Colorectal Cancer, EGFR, T790M (c.2369C>T)

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Expand Collapse Colorectal Cancer  - General Description Colorectal Cancer (CRC) is cancer that initiates in the colon or rectum-the lower part of the digestive system in the body. During digestion, food moves through the stomach and small intestine into the colon. The colon absorbs water and nutrients from food, and stores waste matter (stool) that moves from the colon through the rectum before leaving the body.

Most CRC's and rectal cancers are adenocarcinomas, meaning that they originate in cells that make and release mucus and other fluids. CRC often begins as a growth called a polyp, which may form on the inner wall of the colon or rectum. Over time, some polyps become cancerous. This highlights the importance of colonoscopy screening to find and remove polyps before they become cancerous.

CRC is the fourth most common type of cancer diagnosed in the U.S. Deaths from CRC have decreased with the use of colonoscopies and fecal occult blood tests, which check for blood in the stool. Disparities in survival have been observed between African American and other populations. This may be due to factors such as access to colonoscopy screening, or to other factors not yet identified.

Because of its prevalence, scientists have studied CRC extensively, even creating models of how cancer develops using CRC as an example. There are also families with a very high incidence of CRC occurrence. When these families were studied, certain conditions that create instability in the whole genome were identified that predispose people to CRC. These include what is called the Chromosomal Instability pathway (CIN), as well as MicroSatellite Instability pathway (MSI). These can also occur as spontaneous (uninherited) conditions in some patients. Between 6-10% of CRC's are found to have MSI. Some CRC tumors have been found to have a lot of mutations, or as physicians call it, a "very high mutational load". Some also express a ligand called PD-L1.

These are now recognized features of some CRC's, and immunological treatments may be recommended in these cases. MGH has one of the most extensive Immuno-oncology clinical trials portfolios of any US hospital. Testing for features such as CIN, MSI, a high mutational burden, and the expression of PD-L1 can be conducted at the MGH genetics laboratory, as well as at other large academic centers. Genetic instability such as CIN or MSI lead to the activation of oncogenes such as KRAS, and the inactivation of tumor suppressors such as PTEN, both of which promote tumor growth.

Other genetic alterations in how the DNA in cells is organized have been found to contribute to CRC in families and individuals. These are called epigenetic changes. Normal DNA has methyl groups added in specific regions that regulate gene expression. When the genes that suppress growth-called tumor suppressors-are methylated abnormally, this prevents the production of tumor suppressor proteins important in controlling or stopping cell growth. When tumor suppressor genes are missing, unregulated growth occurs, contributing to the development of cancer. Some tumor suppressor proteins that are frequently inactivated in CRC are APC, TP53, or loss of one arm of chromosome 18 that contains a tumor suppressor.

The study of families with a high prevalence of CRC have lead scientists to discover genetic changes that contribute to the development of CRC in sporadic cases occurring in patients. Mutations in the genes encoding the following proteins have now been associated with subsets of CRC; ALK, AKT, APC, beta-catenin, BRCA1 and BRCA2, BRAF, EGFR, ERBB2 (HER2), ERBB3 (HER3), IDH2, KRAS, MET, NRAS, PI3K, ROS, PTEN, SMO,TP53, TRK 1, 2 and 3, and others that are still being identified. Information on these specific genes is available on this website if you select the gene you want to know more about.

Distinct familial syndromes of CRC such as Lynch syndrome have been studied in patients, leading to the identification of other mechanisms contributing to the development of cancer. Before a cell can divide into two daughter cells, DNA has to be replicated so both daughter cells will have a full complement of chromosomes. DNA replication requires an enzyme called DNA Polymerase. DNA Polymerase occasionally makes errors while it is replicating DNA. Cells therefore have a "proof-reading" process that detects mistakes when they occur during DNA replication. DNA Polymerase mistakes mean that incorrect nucleotides have been incorporated into the DNA, causing mutations. Mistakes in the DNA sequence are repaired in a process called mismatch repair (MMR).
MMR involves a complex of multiple proteins. In Lynch syndrome, one or more of the proteins involved in MMR is mutated, and the mistakes in the DNA do not get corrected. Mutations in MMR proteins are not only found in familial cases of CRC, but also in patients with sporadic (non-inherited) CRC. Defects in MMR also contribute to microsatellite instability (MIS), described above. The accumulation of these mutations can lead to cancer.

