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Expand Collapse Lung Cancer  - General Description This year about 226,000 people in the U.S. will be told by a doctor that they have lung cancer. However, about 390,000 Americans remain alive today after having been diagnosed with this malignancy. Lung cancer includes tumors that begin in tissues lining air passages inside the lungs and bronchi. The bronchi are the 2 branches of the windpipe (trachea) that lead to the lungs. Based on how the cells look under a microscope, lung cancers are divided into 2 main types: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). NSCLC accounts for 85% of these cases.

The main subtypes of NSCLC are squamous cell carcinoma (cancer beginning in thin, flat scaly-looking cells), adenocarcinoma (cancer beginning in cells that make mucus and other substances) and large cell carcinoma (cancer beginning in several types of large cells). The 2 main types of SCLC are small cell carcinoma (oat cell cancer) and combined small cell carcinoma.

Lung cancer (and other tumors) can spread (metastasize) from the place where it started (the primary tumor) in 3 ways. First, it can invade the normal tissue surrounding it. Second, cancer cells can enter the lymph system and travel through lymph vessels to distant parts of the body. Third, the cancer cells can get into the bloodstream and go to other places in the body. In these distant places, the cancer cells cause secondary tumors to grow. The main sites to which lung cancer spreads are the adrenal gland, liver and lungs.

To find out whether the cancer has entered the lymph system, a surgeon removes all or part of a node near the primary tumor and a pathologist looks at it through a microscope to see if cancer cells are present. Several kinds of imaging also can be performed to determine if the cancer has spread. These include MRI, bone scans and endoscopic ultrasound (EUS).

The FDA has approved several targeted therapies to treat patients with NSCLC. These include bevacizumab (Avastin), cetuximab (Erbitux), erlotinib (Tarceva), gefitnib (Iressa) and crizotinib (Xalkori). So far there are no FDA-approved targeted therapies for SCLC.

Despite significant improvements in the treatment of lung cancers, novel therapies and treatment strategies are needed.

Source: National Cancer Institute, 2012
Estimated new cases and deaths from lung cancer (non-small cell and small cell combined) in the United States in 2012:

New cases: 226,160
Deaths: 160,340

Lung cancer is the leading cause of cancer-related mortality in the United States. The 5-year relative survival rate from 1995 to 2001 for patients with lung cancer was 15.7%. The 5-year relative survival rate varies markedly depending on the stage at diagnosis, from 49% to 16% to 2% for patients with local, regional and distant stage disease, respectively.

NSCLC arises from the epithelial cells of the lung, from the central bronchi to the terminal alveoli. The histological type of NSCLC correlates with the site of origin, reflecting the variation in respiratory tract epithelium from the bronchi to the alveoli. Squamous cell carcinoma usually starts near a central bronchus while adenocarcinoma usually originates in peripheral lung tissue.

Tobacco smoking is the strongest risk factor for developing lung cancer, though it should be noted that the majority of patients diagnosed with lung cancer quit smoking years prior to diagnosis or were never-smokers (up to 15% of cases).

The identification of driver oncogene mutations in lung cancer has led to the development of targeted therapy that has vastly broadened treatment options and improved outcomes for subsets of patients with metastatic disease. It is now common practice to determine the genotype of a NSCLC patient early in the course of their diagnosis, to ensure that all possible treatment options are considered.

Source: National Cancer Institute, 2012
This year about 226,000 people in the U.S. will be told by a doctor that they have lung cancer. However, about 390,000 Americans remain alive today after having been diagnosed with this malignancy. Lung cancer includes tumors that begin in tissues lining air passages inside the lungs and bronchi. The bronchi are the 2 branches of the windpipe (trachea) that lead to the lungs. Based on how the cells look under a microscope, lung cancers are divided into 2 main types: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). NSCLC accounts for 85% of these cases.

The main subtypes of NSCLC are squamous cell carcinoma (cancer beginning in thin, flat scaly-looking cells), adenocarcinoma (cancer beginning in cells that make mucus and other substances) and large cell carcinoma (cancer beginning in several types of large cells). The 2 main types of SCLC are small cell carcinoma (oat cell cancer) and combined small cell carcinoma.

Lung cancer (and other tumors) can spread (metastasize) from the place where it started (the primary tumor) in 3 ways. First, it can invade the normal tissue surrounding it. Second, cancer cells can enter the lymph system and travel through lymph vessels to distant parts of the body. Third, the cancer cells can get into the bloodstream and go to other places in the body. In these distant places, the cancer cells cause secondary tumors to grow. The main sites to which lung cancer spreads are the adrenal gland, liver and lungs.

