[18F]FPRGD2 PET/CT imaging of integrin αvβ3 levels in patients with locally advanced rectal carcinoma
Nadia WithofsPhilippe MartiniveJean VanderickNoëlla BlétardI ScagnolFrédéric MiévisFabrice GiacomelliPhilippe CouckePhilippe DelvenneDidier CataldoSanjiv S. GambhirRoland Hustinx
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Although somatic mutations in colorectal cancer are well characterized, little is known about the accumulation of cancer mutations in the normal colon before cancer. Here, we have developed and applied an ultrasensitive, single-molecule mutational test based on CRISPR-DS technology, which enables mutation detection at extremely low frequency (<0.001) in normal colon from patients with and without colorectal cancer. This testing platform revealed that normal colon from patients with and without colorectal cancer carries mutations in common colorectal cancer genes, but these mutations are more abundant in patients with cancer. Oncogenic KRAS mutations were observed in the normal colon of about one third of patients with colorectal cancer but in none of the patients without colorectal cancer. Patients with colorectal cancer also carried more TP53 mutations than patients without cancer and these mutations were more pathogenic and formed larger clones, especially in patients with early-onset colorectal cancer. Most mutations in the normal colon were different from the driver mutations in tumors, suggesting that the occurrence of independent clones with pathogenic KRAS and TP53 mutations is a common event in the colon of individuals who develop colorectal cancer. These results indicate that somatic evolution contributes to clonal expansions in the normal colon and that this process is enhanced in individuals with cancer, particularly in those with early-onset colorectal cancer.
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Hyperplastic Polyp
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Objective To investigate the expression and significance of δ-catenin in colorectal cancer(CRC),and explore the correlation between8-catenin expression and cell proliferation in colorectal cancer.Methods The expressions of 8-catenin and Ki-67 in 120 specimens of colorectal cancer were detected by immunohistochemistry in tissue microassay.The expression of 8-catenin was also determined in 30 paired colorectal cancer and normal colorectum by Western blot.Results Overexpression of 8-catenin was detected in 65.83%(79/120) of the 120 human colorectal cancer tissues,which was significantly higher than that in normal colorectum.The positive expression of 8-catenin was higher in advanced TNM stages(Ⅲ+ Ⅳ)of colorectal cancer(78.05%,32/41),compared to lower stages(Ⅰ+Ⅱ)(59.49%,47/79)(x~2=4.132,P= 0.042).The positive expression of 8-catenin was higher in poor differentiated colorectal cancer(82.14%,23/28),compared to well/moderate differentiated colorectal cancer(60.87%,56/92)(x~2=4-319,P = 0.038).The positive expression of 8-catenin was higher in colorectal cancer with lymph node metastasis(77.05%,47/61),compared to colorectal cancer without lymph node metastasis(54.24%,32/59)(x~2=6-939,P = 0.008).In addition,we also found that the overexpression of 8-catenin was positively correlated with proliferation of colorectal cancer which marked by Ki-67 staining in colorectal cancer(r=0.334,P 0.01).Conclusion 8-catenin overexpression might be involved in the initiation and progression of colorectal cancer.
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Objective To observe the expression of Claudin-2 in colorectal cancer tissues and to explore its relationship with the development and progression of colorectal cancer.Methods Immunohistochemical staining(SP method) was used to detect the expression of Claudin-2 in colorectal cancer tissue,adjacent normal tissue of colorectal cancer and normal tissue and investigate the correlation between expression of Claudin-2 in colorectal cancer tissue and the genesis and development of colorectal cancer.Results The expression of Claudin-2 in colorectal cancer tissues was significantly higher than those in the adjacent tissues of colorectal cancer and normal colorectal tissue(P0.05);besides,the expression of Claudin-2 in the colorectal cancer tissue was correlated with degree of differentiation,Dukes stages of colorectal cancer(P0.05).Conclusion The expression of Claudin-2 in colorectal cancer increases significantly in both positive rate and intensity compared with that in normal tissue.The higher expression of Claudin-2 may play an important role in the genesis and development of colorectal cancer.
Claudin
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Objective To detect the expression and role of PTTG mRNA in human colorectal cancer.Methods The expression of PTTG mRNA was evaluated in 12 normal colorectal tissues,20 colorectal adenoma tissues and 44 colorectal cancer tissues by RT-PCR.Results The expression of PTTG mRNA in colorectal cancer was significantly higher than that in colorectal adenoma and normal colorectal tissues.The PTTG mRNA expression in the Dukes C,D colorectal cancer was higher than that in the Dukes A,B cancer(P0.05).The expression in the colorectal cancer with lymph node metastasis was higher than that in the cancer without lymph node metastasis(P0.05).Conclusion The expression of PTTG mRNA increases in colorectal cancer,and is related with cell differentiation and metastasis.The abnormal expression of PTTG probably participates in genesis and development of colorectal cancers.
