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Expand Collapse Thyroid Tumor  - General Description This year about 56,000 people in the U.S. (77% of them women) will be told by a doctor that they have thyroid cancer. About half of these new patients will be at least 50 years old. However, more than 500,000 patients with thyroid cancer remain alive today.

The thyroid is a butterfly-shaped gland found at the base of the throat, near the windpipe (trachea). The 2 wings (lobes) of the thyroid are connected by a thin piece of tissue called the isthmus. The thyroid uses iodine from food and iodized salts to make hormones that control the heart rate, body temperature, the speed with which food is changed into energy (metabolism) and the level of calcium in the blood. Based on their appearance under the microscope, the 4 main types of thyroid cancer are papillary, follicular, medullary and anaplastic. For treatment purposes, thyroid cancers are often classified as differentiated (papillary or follicular) or poorly differentiated (medullary or anaplastic). If a cancer cell is well-differentiated, it has most of the characteristics of a normal cell. On the other hand, poorly differentiated cancer cells don't look like normal cells.

Follicular thyroid cancer is a slow-growing cancer that forms in follicular cells, which are epithelial cells that take up iodine and make certain thyroid hormones. Papillary thyroid cancer, which appears as finger-like shapes under the microscope, also begins in follicular cells and is slow-growing. It is the most common type of thyroid cancer, usually appearing before the age of 45 years. It is more common in women than in men. Medullary thyroid cancer accounts for about 4% of all thyroid cancers. It begins in C cells, which make calcitonin, a hormone that helps keep calcium at the right level in the blood. Anaplastic thyroid cancer is a rare, aggressive form of cancer whose cells don't look at all like normal thyroid cells.

Thyroid 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 places to which thyroid cancer spreads are the lungs, liver, and bones.

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 can also be performed to determine if the cancer has spread. These include chest x-rays, ultrasound and CT scans.

The FDA has approved the targeted therapy vandetanib (Capreisa) for treatment of medullary thyroid cancer that is locally advanced and can't be removed by surgery or that has metastasized. No targeted therapies are yet available for treatment of anaplastic thyroid cancer. Therefore, novel therapies and treatment strategies are needed.

Source: National Cancer Institute, 2012
Thyroid cancer represents approximately 3% of new malignancies occurring annually in the United States, with an estimated 56,460 cancer diagnoses and 1,780 cancer deaths per year. Of these cancer diagnoses, 2% to 3% are medullary thyroid cancer (MTC).

MTC arises from the calcitonin-secreting parafollicular cells of the thyroid gland. MTC occurs in sporadic and familial forms and may be preceded by C-cell hyperplasia (CCH), although CCH is a relatively common abnormality in middle-aged adults.

Average survival for MTC is lower than that for more common thyroid cancers (e.g., 83% 5-year survival for MTC compared with 90-94% 5-year survival for papillary and follicular thyroid cancer). Survival is correlated with stage at diagnosis. Decreased survival in MTC can be accounted for, in part, by a high proportion of late-stage diagnoses.

In addition to early stage at diagnosis, other factors associated with improved survival in MTC include smaller tumor size, younger age at diagnosis, familial versus sporadic form and diagnosis by biochemical screening (i.e., screening for calcitonin elevation).

A Surveillance, Epidemiology, and End Results (SEER) population-based study of 1,252 MTC patients found that survival varied by extent of local disease. For example, the 10-year survival rates ranged from 95% for disease confined to the thyroid gland to 40% for those with distant metastases.

While the majority of MTC cases are sporadic, approximately 20-25% are hereditary because of mutations in the RET proto-oncogene. Mutations in the RET gene cause multiple endocrine neoplasia type 2 (MEN 2), an autosomal dominant disorder associated with a high lifetime risk of MTC. Multiple endocrine neoplasia type 1 (MEN 1) is an autosomal dominant endocrinopathy that is genetically and clinically distinct from MEN 2. However, the similar nomenclature for MEN 1 and MEN 2 may cause confusion. Of note, there is no increased risk of thyroid cancer for MEN 1.