The importance of accurately replicating DNA following various types of mistakes or damage is reflected in the multiple pathways cells have for correcting or repairing broken DNA. Actual breaks in the DNA strands can happen due to exposure to radiation or other DNA damaging agents. In the case of the occurrence of breaks in DNA, there are also mechanisms for detecting these breaks. Double strand breaks (DSB's) in the DNA can be repaired via several mechanisms, including Non-Homologous End Joining (NHEJ) or Homologous Repair (HR). Many proteins are involved in DSB repair. Mutations in any of the many proteins involved in either of these repair pathways (see BRCA1 and BRCA2 genes) lead to damaged DNA, which results in DNA that is incorrectly replicated, causing mutations that contribute to the development of cancer. DNA repair machinery in the cell is important in keeping the genome stable and accurate.

Testing for the mutations and genomic conditions that contribute to the development or progression of CRC is available at MGH in the sophisticated CLIA certified genomic testing lab, and in other large Centers and some private testing companies used by physicians. Validated treatments, Immune therpies, as well as clinical trials investigating improved targeted and immunologic therapies are available to patients at MGH.

NIH/NCI Cancer Website www.cancer.gov 2017

Colorectal Cancer (CRC) is cancer that initiates in the colon or rectum-the lower part of the digestive system in the body. During digestion, food moves through the stomach and small intestine into the colon. The colon absorbs water and nutrients from food, and stores waste matter (stool) that moves from the colon through the rectum before leaving the body.

Most CRC's and rectal cancers are adenocarcinomas, meaning that they originate in cells that make and release mucus and other fluids. CRC often begins as a growth called a polyp, which may form on the inner wall of the colon or rectum. Over time, some polyps become cancerous. This highlights the importance of colonoscopy screening to find and remove polyps before they become cancerous.

CRC is the fourth most common type of cancer diagnosed in the U.S. Deaths from CRC have decreased with the use of colonoscopies and fecal occult blood tests, which check for blood in the stool. Disparities in survival have been observed between African American and other populations. This may be due to factors such as access to colonoscopy screening, or to other factors not yet identified.

Because of its prevalence, scientists have studied CRC extensively, even creating models of how cancer develops using CRC as an example. There are also families with a very high incidence of CRC occurrence. When these families were studied, certain conditions that create instability in the whole genome were identified that predispose people to CRC. These include what is called the Chromosomal Instability pathway (CIN), as well as MicroSatellite Instability pathway (MSI). These can also occur as spontaneous (uninherited) conditions in some patients. Between 6-10% of CRC's are found to have MSI. Some CRC tumors have been found to have a lot of mutations, or as physicians call it, a "very high mutational load". Some also express a ligand called PD-L1.

These are now recognized features of some CRC's, and immunological treatments may be recommended in these cases. MGH has one of the most extensive Immuno-oncology clinical trials portfolios of any US hospital. Testing for features such as CIN, MSI, a high mutational burden, and the expression of PD-L1 can be conducted at the MGH genetics laboratory, as well as at other large academic centers. Genetic instability such as CIN or MSI lead to the activation of oncogenes such as KRAS, and the inactivation of tumor suppressors such as PTEN, both of which promote tumor growth.

Other genetic alterations in how the DNA in cells is organized have been found to contribute to CRC in families and individuals. These are called epigenetic changes. Normal DNA has methyl groups added in specific regions that regulate gene expression. When the genes that suppress growth-called tumor suppressors-are methylated abnormally, this prevents the production of tumor suppressor proteins important in controlling or stopping cell growth. When tumor suppressor genes are missing, unregulated growth occurs, contributing to the development of cancer. Some tumor suppressor proteins that are frequently inactivated in CRC are APC, TP53, or loss of one arm of chromosome 18 that contains a tumor suppressor.