Colorectal adenoma
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<div>Abstract<p>Although somatic mutations in colorectal cancer are well characterized, little is known about the accumulation of cancer mutations in the normal colon before cancer. Here, we have developed and applied an ultrasensitive, single-molecule mutational test based on CRISPR-DS technology, which enables mutation detection at extremely low frequency (<0.001) in normal colon from patients with and without colorectal cancer. This testing platform revealed that normal colon from patients with and without colorectal cancer carries mutations in common colorectal cancer genes, but these mutations are more abundant in patients with cancer. Oncogenic <i>KRAS</i> mutations were observed in the normal colon of about one third of patients with colorectal cancer but in none of the patients without colorectal cancer. Patients with colorectal cancer also carried more <i>TP53</i> mutations than patients without cancer and these mutations were more pathogenic and formed larger clones, especially in patients with early-onset colorectal cancer. Most mutations in the normal colon were different from the driver mutations in tumors, suggesting that the occurrence of independent clones with pathogenic <i>KRAS</i> and <i>TP53</i> mutations is a common event in the colon of individuals who develop colorectal cancer. These results indicate that somatic evolution contributes to clonal expansions in the normal colon and that this process is enhanced in individuals with cancer, particularly in those with early-onset colorectal cancer.</p>Significance:<p>This work suggests prevalent somatic evolution in the normal colon of patients with colorectal cancer, highlighting the potential of using ultrasensitive gene sequencing to predict disease risk.</p></div>
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Abstract Background: Solute carrier family 25 member 24 (SLC25A24) is a member of the mitochondrial solute vector (MSC) protein superfamily. More and more evidence suggested that SLC family members play an extremely important role in cancers. However, the biological function of SLC25A24 in colorectal cancer has not been reported. Methods: TCGA, GEO, UALCAN, Sangebox3.0 and TIDE databases were used to analyze SLC25A24 in colorectal cancer. The expression of SLC25A24 in 83 pairs of colorectal cancer tissues was detected by immunohistochemistry. qRT-PCR, Western blotting and apoptosis assays were used to explore the biological function of SLC25A24 in colorectal cancer. Results: Through analysis of multiple databases, we found that SLC25A24 expression was higher in colorectal cancer than in adjacent normal tissues, and higher expression of SLC25A24 had a better prognosis. This was verified by clinical case analysis. In addition, based on multiple algorithms of immune infiltration, we found that SLC25A24 was significantly associated with immune infiltration in colorectal cancer. SLC25A24 was significantly associated with clinicopathological features in 83 patients with colorectal cancer. Importantly, SLC25A24 knockdown significantly promoted the apoptosis ability of colorectal cancer cells. In addition, we also found that lower expression of SLC25A24 was associated with poor prognosis and low immunotherapy sensitivity in patients with colorectal cancer. Therefore, SLC25A24 might be a biomarker for the treatment of colorectal cancer. Conclusion: In summary, we found that SLC25A24 was higher expression in colorectal cancer than in adjacent normal tissues, and higher expression of SLC25A24 had a better prognosis. Importantly, we found that SLC25A24 inhibited apoptosis of colorectal cancer cells. In addition, SLC25A24 was associated with immune infiltration of colorectal cancer. Patients with lower expression of SLC25A24 were more prone to immune escape, while patients with higher expression of SLC25A24 were more conducive to immunotherapy. These results suggested that SLC25A24 might be a potential therapeutic target for patients with colorectal cancer.
Infiltration (HVAC)
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Abstract Colorectal cancer is a crucial health-threatening problem. In recent years, the treatment of colorectal cancer has continued improved and update. But the prognosis of advanced colorectal cancer is still disappointing. Galecitn-9 is a member of the galectin family which has been verified to have multiple biological regulatory functions. Our team has been studying the clinical application of the galectin family in gastric and colorectal cancer. However, we do not yet unveil the correlation between Galecitn-9 and colorectal cancer. This study aimed to elucidate the expression of Galecitn-9 in colorectal cancer and the effect of Galecitn-9 on colorectal cancer proliferation, migration and invasion.
Clinical Significance
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Objective To establish colorectal cancer animal model and provide experimental basis for human colorectal cancer research.Method Using dimethylhydrazine to induce Wistar rat colorectal cancer and killed them at 12,18,and 24 weeks after treated,the colorectal mucosa pathological changes of different experiment and control groups were observed.Results During the carcinogensis process,the light,medium and heavy atypical hyperplasia were observed.At 12 weeks,none cancer was observed in experimental groups.At 18 weeks,the incidence of tumor and colorectal cancer were 60% and 50% respectively.At 24 weeks,the incidence of tumor and colorectal cancer were 100% and 80% respectively.Conclusions The incidence of rat colon cancer model induced by dimethylhydrazine were high,the development of which was similar to the human colorectal cancer.The model can be used for the experimental study of human colorectal cancer.
1,2-Dimethylhydrazine
Animal model
Aberrant crypt foci
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