colorectal tumours
Recently Published Documents


TOTAL DOCUMENTS

249
(FIVE YEARS 19)

H-INDEX

35
(FIVE YEARS 2)

2022 ◽  
Vol 9 (1) ◽  
pp. 22-28
Author(s):  
Veysel Barış Turhan ◽  
Mutlu Şahin ◽  
Halil Fatih Gök ◽  
Doğan Öztürk ◽  
Bülent Öztürk ◽  
...  

Objective: Emergency surgical interventions due to colorectal cancer (CRC) obstruction are risk factors for poor prognosis. This study aims to compare emergency and elective surgeries for colorectal tumours performed in a single center. Material and Methods: CRC patients operated on between November 2014 and November 2019 were included in the study. Patients were divided into two groups; Patients operated under elective conditions, and patients operated under the emergency diagnosis of ileus or acute abdomen. Results: A total of 103 CRC patients were included in the study. Forty-five (43.7%) were operated in emergency situations, and 58 (56.3%) electively. 45.6% of the emergency cases were found to be Stage 3B and 4 (p=0.009). Bleeding and constipation were more common in elective cases, whereas in emergency cases, applications related to ileus and perforation were quite frequent (p<0.001). It was found that 62.3% of the tumors in emergency cases were seen in sigmoid and rectosigmoid regions (p=0.015). There was no anastomosis in 60.0% of emergency cases (p<0.001). Conclusion: In the hospital area where the study was applied, compared to other countries, more patients with CRC underwent emergency surgery for intestinal obstruction. Therefore, necessary measures must be taken to prevent further increases in these rates.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tsutomu Yoshihara ◽  
Mitomu Kioi ◽  
Junichi Baba ◽  
Haruki Usuda ◽  
Takaomi Kessoku ◽  
...  

AbstractFusobacterium nucleatum is associated with the progression of colorectal cancer. Thus, the possibility of preventing colorectal cancer or its progression by targeting F. nucleatum has been explored. As F. nucleatum is associated with periodontitis, we analysed whether treating periodontitis could influence F. nucleatum abundance in the colon. Patients with colorectal tumours who underwent colonoscopy were recruited. Patients diagnosed with periodontitis by a dentist were treated for approximately 3 months. Endoscopic resection of colorectal tumours was performed after periodontitis treatment, and resected tumours were pathologically classified as high-(HGD) or low-grade dysplasia (LGD). Saliva and stool samples were collected before and after the treatment. Of the 58 patients with colorectal tumours, 31 were included in the study, 16 showed improvement in periodontitis, and 11 showed no improvement. Stool F. nucleatum levels before treatment were significantly lower in the LGD group than in the HGD group. A significant decrease in faecal F. nucleatum levels was observed in patients who underwent successful treatment but not in those whose treatment failed. Salivary F. nucleatum levels were not altered in patients despite periodontal treatment. Thus, successful periodontitis treatment reduces stool F. nucleatum levels and may aid research on periodontitis and suppression of colorectal cancer development.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shintaro Okumura ◽  
Yusuke Konishi ◽  
Megumi Narukawa ◽  
Yuki Sugiura ◽  
Shin Yoshimoto ◽  
...  

AbstractEmerging evidence is revealing that alterations in gut microbiota are associated with colorectal cancer (CRC). However, very little is currently known about whether and how gut microbiota alterations are causally associated with CRC development. Here we show that 12 faecal bacterial taxa are enriched in CRC patients in two independent cohort studies. Among them, 2 Porphyromonas species are capable of inducing cellular senescence, an oncogenic stress response, through the secretion of the bacterial metabolite, butyrate. Notably, the invasion of these bacteria is observed in the CRC tissues, coinciding with the elevation of butyrate levels and signs of senescence-associated inflammatory phenotypes. Moreover, although the administration of these bacteria into ApcΔ14/+ mice accelerate the onset of colorectal tumours, this is not the case when bacterial butyrate-synthesis genes are disrupted. These results suggest a causal relationship between Porphyromonas species overgrowth and colorectal tumourigenesis which may be due to butyrate-induced senescence.


2021 ◽  
Author(s):  
Guia Cerretelli ◽  
Ying Zhou ◽  
Mike F. Müller ◽  
David J. Adams ◽  
Mark J. Arends

Author(s):  
Sapam Chingkhei Lakpa ◽  
R. Vinoth Kumar ◽  
Mary Lilly

Colorectal cancer is the third most common cancer in men and the second in women globally. There is a marked variation in the incidence of colorectal carcinoma worldwide, where western countries having high rate compared to others. p53 tumour suppressor gene is one of the most intensively studied tumour markers in the colorectal tumours. Two markers were used, p53 (oncoprotein p53) and CEA (carcinoembryonic antigen) in the study. The 102 cases of paraffin-embedded samples were processed for the immunohistochemistry examination. After the analysis of the selected patients regarding the antibodies distribution, statistical analysis was performed. The current study showed that there was a statistically significant correlation existing between p53 and CEA in each tumour type irrespective of its histological grades. The immunohistochemistry (IHC) was performed on 4-µm thick sections from 10% formalin- fixed paraffin-embedded tissue blocks.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Roza H. Ali Masalmeh ◽  
Francesca Taglini ◽  
Cristina Rubio-Ramon ◽  
Kamila I. Musialik ◽  
Jonathan Higham ◽  
...  

AbstractThe aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.


2021 ◽  
Author(s):  
Bence Paul ◽  
Kai Kysenius ◽  
James B. Hilton ◽  
Michael M W Jones ◽  
Robert W. Hutchinson ◽  
...  

Tumours are abnormal growths of cells that reproduce by redirecting essential nutrients and resources from surrounding tissue. Changes to cell metabolism that trigger the growth of tumours are reflected in...


Biomolecules ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1365 ◽  
Author(s):  
Laura Torrente ◽  
Gunjit Maan ◽  
Asma Oumkaltoum Rezig ◽  
Jean Quinn ◽  
Angus Jackson ◽  
...  

Aberrant hyperactivation of nuclear factor erythroid 2 (NF-E2) p45-related factor 2 (NRF2) is a common event in many tumour types and associates with resistance to therapy and poor patient prognosis; however, its relevance in colorectal tumours is not well-established. Measuring the expression of surrogate genes for NRF2 activity in silico, in combination with validation in patients’ samples, we show that the NRF2 pathway is upregulated in colorectal tumours and that high levels of nuclear NRF2 correlate with a poor patient prognosis. These results highlight the need to overcome the protection provided by NRF2 and present an opportunity to selectively kill cancer cells with hyperactive NRF2. Exploiting the CRISPR/Cas9 technology, we generated colorectal cancer cell lines with hyperactive NRF2 and used them to perform a drug screen. We identified AT9283, an Aurora kinase inhibitor, for its selectivity towards killing cancer cells with hyperactive NRF2 as a consequence to either genetic or pharmacological activation. Our results show that hyperactivation of NRF2 in colorectal cancer cells might present a vulnerability that could potentially be therapeutically exploited by using the Aurora kinase inhibitor AT9283.


Sign in / Sign up

Export Citation Format

Share Document