The study of families with a high prevalence of CRC have lead scientists to discover genetic changes that contribute to the development of CRC in sporadic cases occurring in patients. Mutations in the genes encoding the following proteins have now been associated with subsets of CRC; ALK, AKT, APC, beta-catenin, BRCA1 and BRCA2, BRAF, EGFR, ERBB2 (HER2), ERBB3 (HER3), IDH2, KRAS, MET, NRAS, PI3K, ROS, PTEN, SMO,TP53, TRK 1, 2 and 3, and others that are still being identified. Information on these specific genes is available on this website if you select the gene you want to know more about.

Distinct familial syndromes of CRC such as Lynch syndrome have been studied in patients, leading to the identification of other mechanisms contributing to the development of cancer. Before a cell can divide into two daughter cells, DNA has to be replicated so both daughter cells will have a full complement of chromosomes. DNA replication requires an enzyme called DNA Polymerase. DNA Polymerase occasionally makes errors while it is replicating DNA. Cells therefore have a "proof-reading" process that detects mistakes when they occur during DNA replication. DNA Polymerase mistakes mean that incorrect nucleotides have been incorporated into the DNA, causing mutations. Mistakes in the DNA sequence are repaired in a process called mismatch repair (MMR).
MMR involves a complex of multiple proteins. In Lynch syndrome, one or more of the proteins involved in MMR is mutated, and the mistakes in the DNA do not get corrected. Mutations in MMR proteins are not only found in familial cases of CRC, but also in patients with sporadic (non-inherited) CRC. Defects in MMR also contribute to microsatellite instability (MIS), described above. The accumulation of these mutations can lead to cancer.

The importance of accurately replicating DNA following various types of mistakes or damage is reflected in the multiple pathways cells have for correcting or repairing broken DNA. Actual breaks in the DNA strands can happen due to exposure to radiation or other DNA damaging agents. In the case of the occurrence of breaks in DNA, there are also mechanisms for detecting these breaks. Double strand breaks (DSB's) in the DNA can be repaired via several mechanisms, including Non-Homologous End Joining (NHEJ) or Homologous Repair (HR). Many proteins are involved in DSB repair. Mutations in any of the many proteins involved in either of these repair pathways (see BRCA1 and BRCA2 genes) lead to damaged DNA, which results in DNA that is incorrectly replicated, causing mutations that contribute to the development of cancer. DNA repair machinery in the cell is important in keeping the genome stable and accurate.

Testing for the mutations and genomic conditions that contribute to the development or progression of CRC is available at MGH in the sophisticated CLIA certified genomic testing lab, and in other large Centers and some private testing companies used by physicians. Validated treatments, Immune therpies, as well as clinical trials investigating improved targeted and immunologic therapies are available to patients at MGH.

NIH/NCI Cancer Website www.cancer.gov 2017

Colorectal Cancer (CRC) is cancer that initiates in the colon or rectum-the lower part of the digestive system in the body. During digestion, food moves through the stomach and small intestine into the colon. The colon absorbs water and nutrients from food, and stores waste matter (stool) that moves from the colon through the rectum before leaving the body.

Most CRC's and rectal cancers are adenocarcinomas, meaning that they originate in cells that make and release mucus and other fluids. CRC often begins as a growth called a polyp, which may form on the inner wall of the colon or rectum. Over time, some polyps become cancerous. This highlights the importance of colonoscopy screening to find and remove polyps before they become cancerous.

CRC is the fourth most common type of cancer diagnosed in the U.S. Deaths from CRC have decreased with the use of colonoscopies and fecal occult blood tests, which check for blood in the stool. Disparities in survival have been observed between African American and other populations. This may be due to factors such as access to colonoscopy screening, or to other factors not yet identified.

Because of its prevalence, scientists have studied CRC extensively, even creating models of how cancer develops using CRC as an example. There are also families with a very high incidence of CRC occurrence. When these families were studied, certain conditions that create instability in the whole genome were identified that predispose people to CRC. These include what is called the Chromosomal Instability pathway (CIN), as well as MicroSatellite Instability pathway (MSI). These can also occur as spontaneous (uninherited) conditions in some patients. Between 6-10% of CRC's are found to have MSI. Some CRC tumors have been found to have a lot of mutations, or as physicians call it, a "very high mutational load". Some also express a ligand called PD-L1.