Historically, MEN 2 has been classified into three subtypes based on the presence or absence of certain endocrine tumors in the individual or family:

- MEN 2A
- Familial medullary thyroid carcinoma (FMTC)
- MEN 2B

All three subtypes impart a high risk of developing MTC. MEN 2A has an increased risk of pheochromocytoma and parathyroid adenoma and/or hyperplasia. MEN 2B has an increased risk of pheochromocytoma and includes additional clinical features such as mucosal neuromas of the lips and tongue, distinctive faces with enlarged lips, ganglioneuromatosis of the gastrointestinal tract and an asthenic Marfanoid body habitus. FMTC has been defined as the presence of at least four individuals with MTC without any other signs or symptoms of pheochromocytoma or hyperparathyroidism in the proband or other family members.

Some families previously classified as FMTC will go on to develop one or more of the MEN 2A-related tumors, suggesting that FMTC is simply a milder variant of MEN 2A. Offspring of affected individuals have a 50% chance of inheriting the gene mutation.

The age of onset of MTC varies in different subtypes of MEN 2. MTC typically occurs in early childhood for MEN 2B, predominantly early adulthood for MEN 2A and middle age for FMTC.

DNA-based germline testing of the RET gene (chromosomal region 10q11.2) identifies disease-causing mutations in more than 95% of individuals with MEN 2A and MEN 2B and in about 88% of individuals with FMTC.

Source: National Cancer Institute, 2012
This year about 56,000 people in the U.S. (77% of them women) will be told by a doctor that they have thyroid cancer. About half of these new patients will be at least 50 years old. However, more than 500,000 patients with thyroid cancer remain alive today.

The thyroid is a butterfly-shaped gland found at the base of the throat, near the windpipe (trachea). The 2 wings (lobes) of the thyroid are connected by a thin piece of tissue called the isthmus. The thyroid uses iodine from food and iodized salts to make hormones that control the heart rate, body temperature, the speed with which food is changed into energy (metabolism) and the level of calcium in the blood. Based on their appearance under the microscope, the 4 main types of thyroid cancer are papillary, follicular, medullary and anaplastic. For treatment purposes, thyroid cancers are often classified as differentiated (papillary or follicular) or poorly differentiated (medullary or anaplastic). If a cancer cell is well-differentiated, it has most of the characteristics of a normal cell. On the other hand, poorly differentiated cancer cells don't look like normal cells.

Follicular thyroid cancer is a slow-growing cancer that forms in follicular cells, which are epithelial cells that take up iodine and make certain thyroid hormones. Papillary thyroid cancer, which appears as finger-like shapes under the microscope, also begins in follicular cells and is slow-growing. It is the most common type of thyroid cancer, usually appearing before the age of 45 years. It is more common in women than in men. Medullary thyroid cancer accounts for about 4% of all thyroid cancers. It begins in C cells, which make calcitonin, a hormone that helps keep calcium at the right level in the blood. Anaplastic thyroid cancer is a rare, aggressive form of cancer whose cells don't look at all like normal thyroid cells.

Thyroid 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 places to which thyroid cancer spreads are the lungs, liver, and bones.

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 can also be performed to determine if the cancer has spread. These include chest x-rays, ultrasound and CT scans.

The FDA has approved the targeted therapy vandetanib (Capreisa) for treatment of medullary thyroid cancer that is locally advanced and can't be removed by surgery or that has metastasized. No targeted therapies are yet available for treatment of anaplastic thyroid cancer. Therefore, novel therapies and treatment strategies are needed.

Source: National Cancer Institute, 2012
Thyroid cancer represents approximately 3% of new malignancies occurring annually in the United States, with an estimated 56,460 cancer diagnoses and 1,780 cancer deaths per year. Of these cancer diagnoses, 2% to 3% are medullary thyroid cancer (MTC).