To find out whether the cancer has entered the lymph system, a surgeon removes all or part of a node near the primary tumor and a pathologist looks at it through a microscope to see if cancer cells are present. Several kinds of imaging also can be performed to determine if the cancer has spread. These include MRI, bone scans and endoscopic ultrasound (EUS).

The FDA has approved several targeted therapies to treat patients with NSCLC. These include bevacizumab (Avastin), cetuximab (Erbitux), erlotinib (Tarceva), gefitnib (Iressa) and crizotinib (Xalkori). So far there are no FDA-approved targeted therapies for SCLC.

Despite significant improvements in the treatment of lung cancers, novel therapies and treatment strategies are needed.

Source: National Cancer Institute, 2012
Estimated new cases and deaths from lung cancer (non-small cell and small cell combined) in the United States in 2012:

New cases: 226,160
Deaths: 160,340

Lung cancer is the leading cause of cancer-related mortality in the United States. The 5-year relative survival rate from 1995 to 2001 for patients with lung cancer was 15.7%. The 5-year relative survival rate varies markedly depending on the stage at diagnosis, from 49% to 16% to 2% for patients with local, regional and distant stage disease, respectively.

NSCLC arises from the epithelial cells of the lung, from the central bronchi to the terminal alveoli. The histological type of NSCLC correlates with the site of origin, reflecting the variation in respiratory tract epithelium from the bronchi to the alveoli. Squamous cell carcinoma usually starts near a central bronchus while adenocarcinoma usually originates in peripheral lung tissue.

Tobacco smoking is the strongest risk factor for developing lung cancer, though it should be noted that the majority of patients diagnosed with lung cancer quit smoking years prior to diagnosis or were never-smokers (up to 15% of cases).

The identification of driver oncogene mutations in lung cancer has led to the development of targeted therapy that has vastly broadened treatment options and improved outcomes for subsets of patients with metastatic disease. It is now common practice to determine the genotype of a NSCLC patient early in the course of their diagnosis, to ensure that all possible treatment options are considered.

Source: National Cancer Institute, 2012
Expand Collapse FGFR1  - General Description
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FGFR1 is a gene that provides the code for making a protein cell surface receptor called fibroblast growth factor receptor. FGFR has 4 subtypes, FGFR 1,2,3, and 4. When certain growth factors (proteins that stimulate cell growth and division) come into contact with (bind to) this receptor, they activate a signaling system within the cell that tells it to undergo certain changes. In its normal role during development and in cells, the FGFR1 protein is believed to help the nervous system develop, and it also may help regulate the growth of long bones.

Genetic alterations in the FGFR1 gene have been found in several types of cancer. These include lung, esophagus, breast, and oral cavity cancers. Cancers that have altered FGFR1 can have one of several genetic alterations. One form of genetic alteration in cancer is called gene amplification, in which the gene has been copied so there are multiple segments of DNA that code the sequence of the protein. When FGFR1 is amplified, more FGFR1 protein is produced than in normal cells. Another genetic alteration found in the FGFR1 gene in some cancers are genetic mutations, where a single change in the sequence of the DNA leads to a change in the FGFR1 protein. Both gene amplification and mutations in the DNA of FGFR1 that are found in various cancers are activating changes, changes that result in FGFR1 that cannot be regulated normally. Excessive signaling due to either amplification or genetic mutation in FGFR1 contribute to increased cells growth, division and the ability to move from the site of the primary tumor.

Preclinical testing in cancer cell lines suggest that FGFR gene amplification or activation because of mutations can be an important mechanism of tumor progression that may be effectively targeted with FGFR inhibitors. This has led to the development of clinical trials evaluating FGFR inhibitors in FGFR amplified cancers, which are currently underway.

Source: Genetics Home Reference
FGFR1 is a gene that provides the code for making a protein cell surface receptor called fibroblast growth factor receptor. FGFR has 4 subtypes, FGFR 1,2,3, and 4. When certain growth factors (proteins that stimulate cell growth and division) come into contact with (bind to) this receptor, they activate a signaling system within the cell that tells it to undergo certain changes. In its normal role during development and in cells, the FGFR1 protein is believed to help the nervous system develop, and it also may help regulate the growth of long bones.

