Colon cancer screening: Where have we come from and where do we go?

Chorost, Mitchell I.; Datta, Rajiv; Santiago, Rosemary C.; Lee, Byrne; Bollman, Jyoti; Leitman, I. Michael; Ghosh, Bimal C.

doi:10.1002/jso.20008

Cited by 14 publications

(11 citation statements)

References 36 publications

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“…Although the mortality rate is decreasing as the result of improved detection, the incidence of colon cancer continues to increase. 1 Colon cancer has been widely acknowledged to progress from the adenomatous polyp to carcinoma through an accumulation of genetic mutations in molecules, such as K-ras and APC 1-3 ; however, not all colon cancers follow this delineated mutation pathway. 4 Thus, the molecular mechanisms involved in the development and progression of colon cancer are still incompletely understood.…”

mentioning

confidence: 99%

RAGE Activation by S100P in Colon Cancer Stimulates Growth, Migration, and Cell Signaling Pathways

Fuentes¹,

Nigavekar²,

Arumugam³

et al. 2007

Diseases of the Colon &Amp; Rectum

139

134

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mentioning

confidence: 99%

RAGE Activation by S100P in Colon Cancer Stimulates Growth, Migration, and Cell Signaling Pathways

Fuentes¹,

Nigavekar²,

Arumugam³

et al. 2007

Diseases of the Colon &Amp; Rectum

139

134

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“…4 Diagnosis at an early stage of disease is associated with better prognosis and consequently several screening programs, based on different diagnostic techniques, have taken place worldwide with the aim of increasing early diagnosis of adenomas and colorectal cancer. 5 There are several suggestions that proximal colon cancer (adenocarcinoma of the caecum, ascending and transverse colon) and colon cancer distal to the splenic flexure represent the result of different carcinogenic pathways. 6 These findings are mainly based on the different microsatellite and chromosomal instability status of proximal and distal colon cancer.…”

mentioning

confidence: 99%

Search of plasma markers for colorectal cancer by matrix‐assisted laser desorption/ionization mass spectrometry

et al. 2004

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Looking at valid results obtained so far, we thought it of interest to apply the MALDI-MS approach to the study of plasma samples from patients with colon or rectum cancers and to compare the peptide patterns so obtained with those from healthy subjects, with the final aim of establishing some peptides useful as markers of the disease. For this preliminary study, plasma samples from nine healthy subjects, 10 patients affected by colon cancer (stage IV) and 11 patients with rectal cancer, randomly chosen, were analyzed. Interestingly, at first sight, clear differences were observed among the MALDI spectra of plasma samples from healthy subjects and colon and rectal cancer patients, as shown by spectra, typical of the three classes of subjects. However, in order to evaluate the real significance of these differences, some data elaborations were performed. Among the large number of peptides not detected in healthy subjects which are present in colon and rectal cancer patients, some of them are common between the two groups of cancer, whereas some others appear to be specific for colon cancer only. It should be emphasized that the species at m/z 1917, detected for both the sample sets in the case of the different spectra of plasma samples from rectal cancer patients shows a mean relative abundance higher than that observed in the case of colon cancer (21 š8 vs 7š 2, respectively). In conclusion, our data suggest that some ionic species detected by MALDI-MS in the plasma of patients affected by colorectal cancer could be of interest for a more complete molecular classification of the disease, and might provide new information for the development of clinical diagnostic and prognostic tools. Of course, these results represent only preliminary data on low molecular mass plasma peptides. They are, in our opinion, promising but further studies on a larger set of plasma samples and using different fractionation procedures are required, and work is in progress along these lines

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“…Colon cancer is one of the most prevalent tumors worldwide 39. Despite conventional therapies such as surgery, radiation, and chemotherapy, the overall survival rate for colon cancer has not significantly improved 40.…”

Section: Discussionmentioning

confidence: 99%

Niclosamide inhibition of STAT3 synergizes with erlotinib in human colon cancer

Shi¹,

Zheng²,

et al. 2017

OTT

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Niclosamide, an anthelmintic drug approved by the US Food and Drug Administration against cestodes, is used to treat tapeworm infection. In this study, we show that niclosamide can potentially inhibit signal transducer and activator of transcription 3 (STAT3) in colon cancer cell lines. Combined inhibition of epidermal growth factor receptor and STAT3 by erlotinib and niclosamide synergistically induces apoptosis and antiproliferation in colon cancer cell lines. Our findings suggest that erlotinib and niclosamide combination provides an effective therapeutic approach to improving the prognosis of colon cancer.

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Colon cancer screening: Where have we come from and where do we go?

Cited by 14 publications

References 36 publications

RAGE Activation by S100P in Colon Cancer Stimulates Growth, Migration, and Cell Signaling Pathways

RAGE Activation by S100P in Colon Cancer Stimulates Growth, Migration, and Cell Signaling Pathways

Search of plasma markers for colorectal cancer by matrix‐assisted laser desorption/ionization mass spectrometry

Niclosamide inhibition of STAT3 synergizes with erlotinib in human colon cancer

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