MTC arises from the calcitonin-secreting parafollicular cells of the thyroid gland. MTC occurs in sporadic and familial forms and may be preceded by C-cell hyperplasia (CCH), although CCH is a relatively common abnormality in middle-aged adults.

Average survival for MTC is lower than that for more common thyroid cancers (e.g., 83% 5-year survival for MTC compared with 90-94% 5-year survival for papillary and follicular thyroid cancer). Survival is correlated with stage at diagnosis. Decreased survival in MTC can be accounted for, in part, by a high proportion of late-stage diagnoses.

In addition to early stage at diagnosis, other factors associated with improved survival in MTC include smaller tumor size, younger age at diagnosis, familial versus sporadic form and diagnosis by biochemical screening (i.e., screening for calcitonin elevation).

A Surveillance, Epidemiology, and End Results (SEER) population-based study of 1,252 MTC patients found that survival varied by extent of local disease. For example, the 10-year survival rates ranged from 95% for disease confined to the thyroid gland to 40% for those with distant metastases.

While the majority of MTC cases are sporadic, approximately 20-25% are hereditary because of mutations in the RET proto-oncogene. Mutations in the RET gene cause multiple endocrine neoplasia type 2 (MEN 2), an autosomal dominant disorder associated with a high lifetime risk of MTC. Multiple endocrine neoplasia type 1 (MEN 1) is an autosomal dominant endocrinopathy that is genetically and clinically distinct from MEN 2. However, the similar nomenclature for MEN 1 and MEN 2 may cause confusion. Of note, there is no increased risk of thyroid cancer for MEN 1.

Historically, MEN 2 has been classified into three subtypes based on the presence or absence of certain endocrine tumors in the individual or family:

- MEN 2A
- Familial medullary thyroid carcinoma (FMTC)
- MEN 2B

All three subtypes impart a high risk of developing MTC. MEN 2A has an increased risk of pheochromocytoma and parathyroid adenoma and/or hyperplasia. MEN 2B has an increased risk of pheochromocytoma and includes additional clinical features such as mucosal neuromas of the lips and tongue, distinctive faces with enlarged lips, ganglioneuromatosis of the gastrointestinal tract and an asthenic Marfanoid body habitus. FMTC has been defined as the presence of at least four individuals with MTC without any other signs or symptoms of pheochromocytoma or hyperparathyroidism in the proband or other family members.

Some families previously classified as FMTC will go on to develop one or more of the MEN 2A-related tumors, suggesting that FMTC is simply a milder variant of MEN 2A. Offspring of affected individuals have a 50% chance of inheriting the gene mutation.

The age of onset of MTC varies in different subtypes of MEN 2. MTC typically occurs in early childhood for MEN 2B, predominantly early adulthood for MEN 2A and middle age for FMTC.

DNA-based germline testing of the RET gene (chromosomal region 10q11.2) identifies disease-causing mutations in more than 95% of individuals with MEN 2A and MEN 2B and in about 88% of individuals with FMTC.

Source: National Cancer Institute, 2012
Expand Collapse ATR  - General Description
CLICK IMAGE FOR MORE INFORMATION
The protein encoded by ATR is a serine/threonine kinase and DNA damage sensor, activating cell cycle checkpoint signaling and causing a pause in the cell cycle following DNA replication stress or damage. The activated protein can phosphorylate and activate several important proteins that are involved in the inhibition of DNA replication and cell division, which are critical for DNA repair.

The maintenance of intact, correctly sequenced DNA is vital to the life of a cell. If there are mistakes made in replicating DNA before cell division, subsequent daughter cells will have inaccurate or damaged DNA, and may either die or carry mutations that can contribute to the development of cancer. For this reason, cells have evolved multiple pathways to repair mistakes in-or damage to- DNA. The specific repair pathway used by the cell depends on the type of DNA damage that has occurred. The types of DNA repair that we are focusing on relate directly to cancer. These involve a break in BOTH strands of DNA, which can be the result of ionizing radiation or other DNA damaging agents. This type of DNA damage is called Double Strand Breaks (DSB's). There are two main pathways used by cells to repair DSB's in DNA, one is Homologous Recombination (HR), the other is Non-Homologous End Joining (NHEJ). This page of our website focuses on the HR pathway (there is a separate web page for NHEJ repair if you select PKcs from the gene list when you sign on to this page).