These are now recognized features of some CRC's, and immunological treatments may be recommended in these cases. MGH has one of the most extensive Immuno-oncology clinical trials portfolios of any US hospital. Testing for features such as CIN, MSI, a high mutational burden, and the expression of PD-L1 can be conducted at the MGH genetics laboratory, as well as at other large academic centers. Genetic instability such as CIN or MSI lead to the activation of oncogenes such as KRAS, and the inactivation of tumor suppressors such as PTEN, both of which promote tumor growth.

Other genetic alterations in how the DNA in cells is organized have been found to contribute to CRC in families and individuals. These are called epigenetic changes. Normal DNA has methyl groups added in specific regions that regulate gene expression. When the genes that suppress growth-called tumor suppressors-are methylated abnormally, this prevents the production of tumor suppressor proteins important in controlling or stopping cell growth. When tumor suppressor genes are missing, unregulated growth occurs, contributing to the development of cancer. Some tumor suppressor proteins that are frequently inactivated in CRC are APC, TP53, or loss of one arm of chromosome 18 that contains a tumor suppressor.

The study of families with a high prevalence of CRC have lead scientists to discover genetic changes that contribute to the development of CRC in sporadic cases occurring in patients. Mutations in the genes encoding the following proteins have now been associated with subsets of CRC; ALK, AKT, APC, beta-catenin, BRCA1 and BRCA2, BRAF, EGFR, ERBB2 (HER2), ERBB3 (HER3), IDH2, KRAS, MET, NRAS, PI3K, ROS, PTEN, SMO,TP53, TRK 1, 2 and 3, and others that are still being identified. Information on these specific genes is available on this website if you select the gene you want to know more about.

Distinct familial syndromes of CRC such as Lynch syndrome have been studied in patients, leading to the identification of other mechanisms contributing to the development of cancer. Before a cell can divide into two daughter cells, DNA has to be replicated so both daughter cells will have a full complement of chromosomes. DNA replication requires an enzyme called DNA Polymerase. DNA Polymerase occasionally makes errors while it is replicating DNA. Cells therefore have a "proof-reading" process that detects mistakes when they occur during DNA replication. DNA Polymerase mistakes mean that incorrect nucleotides have been incorporated into the DNA, causing mutations. Mistakes in the DNA sequence are repaired in a process called mismatch repair (MMR).
MMR involves a complex of multiple proteins. In Lynch syndrome, one or more of the proteins involved in MMR is mutated, and the mistakes in the DNA do not get corrected. Mutations in MMR proteins are not only found in familial cases of CRC, but also in patients with sporadic (non-inherited) CRC. Defects in MMR also contribute to microsatellite instability (MIS), described above. The accumulation of these mutations can lead to cancer.

The importance of accurately replicating DNA following various types of mistakes or damage is reflected in the multiple pathways cells have for correcting or repairing broken DNA. Actual breaks in the DNA strands can happen due to exposure to radiation or other DNA damaging agents. In the case of the occurrence of breaks in DNA, there are also mechanisms for detecting these breaks. Double strand breaks (DSB's) in the DNA can be repaired via several mechanisms, including Non-Homologous End Joining (NHEJ) or Homologous Repair (HR). Many proteins are involved in DSB repair. Mutations in any of the many proteins involved in either of these repair pathways (see BRCA1 and BRCA2 genes) lead to damaged DNA, which results in DNA that is incorrectly replicated, causing mutations that contribute to the development of cancer. DNA repair machinery in the cell is important in keeping the genome stable and accurate.

Testing for the mutations and genomic conditions that contribute to the development or progression of CRC is available at MGH in the sophisticated CLIA certified genomic testing lab, and in other large Centers and some private testing companies used by physicians. Validated treatments, Immune therpies, as well as clinical trials investigating improved targeted and immunologic therapies are available to patients at MGH.

NIH/NCI Cancer Website www.cancer.gov 2017

Colorectal Cancer (CRC) is cancer that initiates in the colon or rectum-the lower part of the digestive system in the body. During digestion, food moves through the stomach and small intestine into the colon. The colon absorbs water and nutrients from food, and stores waste matter (stool) that moves from the colon through the rectum before leaving the body.

