## 4 Discussion  
The human intestinal microbiota has a complex spectrum of bacteria, estimated to be nearly 1100 species [30]. Likewise, every bacterium influences different biological pathways and drug metabolism due to their enzymatic effects. Increasing evidence shows that understanding the gut microbiome can be a breakthrough discovery for the patient treatment responses, affecting the survival rates in various neoplasms, adenomas, and cancers. The most frequent genus among the microbiome samples that we analyzed with our algorithm, _Bacteroides_, is already published in several studies that have a significant association with human CRC development [31]. This genus has been identified as an important feature from the model we used for comparison of resistant/non-resistant, in favor of the resistant group (\(p\) = 0.003, mean abundance 28). The enterotoxigenic _Bacteroides_ bacteria has a critical impact on the CRC development and proliferation considering their biofilm production for colonization that results in a series of inflammatory reactions that encourages chronic intestinal inflammation and tissue damage [32]. Moreover, the functional studies done on mice verified that the presence of enterotoxigenic _Bacteroides_ could directly promote intestinal carcinogenesis [33]. Additionally, the _Alistipes_ bacteria, which is significantly increased in the non-resistant group, is living in symbiosis with the _Bacteroides_ species because both are resistant to vancomycin, kanamycin, and colistin. These two species have similar pathways for amino acid fermentation supporting colon inflammation and adenoma development [5; 34]. \begin{table}
\begin{tabular}{c c c} \hline \hline
**Genus** & **Our Study Results** & \(p\)**-Values** \\ \hline _Barnesiella_ & Increase in non-resistant & 0.0069 \\ \hline _Alistipes_ & Increase in non-resistant & 0.0017 \\ \hline _Intestinibacter_ & Increase in non-resistant & 0.038 \\ \hline _Flavorinfractor_ & Decrease in non-resistant & 0.04 \\ \hline _Akkermansia_ & Increase in non-resistant & 0.041 \\ \hline _[Ruminococcus] torques group_ & Decrease in non-resistant & 0.043 \\ \hline _Streptococcus_ & Decrease in non-resistant & 0.021 \\ \hline _Butyricimonas_ & Increase in non-resistant & 0.022 \\ \hline _Eggerthella_ & Decrease in non-resistant & 0.024 \\ \hline _Escherichia-Shigella_ & Decrease in non-resistant & 0.026 \\ \hline _Annaercorazacane_ & Increase in non-resistant & 0.027 \\ \hline _Negativibacillus_ & Increase in non-resistant & 0.031 \\ \hline _Leuconostoc_ & Decrease in non-resistant & 0.034 \\ \hline _Ruminococcus_ & Decrease in non-resistant & 0.0017 \\ \hline _Oscillospiraceae_ & Increase in non-resistant & 0.0034 \\ \hline _Bacteroides_ & Decrease in non-resistant & 0.0087 \\ \hline _Clostridium sensu stricto 1_ & Increase in non-resistant & 0.015 \\ \hline \hline \end{tabular}
\end{table} 
Table 6: Bacterial abundance tendency in the non-resistant samples. Additionally, the most compelling genus with the highest \(p\)-value was _Ruminococcus_. This genus is in favor of the non-resistant patients. This study highlights the fundamental role of gut microbiota in cancer development and progression along with chemotherapy outcomes. It is understandable that the _Barnesiella_ species shows high correlation with the non-resistant group since its metabolites indicate infiltration of interferon-\(\gamma\)-producing \(\gamma\)\(\delta\)T cells in cancer tissues. Furthermore, it is shown that this species can interfere with the impact of the anticancer immunomododulatory agents and prevent cancer treatment [15]. The resistance mechanism bacterial function table we composed from our study is summarized and discussed in Table 7.