Bladder Cancer, ERBB2 (HER2), Gene Amplification

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Expand Collapse Bladder Cancer  - General Description This year about 74,000 people in the U.S. (76% of them men and half will be over the age of 73 years old) will be told by a doctor that they have cancer of the urinary bladder. With significant improvements in the treatment of this malignancy, about 550,000 of them remain alive today.

Bladder cancer begins in different types of cells found in the inner lining of the bladder, the flexible muscular organ that stores urine. Transitional cells, which stretch or shrink as the bladder fills or empties, account for 90% of bladder cancers in the United States. Less commonly (in 6-8% of U.S. bladder cancers), the cancer begins in squamous cells that may form in response to irritation or infection that has lasted a long time. Adenocarcinoma begins in cells that make mucous and accounts for only about 2% of U.S. bladder cancers. Adenocarcinoma of the bladder is also believed to be a result of long-lasting irritation or inflammation.

If the cancer stays in the lining of the bladder, it is called superficial bladder cancer. Sometimes, though, transitional cell cancer spreads through the lining and breaks into the muscular wall beneath it or spreads to nearby organs and lymph nodes. In this case it is known as invasive bladder cancer.

Bladder 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, bladder 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 blood stream and go to other places in the body. In these distant places, the bladder cancer cells cause secondary (metastatic) tumors to grow, in the bones, for example. To find out whether the cancer has entered the lymph system, a surgeon removes all or part of a lymph node and a pathologist inspects it under a microscope. Several kinds of imaging can also be performed to determine if bladder cancer has spread. These include CT scans, MRI, chest x-rays and bone scans.

Source: National Cancer Institute, 2012
This year about 74,000 people in the U.S. (76% of them men and half will be over the age of 73 years old) will be told by a doctor that they have cancer of the urinary bladder. With significant improvements in the treatment of this malignancy, about 550,000 of them remain alive today.

Bladder cancer begins in different types of cells found in the inner lining of the bladder, the flexible muscular organ that stores urine. Transitional cells, which stretch or shrink as the bladder fills or empties, account for 90% of bladder cancers in the United States. Less commonly (in 6-8% of U.S. bladder cancers), the cancer begins in squamous cells that may form in response to irritation or infection that has lasted a long time. Adenocarcinoma begins in cells that make mucous and accounts for only about 2% of U.S. bladder cancers. Adenocarcinoma of the bladder is also believed to be a result of long-lasting irritation or inflammation.

If the cancer stays in the lining of the bladder, it is called superficial bladder cancer. Sometimes, though, transitional cell cancer spreads through the lining and breaks into the muscular wall beneath it or spreads to nearby organs and lymph nodes. In this case it is known as invasive bladder cancer.

Bladder 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, bladder 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 blood stream and go to other places in the body. In these distant places, the bladder cancer cells cause secondary (metastatic) tumors to grow, in the bones, for example. To find out whether the cancer has entered the lymph system, a surgeon removes all or part of a lymph node and a pathologist inspects it under a microscope. Several kinds of imaging can also be performed to determine if bladder cancer has spread. These include CT scans, MRI, chest x-rays and bone scans.

Source: National Cancer Institute, 2012
This year about 74,000 people in the U.S. (76% of them men and half will be over the age of 73 years old) will be told by a doctor that they have cancer of the urinary bladder. With significant improvements in the treatment of this malignancy, about 550,000 of them remain alive today.

Bladder cancer begins in different types of cells found in the inner lining of the bladder, the flexible muscular organ that stores urine. Transitional cells, which stretch or shrink as the bladder fills or empties, account for 90% of bladder cancers in the United States. Less commonly (in 6-8% of U.S. bladder cancers), the cancer begins in squamous cells that may form in response to irritation or infection that has lasted a long time. Adenocarcinoma begins in cells that make mucous and accounts for only about 2% of U.S. bladder cancers. Adenocarcinoma of the bladder is also believed to be a result of long-lasting irritation or inflammation.

If the cancer stays in the lining of the bladder, it is called superficial bladder cancer. Sometimes, though, transitional cell cancer spreads through the lining and breaks into the muscular wall beneath it or spreads to nearby organs and lymph nodes. In this case it is known as invasive bladder cancer.

