Gleevec (Imatinib)
| Property | Information |
|---|---|
| Drug Name | Gleevec (Imatinib) |
| FDA Approval | Yes (for chronic myelogenous leukemia and other cancers, not specifically approved for gliomas) |
| Used for | Investigational use in gliomas, specifically targeting overexpression of platelet-derived growth factor receptor (PDGFR) |
| Clinical Trial Phase | Exploratory/Investigational (Specific phase for gliomas not provided) |
| Clinical Trial Explanation | Not specified |
| Common Side Effects | Varies; for leukemia treatment includes fluid retention, nausea, muscle cramps, rashes, and fatigue. Brain tumor studies may have different profiles due to combination treatments and patient population. |
| OS without | Not specified |
| OS with | Not applicable; studies focusing on PFS-6 as a primary endpoint |
| PFS without | Not specified |
| PFS with | PFS-6 value was 53% in a restricted patient population with overexpression of PDGFR |
| Usefulness Rating | 3 |
| Usefulness Explanation | Not specified |
| Toxicity Level | 3 |
| Toxicity Explanation | Gleevec (Imatinib) is at a moderate toxicity level. This is because while it does have side effects such as fluid retention, nausea, muscle cramps, rashes, and fatigue, these are common to most treatments and they vary from patient to patient. Also, it has not been specifically approved for glioma treatment, indicating that it might have unexpected results, slightly increasing the risk factor. However, it has shown some potential benefits in early research, hence the moderate, not high, toxicity rating. |
Notes: Gleevec, known for its role in leukemia treatment, has shown potential in inhibiting glioma growth due to its targeting of PDGF. Its effectiveness in brain tumors has been limited, possibly due to issues crossing the blood-brain barrier and various resistance mechanisms. Its use has been explored in patients with recurrent tumors and PDGFR overexpression, showing some promise in early research.
From Ben Williams Book: Gleevec (also known as imatinib), a small molecule which targets a specific gene involved in the growth of a form of leukemia, received a great deal of publicity because of its unprecedented effectiveness. As will be discussed later, this general strategy of identifying the growth signals for tumor growth and then targeting those signals, or their receptors, is one of the major new areas in cancer research. Such growth signaling channels often are involved in several different types of cancer. Although Gleevec was developed specifically for chronic myelogenous leukemia, it also has been shown to inhibit a more general type of growth signal, platelet-derived growth factor (PDGF), which is also involved in the growth of gliomas and other forms of cancer (e.g., small- cell lung cancer). Laboratory research has supported the importance of this similarity in that gleevec has been shown to strongly inhibit glioma growth, with the result that there now have been a number of studies reporting its use with high-grade gliomas.
The generally disappointing results using gleevec for brain tumors may have occurred
for several different reasons. It may not readily cross the blood-brain-barrier, and it may engender different mechanisms of resistance than other treatment agents. In the study of gleevec for leukemia, for example, high levels of autophagy have been observed, which can be inhibited by the concurrent use of chloroquine or other autophagy inhibitors.
An important variation in the use of gleevec was to restrict its usage to patients with recurrent tumors who tested positive for overexpression of the platelet-derived growth factor receptor (90). PDGFR is overexpressed in 50-65% of tumors, especially tumors
labeled secondary glioblastomas, which are believed to have evolved from lower-grade
tumors (in contrast to de novo glioblastomas that occur without such evolution). For this
restricted patient population, the PFS-6 value was 53%.Property "Has original text" (as page type) with input value "Gleevec (also known as imatinib), a small molecule which targets a specific gene involved</br>in the growth of a form of leukemia, received a great deal of publicity because of its</br>unprecedented effectiveness. As will be discussed later, this general strategy of</br>identifying the growth signals for tumor growth and then targeting those signals, or their</br>receptors, is one of the major new areas in cancer research. Such growth signaling</br>channels often are involved in several different types of cancer. Although Gleevec was</br>developed specifically for chronic myelogenous leukemia, it also has been shown to</br>inhibit a more general type of growth signal, platelet-derived growth factor (PDGF),</br>which is also involved in the growth of gliomas and other forms of cancer (e.g., small-</br>cell lung cancer). Laboratory research has supported the importance of this similarity in</br>that gleevec has been shown to strongly inhibit glioma growth, with the result that there</br>now have been a number of studies reporting its use with high-grade gliomas.</br></br>The generally disappointing results using gleevec for brain tumors may have occurred</br></br>for several different reasons. It may not readily cross the blood-brain-barrier, and it may</br>engender different mechanisms of resistance than other treatment agents. In the study of</br>gleevec for leukemia, for example, high levels of autophagy have been observed, which</br>can be inhibited by the concurrent use of chloroquine or other autophagy inhibitors.</br></br>An important variation in the use of gleevec was to restrict its usage to patients with</br>recurrent tumors who tested positive for overexpression of the platelet-derived growth</br>factor receptor (90). PDGFR is overexpressed in 50-65% of tumors, especially tumors</br></br></br>labeled secondary glioblastomas, which are believed to have evolved from lower-grade</br>tumors (in contrast to de novo glioblastomas that occur without such evolution). For this</br>restricted patient population, the PFS-6 value was 53%." contains invalid characters or is incomplete and therefore can cause unexpected results during a query or annotation process.
