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--- worked_example_perturbation_effect [2021/01/26 16:10] – mpena
+++ worked_example_perturbation_effect [2024/02/27 13:31] (current) – [References] krian
@@ Line 81: / Line 81: @@
 Focusing on the //Ras signaling pathway// (hsa04014), three circuits appear as inhibited by the knock-down of c-Raf:
   * The ELK-1 circuit, which is generally activated in pancreatic cancer [3].
-  * The ETS-1 circuit. The ETS Proto-Oncogene family (//ETS//) has been linked to pancreatic cancer progression and, specifically, //ETS-1// has been described as potential targets reducing angiogenesis and progression in pancreatic cancer [4, 5].
+  * The ETS-1 circuit. The ETS Proto-Oncogene family (//ETS//) has been linked to pancreatic cancer progression and, specifically, //ETS-1// has been described as potential target reducing angiogenesis and progression in pancreatic cancer [4, 5].
   * The PLA2G4B circuit. //PLA2G4B// is highly expressed in the pancreas and this gene has been described to modulate the sensitivity of pancreatic cancer cells to chemoradiation treatment [6].
-Among the most represented effector genes affected by the knock-down simulation, we want to highlight the roles of //PLA2G4B//, //MAPK1//, //CDKN1A//, //ELK1//, //PRKCA//, and //CAMK2A// in processes such as signal transduction, calcium metabolism, and cell cycle regulation. These mechanisms have been highly related to cell proliferation and cancer progression, therefore inactivating the circuits that trigger these effectors would result in a potential reduction of cancer prognosis, consistent with the results observed in //Blasco et al.// [1].
+Among the most represented effector genes affected by the knock-down simulation, we want to highlight the roles of //PLA2G4B//, //MAPK1//, //CDKN1A//, //ELK1//, //PRKCA//, and //CAMK2A// in processes such as signal transduction, calcium metabolism, and cell cycle regulation. These mechanisms have been highly related to cell proliferation and cancer progression, therefore inactivating the circuits that trigger these effectors would result in a potential reduction in cancer progression, which is consistent with the results observed in //Blasco et al.// [1].
 ==== References ====
@@ Line 100: / Line 100: @@
 [6]    D. Wei et al., “Inhibition of protein phosphatase 2A radiosensitizes pancreatic cancers by modulating CDC25C/CDK1 and homologous recombination repair,” Clin. Cancer Res. Off. J. Am. Assoc. Cancer Res., vol. 19, no. 16, pp. 4422–4432, Aug. 2013, doi: 10.1158/1078-0432.CCR-13-0788.
+/* Visualize the results. For further information in the interpretation of the results, see [[Perturbation effect results|Perturbation effect results]].*/
-  /* Visualize the results. For further information in the interpretation of the results, see [[Perturbation effect results|Perturbation effect results]].*/