Bladder 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, bladder 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 blood stream and go to other places in the body. In these distant places, the bladder cancer cells cause secondary (metastatic) tumors to grow, in the bones, for example. To find out whether the cancer has entered the lymph system, a surgeon removes all or part of a lymph node and a pathologist inspects it under a microscope. Several kinds of imaging can also be performed to determine if bladder cancer has spread. These include CT scans, MRI, chest x-rays and bone scans.

Source: National Cancer Institute, 2012
This year about 74,000 people in the U.S. (76% of them men and half will be over the age of 73 years old) will be told by a doctor that they have cancer of the urinary bladder. With significant improvements in the treatment of this malignancy, about 550,000 of them remain alive today.

Bladder cancer begins in different types of cells found in the inner lining of the bladder, the flexible muscular organ that stores urine. Transitional cells, which stretch or shrink as the bladder fills or empties, account for 90% of bladder cancers in the United States. Less commonly (in 6-8% of U.S. bladder cancers), the cancer begins in squamous cells that may form in response to irritation or infection that has lasted a long time. Adenocarcinoma begins in cells that make mucous and accounts for only about 2% of U.S. bladder cancers. Adenocarcinoma of the bladder is also believed to be a result of long-lasting irritation or inflammation.

If the cancer stays in the lining of the bladder, it is called superficial bladder cancer. Sometimes, though, transitional cell cancer spreads through the lining and breaks into the muscular wall beneath it or spreads to nearby organs and lymph nodes. In this case it is known as invasive bladder cancer.

Bladder 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, bladder 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 blood stream and go to other places in the body. In these distant places, the bladder cancer cells cause secondary (metastatic) tumors to grow, in the bones, for example. To find out whether the cancer has entered the lymph system, a surgeon removes all or part of a lymph node and a pathologist inspects it under a microscope. Several kinds of imaging can also be performed to determine if bladder cancer has spread. These include CT scans, MRI, chest x-rays and bone scans.

Source: National Cancer Institute, 2012
Expand Collapse ERBB2 (HER2)  - General Description
CLICK IMAGE FOR MORE INFORMATION
ERBB2, often called HER2, is a gene that provides the code for making a cell surface growth receptor called the ERBB2 (HER2). When certain growth factors (proteins that stimulate cell growth and division) bind to this receptor, they activate a signaling system inside the cell that ultimately promotes diverse functions such as growth, interaction and adhesion between cells, and ability of the cell to migrate within tissues. In some tumors, the activation of HER2 signaling is an important mechanism that drives the disease process. This can occur through HER2 gene amplification (the most common mechanism) or HER2 gene mutation in cancer cells.

Extra copies of the ERBB2 (HER2) gene (gene amplification) have been found in a number of different cancers. This causes the cancer cells to make excess HER2 (overexpression), which in turn, tells the cells to grow and divide in an uncontrolled manner. Genetic mutations (changes in the DNA sequence that codes the ERBB2 (HER2) protein have also been found in certain tumors.

Source: Genetics Home Reference
ERBB2, often called HER2, is a gene that provides the code for making a cell surface growth receptor called the ERBB2 (HER2). When certain growth factors (proteins that stimulate cell growth and division) bind to this receptor, they activate a signaling system inside the cell that ultimately promotes diverse functions such as growth, interaction and adhesion between cells, and ability of the cell to migrate within tissues. In some tumors, the activation of HER2 signaling is an important mechanism that drives the disease process. This can occur through HER2 gene amplification (the most common mechanism) or HER2 gene mutation in cancer cells.

Extra copies of the ERBB2 (HER2) gene (gene amplification) have been found in a number of different cancers. This causes the cancer cells to make excess HER2 (overexpression), which in turn, tells the cells to grow and divide in an uncontrolled manner. Genetic mutations (changes in the DNA sequence that codes the ERBB2 (HER2) protein have also been found in certain tumors.

Source: Genetics Home Reference
PubMed ID's
15864276, 9130710, 15457249, 16397024, 18772890, 16843263, 16988931, 22899400
Expand Collapse Gene Amplification  in ERBB2 (HER2)
Genetic alterations in HER2 have been found in several types of cancer. The alterations found in different tumors include gene amplification, in which multiple copies of the HER2 gene are found in cancer cells. Overexpression of HER2 has also been found in some cancers, resulting in a higher level of the ERBB2 (HER2) protein being produced in cells, and therefore a higher level of activity. Other genetic alterations include the insertion of nucleotides in one portion of the gene called exon 20. All of these changes result in ERBB2 (HER2) proteins that cannot be regulated normally by the cell, and the protein sends constant signals to the tumor cells to grow and proliferate.