Many proteins are involved in the complex HR pathway to repair DSB's in DNA. There is a graphic above that depicts the HR pathway (if you click on the graphic, it will enlarge and become a bit easier to follow). While complicated, the DSB at the top right of the graphic is acted upon by a series of proteins in the circle of steps shown that ultimately lead to the complete and accurate repair of the DSB in the DNA.

Some of the proteins involved in the HR DSB repair pathway are MRE11, NBS1, RAD50. These three proteins make up the MRN complex. This complex detects DSB's in the DNA. Once the DSB is found by the MRN complex, the MRN complex functions with BRCA1 and CtIP to resect the DSB’s to form single stranded DNA “tails”. Meanwhile, DSB's also activate the ATM protein, which in turn acts upon CHK2 to activate it, as well as directly activating the tumor suppressor TP53. TP53 can cause cell cycle delay, giving the cell time to repair DNA breaks or mistakes before the cell cycle leading to division resumes. In the next step, RPA binds to the single stranded DNA "tails" that have been created by BRCA1 and CtIP in conjunction with the MRN. The binding of RPA activates another protein called ATR. ATR has many important functions, including activating CHK1, which can cause cell cycle delay giving cells time to repair DNA. ATR also regulates BRCA1 which recruits a bound group of proteins including PALB2/BRCA2/RAD51. In the next step, RAD51 displaces the RPA that is on the single stranded DNA, with the involvement of BRCA2/PALB2 and RAD51c. BRCA1/BARD1 helps RAD51 coated single stranded DNA invade double stranded DNA with homologous sequences to form a DNA repair loop. With the help of DNA polymerases, the repair loop creates the opportunity to use the intact homologous DNA as a template to correctly repair DSB’s. Enzymes called ligases reconnect the ends of the DNA, leading to complete and accurate repair of the DSB in DNA.

After studying familial cancer syndromes, germline or inherited BRCA1 and BRCA2 were identified a while ago as proteins that when altered by mutation, cause certain cancers. Some BRCA1 and BRCA2 genes become mutated somatically, meaning in a non-inherited way. When either gene is mutated, the resulting protein cannot perform its role in DNA repair correctly. This turns out to be true for other proteins in the HR pathway as well. Recently, scientists have found mutations in many of the other genes that encode the proteins involved in the HR pathway. Mutations in HR pathway members include MRE11, NBS1, RAD50, ATM, CHK2, BRCA1, PALB2, RAD51, BRCA2, BARD1, and RAD51c (these are depicted in red in the above graphic). This remarkable number of mutations in proteins involved in the DNA repair pathway found in cancer highlights how important the HR DSB DNA repair pathway is in cells. The mutations in HR pathway proteins result in proteins that do not function properly in their role in DNA repair. Without proper function of the proteins involved in DNA repair, DNA mistakes or breaks are not properly repaired, and the damaged DNA contributes to the development of cancer.

ATR is only rarely mutated in cancer, however, the frequent mutations in ATM result in cells that are completely reliant on the ATR pathway to repair DSB's in the DNA. This has therapeutic implications for treatment of tumors that have mutations in the HR DNA repair pathway.

Testing for mutations in the many genes/proteins involved in DNA repair discussed above is available in the MGH genetics lab. Treatment as well as clinical trials studying new drugs that target defects in these proteins-including ATR- are available at the MGH Cancer Center.

The protein encoded by ATR is a serine/threonine kinase and DNA damage sensor, activating cell cycle checkpoint signaling and causing a pause in the cell cycle following DNA replication stress or damage. The activated protein can phosphorylate and activate several important proteins that are involved in the inhibition of DNA replication and cell division, which are critical for DNA repair.

