198P Use of chemotherapy and mismatch repair deficiency testing in resected stage II colon cancer

2016 ◽  
Vol 27 (suppl_9) ◽  
Author(s):  
L. Au ◽  
M. Grant ◽  
A. Haydon ◽  
K. Oliva ◽  
S. Wilkins ◽  
...  
2016 ◽  
Vol 27 ◽  
pp. ix62
Author(s):  
L. Au ◽  
M. Grant ◽  
A. Haydon ◽  
K. Oliva ◽  
S. Wilkins ◽  
...  

2012 ◽  
Vol 23 ◽  
pp. xi151
Author(s):  
Y.S. Hong ◽  
J.E. Kim ◽  
K. Kim ◽  
J.-L. Lee ◽  
S.-J. Jang ◽  
...  

Author(s):  
Nancy N. Baxter ◽  
Erin B. Kennedy ◽  
Emily Bergsland ◽  
Jordan Berlin ◽  
Thomas J. George ◽  
...  

PURPOSE To develop recommendations for adjuvant therapy for patients with resected stage II colon cancer. METHODS ASCO convened an Expert Panel to conduct a systematic review of relevant studies and develop recommendations for clinical practice. RESULTS Twenty-one observational studies and six randomized controlled trials met the systematic review inclusion criteria. RECOMMENDATIONS Adjuvant chemotherapy (ACT) is not routinely recommended for patients with stage II colon cancer who are not in a high-risk subgroup. Patients with T4 tumors are at higher risk of recurrence and should be offered ACT, whereas patients with other high-risk factors, including sampling of fewer than 12 lymph nodes in the surgical specimen, perineural or lymphatic invasion, poorly or undifferentiated tumor grade, intestinal obstruction, tumor perforation, or grade BD3 tumor budding, may be offered ACT. The addition of oxaliplatin to fluoropyrimidine-based ACT is not routinely recommended, but may be offered as a result of shared decision making. Patients with mismatch repair deficiency/microsatellite instability tumors should not be routinely offered ACT; if the combination of mismatch repair deficiency/microsatellite instability and high-risk factors results in a decision to offer ACT, oxaliplatin-containing chemotherapy is recommended. Duration of oxaliplatin-containing chemotherapy is also addressed, with recommendations for 3 or 6 months of treatment with capecitabine and oxaliplatin or fluorouracil, leucovorin, and oxaliplatin, with decision making informed by key evidence of 5-year disease-free survival in each treatment subgroup and the rate of adverse events, including peripheral neuropathy. Additional information is available at www.asco.org/gastrointestinal-cancer-guidelines .


Author(s):  
Sebastian Dwertmann Rico ◽  
Doris Höflmayer ◽  
Franziska Büscheck ◽  
David Dum ◽  
Andreas M. Luebke ◽  
...  

AbstractMucin 5AC (MUC5AC) is a secreted gel-forming mucin expressed by several epithelia. In the colon, MUC5AC is expressed in scattered normal epithelial cells but can be abundant in colorectal cancers. To clarify the relationship of MUC5AC expression with parameters of tumor aggressiveness and mismatch repair deficiency (dMMR) in colorectal cancer, a tissue microarray containing 1812 colorectal cancers was analyzed by immunohistochemistry. MUC5AC expression was found in 261 (15.7%) of 1,667 analyzable colorectal cancers. MUC5AC expression strongly depended on the tumor location and gradually decreased from proximal (27.4% of cecum cancers) to distal (10.6% of rectal cancers; p < 0.0001). MUC5AC expression was also strongly linked to dMMR. dMMR was found in 21.3% of 169 cancers with MUC5AC positivity but in only 4.6% of 1051 cancers without detectable MUC5AC expression (p < 0.0001). A multivariate analysis showed that dMMR status and tumor localization predicted MUC5AC expression independently (p < 0.0001 each). MUC5AC expression was unrelated to pT and pN status. This also applied to the subgroups of 1136 proficient MMR (pMMR) and of 84 dMMR cancers. The results of our study show a strong association of MUC5AC expression with proximal and dMMR colorectal cancers. However, MUC5AC expression is unrelated to colon cancer aggressiveness.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Brendan L. Hagerty ◽  
John G. Aversa ◽  
Dana A. Dominguez ◽  
Jeremy L. Davis ◽  
Jonathan M. Hernandez ◽  
...  

2018 ◽  
Vol 51 ◽  
pp. 71-75 ◽  
Author(s):  
Matthew Grant ◽  
Andrew Haydon ◽  
Lewis Au ◽  
Simon Wilkins ◽  
Karen Oliva ◽  
...  

2019 ◽  
Vol 121 (2) ◽  
pp. 392-401 ◽  
Author(s):  
I. Gkekas ◽  
J. Novotny ◽  
P. Fabian ◽  
R. Nemecek ◽  
R. Palmqvist ◽  
...  

2019 ◽  
Vol 45 (10) ◽  
pp. 1854-1861 ◽  
Author(s):  
Ioannis Gkekas ◽  
Jan Novotny ◽  
Pavel Fabian ◽  
Radim Nemecek ◽  
Richard Palmqvist ◽  
...  

2011 ◽  
Vol 29 (23) ◽  
pp. 3146-3152 ◽  
Author(s):  
Donna Niedzwiecki ◽  
Monica M. Bertagnolli ◽  
Robert S. Warren ◽  
Carolyn C. Compton ◽  
Nancy E. Kemeny ◽  
...  

Purpose We conducted a randomized trial comparing adjuvant treatment with edrecolomab versus observation in patients with resected, low-risk, stage II colon cancer. This study also prospectively studied patient- and tumor-specific markers of treatment outcome. Patients and Methods After surgical resection, patients with stage II colon cancer were randomly assigned to either five infusions of edrecolomab at 28-day intervals or observation without adjuvant therapy. Results Final accrual included 1,738 patients; 865 patients received edrecolomab, and 873 patients were observed without adjuvant treatment. Median follow-up time was 7.9 years. There were no significant outcome differences between study arms (overall survival [OS], P = .71; disease-free survival, P = .64). The combined 5-year all-cause OS was 0.86 (95% CI, 0.84 to 0.88), and the combined 5-year disease-specific OS was 0.93 (95% CI, 0.91 to 0.94). The relationships between demographic and histopathologic factors and survival differed for all-cause and disease-specific survival outcomes, but no combined prognostic factor model was found to adequately classify patients at higher risk of recurrence or death as a result of colon cancer. Conclusion Edrecolomab did not prolong survival. Consequently, this large study with a long duration of follow-up provided unique data concerning the natural history of resected stage II colon cancer. Prognostic factors identified in previous retrospective and pooled analyses were associated with survival outcomes in this stage II patient cohort. Results from ongoing molecular marker studies may enhance our ability to determine the risk profile of these patients.


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