Most CRC's and rectal cancers are adenocarcinomas, meaning that they originate in cells that make and release mucus and other fluids. CRC often begins as a growth called a polyp, which may form on the inner wall of the colon or rectum. Over time, some polyps become cancerous. This highlights the importance of colonoscopy screening to find and remove polyps before they become cancerous.

CRC is the fourth most common type of cancer diagnosed in the U.S. Deaths from CRC have decreased with the use of colonoscopies and fecal occult blood tests, which check for blood in the stool. Disparities in survival have been observed between African American and other populations. This may be due to factors such as access to colonoscopy screening, or to other factors not yet identified.

Because of its prevalence, scientists have studied CRC extensively, even creating models of how cancer develops using CRC as an example. There are also families with a very high incidence of CRC occurrence. When these families were studied, certain conditions that create instability in the whole genome were identified that predispose people to CRC. These include what is called the Chromosomal Instability pathway (CIN), as well as MicroSatellite Instability pathway (MSI). These can also occur as spontaneous (uninherited) conditions in some patients. Between 6-10% of CRC's are found to have MSI. Some CRC tumors have been found to have a lot of mutations, or as physicians call it, a "very high mutational load". Some also express a ligand called PD-L1.

These are now recognized features of some CRC's, and immunological treatments may be recommended in these cases. MGH has one of the most extensive Immuno-oncology clinical trials portfolios of any US hospital. Testing for features such as CIN, MSI, a high mutational burden, and the expression of PD-L1 can be conducted at the MGH genetics laboratory, as well as at other large academic centers. Genetic instability such as CIN or MSI lead to the activation of oncogenes such as KRAS, and the inactivation of tumor suppressors such as PTEN, both of which promote tumor growth.

Other genetic alterations in how the DNA in cells is organized have been found to contribute to CRC in families and individuals. These are called epigenetic changes. Normal DNA has methyl groups added in specific regions that regulate gene expression. When the genes that suppress growth-called tumor suppressors-are methylated abnormally, this prevents the production of tumor suppressor proteins important in controlling or stopping cell growth. When tumor suppressor genes are missing, unregulated growth occurs, contributing to the development of cancer. Some tumor suppressor proteins that are frequently inactivated in CRC are APC, TP53, or loss of one arm of chromosome 18 that contains a tumor suppressor.

The study of families with a high prevalence of CRC have lead scientists to discover genetic changes that contribute to the development of CRC in sporadic cases occurring in patients. Mutations in the genes encoding the following proteins have now been associated with subsets of CRC; ALK, AKT, APC, beta-catenin, BRCA1 and BRCA2, BRAF, EGFR, ERBB2 (HER2), ERBB3 (HER3), IDH2, KRAS, MET, NRAS, PI3K, ROS, PTEN, SMO,TP53, TRK 1, 2 and 3, and others that are still being identified. Information on these specific genes is available on this website if you select the gene you want to know more about.

Distinct familial syndromes of CRC such as Lynch syndrome have been studied in patients, leading to the identification of other mechanisms contributing to the development of cancer. Before a cell can divide into two daughter cells, DNA has to be replicated so both daughter cells will have a full complement of chromosomes. DNA replication requires an enzyme called DNA Polymerase. DNA Polymerase occasionally makes errors while it is replicating DNA. Cells therefore have a "proof-reading" process that detects mistakes when they occur during DNA replication. DNA Polymerase mistakes mean that incorrect nucleotides have been incorporated into the DNA, causing mutations. Mistakes in the DNA sequence are repaired in a process called mismatch repair (MMR).
MMR involves a complex of multiple proteins. In Lynch syndrome, one or more of the proteins involved in MMR is mutated, and the mistakes in the DNA do not get corrected. Mutations in MMR proteins are not only found in familial cases of CRC, but also in patients with sporadic (non-inherited) CRC. Defects in MMR also contribute to microsatellite instability (MIS), described above. The accumulation of these mutations can lead to cancer.