The maintenance of intact, correctly sequenced DNA is vital to the life of a cell. If there are mistakes made in replicating DNA before cell division, subsequent daughter cells will have inaccurate or damaged DNA, and may either die or carry mutations that can contribute to the development of cancer. For this reason, cells have evolved multiple pathways to repair mistakes in-or damage to- DNA. The specific repair pathway used by the cell depends on the type of DNA damage that has occurred. The types of DNA repair that we are focusing on relate directly to cancer. These involve a break in BOTH strands of DNA, which can be the result of ionizing radiation or other DNA damaging agents. This type of DNA damage is called Double Strand Breaks (DSB's). There are two main pathways used by cells to repair DSB's in DNA, one is Homologous Recombination (HR), the other is Non-Homologous End Joining (NHEJ). This page of our website focuses on the HR pathway (there is a separate web page for NHEJ repair if you select PKcs from the gene list when you sign on to this page).

Many proteins are involved in the complex HR pathway to repair DSB's in DNA. There is a graphic above that depicts the HR pathway (if you click on the graphic, it will enlarge and become a bit easier to follow). While complicated, the DSB at the top right of the graphic is acted upon by a series of proteins in the circle of steps shown that ultimately lead to the complete and accurate repair of the DSB in the DNA.

Some of the proteins involved in the HR DSB repair pathway are MRE11, NBS1, RAD50. These three proteins make up the MRN complex. This complex detects DSB's in the DNA. Once the DSB is found by the MRN complex, the MRN complex functions with BRCA1 and CtIP to resect the DSB’s to form single stranded DNA “tails”. Meanwhile, DSB's also activate the ATM protein, which in turn acts upon CHK2 to activate it, as well as directly activating the tumor suppressor TP53. TP53 can cause cell cycle delay, giving the cell time to repair DNA breaks or mistakes before the cell cycle leading to division resumes. In the next step, RPA binds to the single stranded DNA "tails" that have been created by BRCA1 and CtIP in conjunction with the MRN. The binding of RPA activates another protein called ATR. ATR has many important functions, including activating CHK1, which can cause cell cycle delay giving cells time to repair DNA. ATR also regulates BRCA1 which recruits a bound group of proteins including PALB2/BRCA2/RAD51. In the next step, RAD51 displaces the RPA that is on the single stranded DNA, with the involvement of BRCA2/PALB2 and RAD51c. BRCA1/BARD1 helps RAD51 coated single stranded DNA invade double stranded DNA with homologous sequences to form a DNA repair loop. With the help of DNA polymerases, the repair loop creates the opportunity to use the intact homologous DNA as a template to correctly repair DSB’s. Enzymes called ligases reconnect the ends of the DNA, leading to complete and accurate repair of the DSB in DNA.

After studying familial cancer syndromes, germline or inherited BRCA1 and BRCA2 were identified a while ago as proteins that when altered by mutation, cause certain cancers. Some BRCA1 and BRCA2 genes become mutated somatically, meaning in a non-inherited way. When either gene is mutated, the resulting protein cannot perform its role in DNA repair correctly. This turns out to be true for other proteins in the HR pathway as well. Recently, scientists have found mutations in many of the other genes that encode the proteins involved in the HR pathway. Mutations in HR pathway members include MRE11, NBS1, RAD50, ATM, CHK2, BRCA1, PALB2, RAD51, BRCA2, BARD1, and RAD51c (these are depicted in red in the above graphic). This remarkable number of mutations in proteins involved in the DNA repair pathway found in cancer highlights how important the HR DSB DNA repair pathway is in cells. The mutations in HR pathway proteins result in proteins that do not function properly in their role in DNA repair. Without proper function of the proteins involved in DNA repair, DNA mistakes or breaks are not properly repaired, and the damaged DNA contributes to the development of cancer.

ATR is only rarely mutated in cancer, however, the frequent mutations in ATM result in cells that are completely reliant on the ATR pathway to repair DSB's in the DNA. This has therapeutic implications for treatment of tumors that have mutations in the HR DNA repair pathway.