Genetic alterations in the FGFR1 gene have been found in several types of cancer. These include lung, esophagus, breast, and oral cavity cancers. Cancers that have altered FGFR1 can have one of several genetic alterations. One form of genetic alteration in cancer is called gene amplification, in which the gene has been copied so there are multiple segments of DNA that code the sequence of the protein. When FGFR1 is amplified, more FGFR1 protein is produced than in normal cells. Another genetic alteration found in the FGFR1 gene in some cancers are genetic mutations, where a single change in the sequence of the DNA leads to a change in the FGFR1 protein. Both gene amplification and mutations in the DNA of FGFR1 that are found in various cancers are activating changes, changes that result in FGFR1 that cannot be regulated normally. Excessive signaling due to either amplification or genetic mutation in FGFR1 contribute to increased cells growth, division and the ability to move from the site of the primary tumor.

Preclinical testing in cancer cell lines suggest that FGFR gene amplification or activation because of mutations can be an important mechanism of tumor progression that may be effectively targeted with FGFR inhibitors. This has led to the development of clinical trials evaluating FGFR inhibitors in FGFR amplified cancers, which are currently underway.

Source: Genetics Home Reference
Expand Collapse FGFR1  in Lung Cancer
FGFR1 is amplified in 10-20% of squamous non-small cell lung cancer.

Preclinical studies clearly demonstrate that FGFR1 gene amplification promotes dependence upon FGFR signaling, thus identifying an important target for drug intervention. In preclinical laboratory models, treatment of FGFR1-amplified lung cancer with a selective FGFR kinase inhibitor resulted in growth inhibition and reduction of tumor size. The FGFR inhibitor had no effect on cells without FGFR amplification. Clinical trials with FGFR inhibitors are currently being conducted across a number of cancer types, including lung cancer.

FGFR1 is amplified in 10-20% of squamous non-small cell lung cancer.

Preclinical studies clearly demonstrate that FGFR1 gene amplification promotes dependence upon FGFR signaling, thus identifying an important target for drug intervention. In preclinical laboratory models, treatment of FGFR1-amplified lung cancer with a selective FGFR kinase inhibitor resulted in growth inhibition and reduction of tumor size. The FGFR inhibitor had no effect on cells without FGFR amplification. Clinical trials with FGFR inhibitors are currently being conducted across a number of cancer types, including lung cancer.

PubMed ID's
23182986, 21160078, 23082000
Expand Collapse No mutation selected
The mutation of a gene provides clinicians with a very detailed look at your cancer. Knowing this information could change the course of your care. To learn how you can find out more about genetic testing please visit http://www.massgeneral.org/cancer/news/faq.aspx or contact the Cancer Center.
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Your Matched Clinical Trials

Trial Matches: (D) - Disease, (G) - Gene
Trial Status: Showing Results: 1-10 of 59 Per Page:
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Protocol # Title Location Status Match
NCT02052778 A Dose Finding Study Followed by a Safety and Efficacy Study in Patients With Advanced Solid Tumors or Multiple Myeloma With FGF/FGFR-Related Abnormalities A Dose Finding Study Followed by a Safety and Efficacy Study in Patients With Advanced Solid Tumors or Multiple Myeloma With FGF/FGFR-Related Abnormalities MGH Open DG
NCT01948297 Debio 1347-101 Phase I Trial in Advanced Solid Tumours With Fibroblast Growth Factor Receptor (FGFR) Alterations Debio 1347-101 Phase I Trial in Advanced Solid Tumours With Fibroblast Growth Factor Receptor (FGFR) Alterations MGH Open DG
NCT02335918 A Dose Escalation and Cohort Expansion Study of Anti-CD27 (Varlilumab) and Anti-PD-1 (Nivolumab) in Advanced Refractory Solid Tumors A Dose Escalation and Cohort Expansion Study of Anti-CD27 (Varlilumab) and Anti-PD-1 (Nivolumab) in Advanced Refractory Solid Tumors MGH Open D
NCT02637531 A Dose-Escalation Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of IPI-549 A Dose-Escalation Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of IPI-549 MGH Open D
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
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
NCT02108964 A Phase I/II, Multicenter, Open-label Study of EGFRmut-TKI EGF816, Administered Orally in Adult Patients With EGFRmut Solid Malignancies A Phase I/II, Multicenter, Open-label Study of EGFRmut-TKI EGF816, Administered Orally in Adult Patients With EGFRmut Solid Malignancies MGH Open D
NCT01714739 A Study of an Anti-KIR Antibody in Combination With an Anti-PD1 Antibody in Patients With Advanced Solid Tumors A Study of an Anti-KIR Antibody in Combination With an Anti-PD1 Antibody in Patients With Advanced Solid Tumors MGH Open D
Trial Status: Showing Results: 1-10 of 59 Per Page:
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