The importance of accurately replicating DNA following various types of mistakes or damage is reflected in the multiple pathways cells have for correcting or repairing broken DNA. Actual breaks in the DNA strands can happen due to exposure to radiation or other DNA damaging agents. In the case of the occurrence of breaks in DNA, there are also mechanisms for detecting these breaks. Double strand breaks (DSB's) in the DNA can be repaired via several mechanisms, including Non-Homologous End Joining (NHEJ) or Homologous Repair (HR). Many proteins are involved in DSB repair. Mutations in any of the many proteins involved in either of these repair pathways (see BRCA1 and BRCA2 genes) lead to damaged DNA, which results in DNA that is incorrectly replicated, causing mutations that contribute to the development of cancer. DNA repair machinery in the cell is important in keeping the genome stable and accurate.

Testing for the mutations and genomic conditions that contribute to the development or progression of CRC is available at MGH in the sophisticated CLIA certified genomic testing lab, and in other large Centers and some private testing companies used by physicians. Validated treatments, Immune therpies, as well as clinical trials investigating improved targeted and immunologic therapies are available to patients at MGH.

NIH/NCI Cancer Website www.cancer.gov 2017

PubMed ID's
2188735, 23897299, 20965415
Expand Collapse EGFR  - General Description
CLICK IMAGE FOR MORE INFORMATION
The EGFR gene encodes for a cell-surface protein known as the epidermal growth factor receptor, which is found in many normal epithelial tissues such as the skin and hair follicles. When epidermal growth factor ligand bind to EGFR, they activate several different cell signaling pathways that control various cell functions, including cell growth and proliferation.

Mutations in EGFR can lead to unregulated activation of the protein. These types of activating mutations are often found in NSCLC (non-small cell lung cancer), glioblastoma and head and neck squamous cell carcinoma. Sometimes, excess EGFR protein is produced due to the presence of too many copies of the EGFR gene, leading to excessive cell division and growth in the presence of epidermal growth factor. Among the human cancers in which EGFR overabundance is present are cancers of the head and neck (squamous cell), colon, rectum, lung (NSCLC), central nervous system (glioblastoma), pancreas and breast (HER2-positive metastatic). Blocking EGFR in tumors may keep cancer cells from growing. The FDA has approved several therapies that target EGFR in one or more cancers. Testing for genetic alterations of EGFR is available at the MGH genetics lab. Treatment for EGFR-mutant tumors, along with clinical trials testing new drugs for the treatment of EGFR-mutant tumors are available at the MGH Cancer Center.

Tumor mutation profiling performed clinically at the MGH Cancer Center has indicated that EGFR mutations occur primarily in lung cancer (~15%), but also in a minor subset of gastric (2%), brain (1%) and pancreatic (1%) cancers.

Source: Genetics Home Reference
The EGFR gene encodes for a cell-surface protein known as the epidermal growth factor receptor, which is found in many normal epithelial tissues such as the skin and hair follicles. When epidermal growth factor ligand bind to EGFR, they activate several different cell signaling pathways that control various cell functions, including cell growth and proliferation.

Mutations in EGFR can lead to unregulated activation of the protein. These types of activating mutations are often found in NSCLC (non-small cell lung cancer), glioblastoma and head and neck squamous cell carcinoma. Sometimes, excess EGFR protein is produced due to the presence of too many copies of the EGFR gene, leading to excessive cell division and growth in the presence of epidermal growth factor. Among the human cancers in which EGFR overabundance is present are cancers of the head and neck (squamous cell), colon, rectum, lung (NSCLC), central nervous system (glioblastoma), pancreas and breast (HER2-positive metastatic). Blocking EGFR in tumors may keep cancer cells from growing. The FDA has approved several therapies that target EGFR in one or more cancers. Testing for genetic alterations of EGFR is available at the MGH genetics lab. Treatment for EGFR-mutant tumors, along with clinical trials testing new drugs for the treatment of EGFR-mutant tumors are available at the MGH Cancer Center.

Tumor mutation profiling performed clinically at the MGH Cancer Center has indicated that EGFR mutations occur primarily in lung cancer (~15%), but also in a minor subset of gastric (2%), brain (1%) and pancreatic (1%) cancers.

Source: Genetics Home Reference
PubMed ID's
15864276, 15118073, 15118125, 15329413, 18772890, 15837736, 16720329, 21057220
Expand Collapse T790M (c.2369C>T)  in EGFR
The EGFR T790M mutation arises from the nucleotide change c.2369C>T in exon 20, resulting in an amino acid substitution of the threonine (T) at position 790 by a methionine (M).
The EGFR T790M mutation arises from the nucleotide change c.2369C>T in exon 20, resulting in an amino acid substitution of the threonine (T) at position 790 by a methionine (M).