Testing for mutations in the many genes/proteins involved in DNA repair discussed above is available in the MGH genetics lab. Treatment as well as clinical trials studying new drugs that target defects in these proteins-including ATR- are available at the MGH Cancer Center.



PubMed ID's
27617969, 24003211, PMC2988877
Expand Collapse ATR  in Thyroid Tumor
Alterations in the gene encoding ATR are not found in cancers of the thyroid. ATR is an important protein in the DNA repair pathway. ATR controls a signaling pathway in the cell by activating CHK1, which causes a delay in the cell cycle (see graphic above). Without this delay, cells would not have time to repair broken or damaged DNA. The accumulation of damaged DNA in the cell can lead to cancer.

ATR has become an important protein to inhibit with drugs in cancer. Cancer cells often have genetic alterations in other proteins in the DNA repair pathway (see red proteins in graphic above). If the ATM protein is mutated and unable to cause cell cycle arrest for DNA repair, then ATR is the only option for cancer cells to use to delay the cell cycle and repair DNA. Drugs targeting ATR block this pathway, leaving cancer cells no way to pause the cell cycle to achieve DNA repair. The tumor cells die as the result of accumulated damaged or broken DNA.

Alterations in the gene encoding ATR are not found in cancers of the thyroid. ATR is an important protein in the DNA repair pathway. ATR controls a signaling pathway in the cell by activating CHK1, which causes a delay in the cell cycle (see graphic above). Without this delay, cells would not have time to repair broken or damaged DNA. The accumulation of damaged DNA in the cell can lead to cancer.

ATR has become an important protein to inhibit with drugs in cancer. Cancer cells often have genetic alterations in other proteins in the DNA repair pathway (see red proteins in graphic above). If the ATM protein is mutated and unable to cause cell cycle arrest for DNA repair, then ATR is the only option for cancer cells to use to delay the cell cycle and repair DNA. Drugs targeting ATR block this pathway, leaving cancer cells no way to pause the cell cycle to achieve DNA repair. The tumor cells die as the result of accumulated damaged or broken DNA.

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 all 5 results Per Page:
Protocol # Title Location Status Match
NCT00585195 A Study Of Oral PF-02341066, A C-Met/Hepatocyte Growth Factor Tyrosine Kinase Inhibitor, In Patients With Advanced Cancer A Study Of Oral PF-02341066, A C-Met/Hepatocyte Growth Factor Tyrosine Kinase Inhibitor, In Patients With Advanced Cancer MGH Open D
NCT02303444 An Observational Study in Differentiated Thyroid Cancer Which is Radioactive Iodine (RAI) Refractory to Assess the Use of Multikinase Inhibitors An Observational Study in Differentiated Thyroid Cancer Which is Radioactive Iodine (RAI) Refractory to Assess the Use of Multikinase Inhibitors MGH Open D
NCT02568267 Basket Study of Entrectinib (RXDX-101) for the Treatment of Patients With Solid Tumors Harboring NTRK 1/2/3 (Trk A/B/C), ROS1, or ALK Gene Rearrangements (Fusions) Basket Study of Entrectinib (RXDX-101) for the Treatment of Patients With Solid Tumors Harboring NTRK 1/2/3 (Trk A/B/C), ROS1, or ALK Gene Rearrangements (Fusions) MGH Open D
NCT02393690 Iodine I-131 With or Without Selumetinib in Treating Patients With Recurrent or Metastatic Thyroid Cancer Iodine I-131 With or Without Selumetinib in Treating Patients With Recurrent or Metastatic Thyroid Cancer 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
MGH has many open clinical trials for other cancers not shown on the Targeted Cancer Care website. They can be found on the MassGeneral.org clinical trials search page.

Additional clinical trials may be applicable to your search criteria, but they may not be available at MGH. These clinical trials can typically be found by searching the clinicaltrials.gov website.
Trial Status: Showing all 5 results Per Page:

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