KRAS is one of the most challenging goals in cancer. Although found over 60 years, cancer caused by KRAS mutations is common and fatal, and researchers are working hard to find the target drugs that can overcome them.

 The researchers have successfully developed other personal targeted mutagenic cancer treatments such as EGFR and BRAF. However, KRAS is still a very difficult study. This study will be able to save millions of cancer patients worldwide with the KRAS mutation if a promising compound, PHT-7.3 KRAS, is available.

KRAS is a protein that regulates cell growth. When a mutation occurs, the signal path switch opens and the cell is not controlled and causes cancer. This mutation occurs in about 25% of human cancers, including more than 90% of pancreatic cancer, 35-45% of colorectal cancer, and about 25% of lung cancer. Currently, there is no effective cure for KRAS positive cancer. 

In this study, scientists focused on a protein called Cnksr1 (augmentation of the ligase 1 kinase inhibitor) in the co-event of the KRAS mutation. The membrane membrane mutant KRAS floats mounted on the carrier and activates. Studies have shown that inhibition of Cnksr1 protein can prevent the growth of lung and colon cancer cells, the researchers have carried out molecular modeling and structural modification to develop PHT-7.3 drugs and have reduced KRAS-induced tumors in mouse models of non-small cell lung cancer . Importantly, this drug does not affect the function of healthy KRAS, suggesting that there are few potential side effects, so it is effective for cancer patients, effective for cancer, and almost free from side effects. Although there is no clear target drug for the clinical application of the KRAS gene, KRAS is a gene target that must be detected for whole genome detection. You can ask if there are any drugs that can be used to detect mutations and why they should be detected.

The Importance of KRAS Detection in Lung Cancer.

Previous studies have shown that EGFR (members of the ERBB family ERBB1) and KRAS are two members of the signaling pathway with EGFR on the anterior side and KRAS on the posterior side. Scientists believe that drugs that block EGFR can block cancer progression in KRAS, but EGFR generation, such as the target drug, erlotinib, and gefitinib, do not have that effect.

The Importance of KRAS Detection in Colorectal Cancer

This study confirms that the EGFR monoclonal antibody does not directly detect KRAS mutations in cancer patients, as drugs are effective targets for KRAS mutations in colorectal cancer patients, but in patients with colorectal cancer for KRAS mutations, but Cetuximab is used Do not recommend Infliximab and panitumumab. If KRAS gene test results are wild type, chemotherapy combined with cetuximab has better therapeutic effect than chemotherapy monotherapy.

VOLFI Phase II trial, mFOLFOXIRI should be detected in patients with metastatic colorectal cancer (fluorouracil + leucovorin + oxycarbital, irinotecan) EGFR inhibitor plus panitumumab, these gene patients should be detected in the following cases: KRAS / NRAS / BRAF wild type and unresectable metastatic colorectal cancer patients tumor.

In the VOLFI study, randomly divided into either the panitumumab (N = 63) or the exclusive mFOLFOXIRI (N = 33) of the US mFOLFOXIRI at a ratio of 96: 1 in 2 wild-type RAS metastatic colorectal cancer patients. The joint panitumumab group was 85.7%, alone using mFOLFOXIRI 54.5% and more than 30% efficiency. Therefore, the KRAS gene is an important goal in inducing target therapy. Cancer patients who want accurate treatment should perform a full genetic test and maximize the survival rate to find a target drug with a target drug or other disease.