The T790M mutation in the gene encoding EGFR have been found in CRC. This mutation may have different therapeutic implications than some of the other genetic alterations found in EGFR. Your Oncologist can interpret the results of your genetic testing, and make treatment recommendations or suggest clinical trials you may be eligible for to treat T790M-mutant CRC.

The T790M mutation in the gene encoding EGFR have been found in CRC. This mutation may have different therapeutic implications than some of the other genetic alterations found in EGFR. Your Oncologist can interpret the results of your genetic testing, and make treatment recommendations or suggest clinical trials you may be eligible for to treat T790M-mutant CRC.

PubMed ID's
15118125, 15118073, 15863375, 16166444, 15746034, 20184776, 20184776, 15625347, 16012179
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Your Matched Clinical Trials

Trial Matches: (D) - Disease, (G) - Gene, (M) - Mutation
Trial Status: Showing Results: 1-10 of 39 Per Page:
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Protocol # Title Location Status Match
NCT01953926 Neratinib HER Mutation Basket Study (SUMMIT) Neratinib HER Mutation Basket Study (SUMMIT) MGH Open DGM
NCT03192345 A First-in-human Study of the Safety, Pharmacokinetics, Pharmacodynamics and Anti-tumor Activity of SAR439459 Monotherapy and Combination of SAR439459 and REGN2810 in Patients With Advanced Solid Tumors A First-in-human Study of the Safety, Pharmacokinetics, Pharmacodynamics and Anti-tumor Activity of SAR439459 Monotherapy and Combination of SAR439459 and REGN2810 in Patients With Advanced Solid Tumors MGH Open D
NCT02715284 A Phase 1 Dose Escalation and Cohort Expansion Study of TSR-042, an Anti-PD-1 Monoclonal Antibody, in Patients With Advanced Solid Tumors A Phase 1 Dose Escalation and Cohort Expansion Study of TSR-042, an Anti-PD-1 Monoclonal Antibody, in Patients With Advanced Solid Tumors MGH Open D
NCT02817633 A Phase 1 Study of TSR-022, an Anti-TIM-3 Monoclonal Antibody, in Patients With Advanced Solid Tumors A Phase 1 Study of TSR-022, an Anti-TIM-3 Monoclonal Antibody, in Patients With Advanced Solid Tumors MGH Open D
NCT03057509 A Pilot Study Of Ga-68-DOTA-TOC Imaging In Participants With Small Bowel Carcinoid Tumors A Pilot Study Of Ga-68-DOTA-TOC Imaging In Participants With Small Bowel Carcinoid Tumors MGH Open D
NCT02099058 A Study Evaluating the Safety, Pharmacokinetics (PK), and Preliminary Efficacy of ABBV-399 in Subjects With Advanced Solid Tumors. A Study Evaluating the Safety, Pharmacokinetics (PK), and Preliminary Efficacy of ABBV-399 in Subjects With Advanced Solid Tumors. MGH Open D
NCT02908451 A Study of AbGn-107 in Patients With Gastric, Colorectal, or Pancreatic Cancer A Study of AbGn-107 in Patients With Gastric, Colorectal, or Pancreatic Cancer MGH Open D
NCT02880371 A Study of ARRY-382 in Combination With Pembrolizumab for the Treatment of Patients With Advanced Solid Tumors A Study of ARRY-382 in Combination With Pembrolizumab for the Treatment of Patients With Advanced Solid Tumors MGH Open D
NCT01351103 A Study of LGK974 in Patients With Malignancies Dependent on Wnt Ligands A Study of LGK974 in Patients With Malignancies Dependent on Wnt Ligands MGH Open D
NCT02857270 A Study of LY3214996 Administered Alone or in Combination With Other Agents in Participants With Advanced/Metastatic Cancer A Study of LY3214996 Administered Alone or in Combination With Other Agents in Participants With Advanced/Metastatic Cancer MGH Open D
Trial Status: Showing Results: 1-10 of 39 Per Page:
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