摘要:
The invention provides anti-human pro-epiregulin and anti-human amphiregulin antibodies and methods of using the same. Anti-EREG antibodies raised against amino acids 148-169 and 156-169 of the human EREG protein, and anti-AREG antibodies raised against amino acids 238-252 of the human AREG protein are disclosed. Methods of using these antibodies to detect EREG and AREG and kits and other products for performing such methods are also disclosed.
摘要:
Provided herein are methods of analyzing stage II colorectal cancer (CRC) samples (such as those that are mis-match repair proficient, pMMR), by scoring G-alpha interacting vesicle associated protein (GIV, also known as girdin) full-length (GIV-fl) expression in combination with lymphovascular invasion (LVI) status or clinical variables. The disclosed methods can be used to identify GIV-fl expressing tumors that are likely to recur (high risk) and those that are not likely to recur (high risk). Subjects identified as having a high risk CRC can be selected to receive chemotherapy or biotherapy for the CRC. Thus, in some examples, the disclosed methods can be used to identify CRC tumors that are likely to respond to chemotherapy or biotherapy. Also provided are computer implemented methods, systems, and kits that can be used with these methods.
摘要:
The invention provides anti-human pro-epiregulin and anti-human amphiregulin antibodies and methods of using the same. Anti-EREG antibodies raised against amino acids 148-169 and 156-169 of the human EREG protein, and anti-AREG antibodies raised against amino acids 238-252 of the human AREG protein are disclosed. Methods of using these antibodies to detect EREG and AREG and kits and other products for performing such methods are also disclosed.
摘要:
The invention provides anti-human pro-epiregulin and anti-human amphiregulin antibodies and methods of using the same. Anti-EREG antibodies raised against amino acids 148-169 and 156-169 of the human EREG protein, and anti-AREG antibodies raised against amino acids 238-252 of the human AREG protein are disclosed. Methods of using these antibodies to detect EREG and AREG and kits and other products for performing such methods are also disclosed.
摘要:
The invention provides anti-human pro-epiregulin and anti-human amphiregulin antibodies and methods of using the same. Anti-EREG antibodies raised against amino acids 148-169 and 156-169 of the human EREG protein, and anti-AREG antibodies raised against amino acids 238-252 of the human AREG protein are disclosed. Methods of using these antibodies to detect EREG and AREG and kits and other products for performing such methods are also disclosed.
摘要:
Methods and systems for predictive measures of anti-EGFR therapy response in wild type RAS/EGFR+ samples, e.g., histochemical staining methods for staining EGFR, AREG, and EREG, digital analysis of stained slides, and scoring algorithms that allow prediction of a response to anti-EGFR therapies. Analysis of the stained slides and scoring algorithms may include but are not limited to: a percent tumor cell positivity, computerized clustering algorithms, area density (e.g., area of tumor positive for one or more markers over total tumor area), average intensity (e.g., computerized methodology measuring average gray scale pixel intensity), average intensity broken down according to membrane, cytoplasmic, or punctate staining patterns), or any other appropriate parameter or combination of parameters. The methods of the present invention allow for resolving spatial expression patterns of the ligands and the receptor to determine what patterns are predictive for response to anti-EGFR therapies.
摘要:
The invention provides anti-human pro-epiregulin and anti-human amphiregulin antibodies and methods of using the same. Anti-EREG antibodies raised against amino acids 148-169 and 156-169 of the human EREG protein, and anti-AREG antibodies raised against amino acids 238-252 of the human AREG protein are disclosed. Methods of using these antibodies to detect EREG and AREG and kits and other products for performing such methods are also disclosed.
摘要:
A combination of mismatch repair (MMR) and Metastasis Associated in Colon Cancer 1 (MACC1) gene expression status of the patient serve as a basis for risk stratification of early stage colon cancer patients. Patients with defective MMR (dMMR) status have improved survival and do not benefit from 5-fluorouracil (5-FU) therapies. In contrast, patients with a proficient MMR (pMMR) status have a higher risk of recurrence and worse survival. The pMMR patients are then further stratified on the basis of MACC1 gene expression. Patients with a pMMR status and a low MACC1 expression have a favorable prognosis similar to patients having a dMMR status, whereas patients having a pMMR status and high MACC1 expression have a less favorable prognosis.