Yanyan Xu1, Hongliang Sun1, Queenie Chan2, and Wu Wang1
1Radiology, China-Japan Friendship Hospital, Beijing, China, 2Philips Healthcare, Hongkong, China
Synopsis
KRAS mutations are well known
as predictive markers of resistance to epidermal growth factor
receptor-targeted antibodies in rectal cancers. Approximately 30%-40% colorectal
cancers are observed with KRAS mutation,
and rectal cancer accounts for 30%-35% among CRC. The pre-operative
neoadjuvant therapy including anti-EGFR chemotherapy demonstrated robust value
is the current trend in the management of rectal cancer. Therefore, it is
important to select suitable patients who would benefit from the aggressive
multimodality approaches and tailor individual treatment to better combat
disease. Currently, few data are available regarding the potential relationship
between MRI characteristics and genetic biomarkers.
Synopsis
KRAS mutations are well known as predictive markers
of resistance to epidermal growth factor receptor-targeted antibodies in rectal
cancers. Approximately 30%-40% colorectal cancers are observed with KRAS mutation, and rectal
cancer accounts for 30%-35% among CRC 1-3. The pre-operative neoadjuvant
therapy including anti-EGFR chemotherapy demonstrated robust value is the
current trend in the management of rectal cancer. Therefore, it is important to
select suitable patients who would benefit from the aggressive multimodality
approaches and tailor individual treatment to better combat disease. Currently,
few data are available regarding the potential relationship between MRI characteristics
and genetic biomarkers.Purpose
To
evaluate the MRI features and texture analysis of different KRAS mutation
status in rectal cancer.Material and Methods
This
is an institutional review board approved retrospective case-control study. Totally,
158 patients(mean age,[60.66±13.38] years;
range 26-87 years)including106 men and 52 women with
pathologically proved rectal cancers and preoperative pelvic MRI examinations
were enrolled. Patients were stratified into two groups: wild-type and mutant
according to genomic DNA extraction and analysis. MRI features of rectal
cancers (including histogram-based texture features onT2 weighted images) and
relevant clinical characteristics were statistically evaluated to identify the
differences between wild-type and mutant groups. The independent samples t test or Mann-Whitney U test were used
for continuous variables. The differences of the remaining categorical other polytomous
variables were analyzed using the chi-square test or Fisher exact test. A receiver
operating characteristic (ROC) curve analysis was performed to evaluate the discriminatory
power of MRI features in predicting tumor KRAS status. The area under the
ROC curve (AUC) and the optimal cut-off values were calculated, meanwhile
sensitivity, specificity, and accuracy rate were determined. The
interobserver agreement for continuous variables was evaluated using the interclass
correlation coefficient (ICC), and for categorical
varivables using Kappa of
agreement. P<0.05 was considered to
indicate a statistically significant difference.Results
Relatively good to excellent interobserver agreement was obtained for continuous
and categorical variables. Statistically
difference of tumor shape distribution was observed between wild-type and
mutant group (=7.591, p=0.022). Higher T stage was
observed more frequently in the mutant group than that of wild-type group (=7.086, p=0.029). Higher
ADC values were observed in KRAS mutant group than those in wild-type group (t=-2.708,
p=0.008). Textural parameters (Mean,
Variance, Kurtosis, Entropy) value derived from T2-weighted
images showed significant differences in rectal cancer with different KRAS
status (p=0.008, p=0.046, p=0.031, p=0.001,
respectively). The AUC values for MRI
features including textural parameters ranged from 0.595 to 0.682.Conclusion
The MRI features
of rectal cancer including
histogram-based texture features showed potential value in identifying KRAS status, however, more effort need
to verify our results.Acknowledgements
No acknowledgement found.References
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al. Mutations of KRAS and
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AR, Cunningham D, et al. Kirsten
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