer control
No full textScreening should allow for the anticipation of cancer diagnosis at an earlier stage, when curative treatment is possible. Screening for cervical, large bowel, and breast cancer were shown to be effective in reducing mortality. The wide acceptance of the screening concept led to the wide diffusion also of screening of uncertain benefit against prostate cancer and skin melanoma. Diagnostic technologies are continuously evolving, and new tests are proposed to improve existing screenings or as screening tests for additional cancer sites (e.g., lung cancer). Cancer screening, however, is a complex and costly intervention that does not result only in benefits but also may cause harm. A major emerging problem of screening is overdiagnosis, or the detection of cases that would have not progressed to the symptomatic phase in the absence of screening. Thus, both experimental and observational evaluation studies are needed to reduce harm caused by screenings and to select effective interventions among many proposed innovations. Finally, the research of markers to assess the aggressive nature of screen-detected lesions is of great importance to improve screenings ’ harm/benefit ratio
Il ruolo della mutazione del gene oncosoppressore APC nel processo di cancerogenesi colorettale
No full textSecondo le attuali conoscenze degli aspetti genetici della cancerogenesi colorettale, almeno due distinti meccanismi sembrano coinvolti nella genesi del cancro, la mutazione somatica o germinale (HNPCC) di uno dei geni costituenti un sistema di riparazione del DNA o l'inattivazione di alcuni geni oncosoppressori (APC, DCC, p53) ed oncogeni (k-ras)
Epidemiological changes in breast tumours in Italy: the IMPACT study on mammographic screening programmes.
No full textHuman papillomavirus and gastrointestinal cancer: A review
Full text linkHuman papillomavirus (HPV) is one of the most common sexually transmitted infections worldwide. Exposure to HPV is very common, and an estimated 65%-100% of sexually active adults are exposed to HPV in their lifetime. The majority of HPV infections are asymptomatic, but there is a 10% chance that individuals will develop a persistent infection and have an increased risk of developing a carcinoma. The International Agency
for Research on Cancer has found that the following cancer sites have a strong causal relationship with HPV: cervix uteri, penis, vulva, vagina, anus and oropharynx, including the base of the tongue and the tonsils. However, studies of the aetiological role of HPV in colorectal and esophageal malignancies have conflicting results. The aim of this review was to organize recent evidence and issues about the association between HPV infection and gastrointestinal tumours with a focus on esophageal, colorectal and anal cancers. The ultimate goal was to highlight possible implications for prognosis and prevention
Cytotoxic synergism of Clostridioides difficile toxin B with proinflammatory cytokines in subjects with inflammatory bowel diseases
Full text linkClostridioides difficile (C. difficile) is progressively colonizing humans and animals living with humans. During this process, hypervirulent strains and mutated toxin A and B of C. difficile (TcdA and TcdB) are originating and developing. While in healthy subjects colonization by C. difficile becomes a risk after the use of antibiotics that alter the microbiome, other categories of people are more susceptible to infection and at risk of relapse, such as those with inflammatory bowel disease (IBD). Recent in vitro studies suggest that this increased susceptibility could be due to the strong cytotoxic synergism between TcdB and proinflammatory cytokines the tumor necrosis factor-alpha and interferon-gamma (CKs). Therefore, in subjects with IBD the presence of an inflammatory state in the colon could be the driver that increases the susceptibility to C. difficile infection and its progression and relapses. TcdB is internalized in the cell via three receptors: chondroitin sulphate proteoglycan 4; poliovirus receptor-like 3; and Wnt receptor frizzled family. Chondroitin sulphate proteoglycan 4 and Wnt receptor frizzled family are involved in cell death by apoptosis or necrosis depending on the concentration of TcdB and cell types, while poliovirus receptor-like 3 induces only necrosis. It is possible that cytokines could also induce a greater expression of receptors for TcdB that are more involved in necrosis than in apoptosis. Therefore, in subjects with IBD there are the conditions: (1) For greater susceptibility to C. difficile infection, such as the inflammatory state, and abnormalities of the microbiome and of the immune system; (2) for the enhancement of the cytotoxic activity of TcdB +Cks; and (3) for a greater expression of TcdB receptors stimulated by cytokines that induce cell death by necrosis rather than apoptosis. The only therapeutic approach currently possible in IBD patients is monitoring of C. difficile colonization for interventions aimed at reducing tumor necrosis factor-alpha and interferon-gamma levels when the infection begins. The future perspective is to generate bacteriophages against C. difficile for targeted therapy
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