Testing for gene amplification, exon 20 insertion, and all ERBB2 (HER2) mutations is performed at the Center for Integrated Diagnostics at MGH. Treatment is available at the MGH Cancer Center. In addition, clinical trials are available investigating novel HER2 inhibitors and combination drug strategies.
Genetic alterations in HER2 have been found in several types of cancer. The alterations found in different tumors include gene amplification, in which multiple copies of the HER2 gene are found in cancer cells. Overexpression of HER2 has also been found in some cancers, resulting in a higher level of the ERBB2 (HER2) protein being produced in cells, and therefore a higher level of activity. Other genetic alterations include the insertion of nucleotides in one portion of the gene called exon 20. All of these changes result in ERBB2 (HER2) proteins that cannot be regulated normally by the cell, and the protein sends constant signals to the tumor cells to grow and proliferate.

Testing for gene amplification, exon 20 insertion, and all ERBB2 (HER2) mutations is performed at the Center for Integrated Diagnostics at MGH. Treatment is available at the MGH Cancer Center. In addition, clinical trials are available investigating novel HER2 inhibitors and combination drug strategies.

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Your Matched Clinical Trials

Trial Matches: (D) - Disease, (G) - Gene, (M) - Mutation
Trial Status: Showing Results: 1-10 of 18 Per Page:
12Next »
Protocol # Title Location Status Match
NCT01953926 Neratinib HER Mutation Basket Study (SUMMIT) Neratinib HER Mutation Basket Study (SUMMIT) MGH Open DGM
NCT02897765 A Personal Cancer Vaccine (NEO-PV-01) w/ Nivolumab for Patients With Melanoma, Lung Cancer or Bladder Cancer A Personal Cancer Vaccine (NEO-PV-01) w/ Nivolumab for Patients With Melanoma, Lung Cancer or Bladder Cancer MGH Open D
NCT02450331 A Study of Atezolizumab Versus Observation as Adjuvant Therapy in Participants With High-Risk Muscle-Invasive Urothelial Carcinoma (UC) After Surgical Resection A Study of Atezolizumab Versus Observation as Adjuvant Therapy in Participants With High-Risk Muscle-Invasive Urothelial Carcinoma (UC) After Surgical Resection MGH Open D
NCT02603432 A Study Of Avelumab In Patients With Locally Advanced Or Metastatic Urothelial Cancer (JAVELIN Bladder 100) A Study Of Avelumab In Patients With Locally Advanced Or Metastatic Urothelial Cancer (JAVELIN Bladder 100) MGH Open D
NCT03219333 A Study of Enfortumab Vedotin for Patients With Locally Advanced or Metastatic Urothelial Bladder Cancer A Study of Enfortumab Vedotin for Patients With Locally Advanced or Metastatic Urothelial Bladder Cancer MGH Open D
NCT02052778 A Study of TAS-120 in Patients With Advanced Solid Tumors A Study of TAS-120 in Patients With Advanced Solid Tumors MGH Open D
NCT02567409 Cisplatin and Gemcitabine Hydrochloride With or Without ATR Kinase Inhibitor VX-970 in Treating Patients With Metastatic Urothelial Cancer Cisplatin and Gemcitabine Hydrochloride With or Without ATR Kinase Inhibitor VX-970 in Treating Patients With Metastatic Urothelial Cancer MGH Open D
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 D
NCT02989064 MAGE-A10ᶜ⁷⁹⁶T for Urothelial Cancer, Melanoma or Head and Neck Cancers MAGE-A10ᶜ⁷⁹⁶T for Urothelial Cancer, Melanoma or Head and Neck Cancers MGH Open D
NCT02465060 NCI-MATCH: Targeted Therapy Directed by Genetic Testing in Treating Patients With Advanced Refractory Solid Tumors, Lymphomas, or Multiple Myeloma NCI-MATCH: Targeted Therapy Directed by Genetic Testing in Treating Patients With Advanced Refractory Solid Tumors, Lymphomas, or Multiple Myeloma MGH Open D
Trial Status: Showing Results: 1-10 of 18 Per Page:
12Next »
Our Bladder Cancer Team

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