Colorectal Cancer, PIK3CA, activating mutations

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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 PIK3CA  - General Description
CLICK IMAGE FOR MORE INFORMATION
PIK3CA is a gene that provides the code for making one piece of the phosphatidylinositol 3-kinase (PI3K) protein, which is an enzyme that is part of an important signaling pathway (PI3K/AKT) involved in controlling the growth, division, survival, nutrient utilization, movement and structure of cells. PIK3CA encodes the catalytic subunit of PI3K, which is the part of the protein that lets it function as an enzyme. PI3K function is tightly maintained in normal cells. The enzymatic activity is activated by specific signals from growth factor receptor tyrosine kinases (RTKs) or from activated RAS proteins. PI3K then generates molecules that attract another enzyme (particularly AKT) to the cell membrane, where it is activated. The activated AKT acts on other proteins that regulate various cell processes that promotes cell growth and survival.

Mutations in PIK3CA lead to enhanced activation of its signaling function, thereby driving the tumorigenic process. These activating mutations are commonly associated with breast and colon cancer, and more rarely with melanoma of the skin. Defects in this gene have also been associated with ovarian cancer, endometrial cancer, and liver cancer.

Tumor mutation profiling performed clinically at the MGH Cancer Center has identified PIK3CA mutations across a broad-spectrum of cancer types. The highest incidence of PIK3CA mutations have been found in endometrial cancer (25%), breast cancer (20%), colon cancer (25%) and cancers of the head and neck (10%). In the other major tumor types, PIK3CA mutations have been found in less than 10% of cases that have been tested.

Sources: Genetics Home Reference
The PIK3CA gene encodes the p110 alpha catalytic subunit of the phosphoinositol 3-kinase (PI3K) complex. PI3K receives upstream activation signals from growth factor receptor tyrosine kinases (e.g. EGFR family members), and in turn signals through AKT and mTOR in order to promote cell survival, cell growth and cellular proliferation. PIK3CA mutations lead to increased activation of PI3K/AKT/mTOR signaling. PI3K function is opposed by PTEN, a lipid phosphatase that is often inactivated by mutations or silenced by methylation in many cancers.

Tumor mutation profiling performed clinically at the MGH Cancer Center has identified PIK3CA mutations across a broad-spectrum of cancer types. The highest incidence of PIK3CA mutations have been found in endometrial cancer (25%), breast cancer (20%), colon cancer (25%) and cancers of the head and neck (10%). In the other major tumor types, PIK3CA mutations have been found in less than 10% of cases that have been tested.

Sources: Genetics Home Reference
Expand Collapse activating mutations  in PIK3CA
Many of the mutations in PIK3CA associated with tumors are gain of function mutations, rendering the kinase in a constantly activated state. Instead of reacting to appropriate stimulation to induce a growth signal, activating mutations keep the PI3 Kinase in a constant state of stimulating growth.
Many of the mutations in PIK3CA associated with tumors are gain of function mutations, rendering the kinase in a constantly activated state. Instead of reacting to appropriate stimulation to induce a growth signal, activating mutations keep the PI3 Kinase in a constant state of stimulating growth.

Mutations in the gene that provides the cell with the genetic sequence to produce the PI3K protein cause it to be abnormally regulated. The protein is constantly sending growth signals to the cell, contributing to the development of cancer.

Mutations in the gene that provides the cell with the genetic sequence to produce the PI3K protein cause it to be abnormally regulated. The protein is constantly sending growth signals to the cell, contributing to the development of cancer.

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Your Matched Clinical Trials

Trial Matches: (D) - Disease, (G) - Gene, (M) - Mutation
Trial Status: Showing Results: 1-10 of 46 Per Page:
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Protocol # Title Location Status Match
NCT02961283 Study of ASN003 in Subjects With Advanced Solid Tumors Study of ASN003 in Subjects With Advanced Solid Tumors MGH Open DGM
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NCT02279433 A First-in-human Study to Evaluate the Safety, Tolerability and Pharmacokinetics of DS-6051b A First-in-human Study to Evaluate the Safety, Tolerability and Pharmacokinetics of DS-6051b 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
NCT02099058 A Phase 1/1b Study With ABBV-399, an Antibody Drug Conjugate, in Subjects With Advanced Solid Cancer Tumors A Phase 1/1b Study With ABBV-399, an Antibody Drug Conjugate, in Subjects With Advanced Solid Cancer Tumors MGH Open D
NCT02482441 A Phase 1a/b Dose Escalation Study of the Safety, Pharmacokinetics, and Pharmacodynamics of OMP-131R10 A Phase 1a/b Dose Escalation Study of the Safety, Pharmacokinetics, and Pharmacodynamics of OMP-131R10 MGH Open D
NCT02327169 A Phase 1B Study of MLN2480 in Combination With MLN0128 or Alisertib, or Paclitaxel, or Cetuximab, or Irinotecan in Adult Patients With Advanced Nonhematologic Malignancies A Phase 1B Study of MLN2480 in Combination With MLN0128 or Alisertib, or Paclitaxel, or Cetuximab, or Irinotecan in Adult Patients With Advanced Nonhematologic Malignancies MGH Open D
NCT03144804 A Phase 2 Study of Lamivudine in Patients With p53 Mutant Metastatic Colorectal Cancer A Phase 2 Study of Lamivudine in Patients With p53 Mutant Metastatic Colorectal Cancer 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
NCT01714739 A Study of an Anti-KIR Antibody Lirilumab in Combination With an Anti-PD1 Antibody Nivolumab and Nivolumab Plus an Anti-CTLA-4 Ipilimumab Antibody in Patients With Advanced Solid Tumors A Study of an Anti-KIR Antibody Lirilumab in Combination With an Anti-PD1 Antibody Nivolumab and Nivolumab Plus an Anti-CTLA-4 Ipilimumab Antibody in Patients With Advanced Solid Tumors MGH Open D
Trial Status: Showing Results: 1-10 of 46 Per Page:
12345Next »
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