S18 Ep48: OncoBytes Adaptive Learning Pathways™: Decoding Precision Diagnostics and Targeted Therapies in Glioma

Today we're gonna talk about the treatment options for first-line treatment of, uh, low-grade gliomas in adults.

So we cannot start without talking about the surgical management of these tumors.

It remains the mainstay of management, and we always aim for maximal safe resection while preserving the neurological function.

Of course, we talk about the extent of resection.

This matters.

It matters because we want less of the tumor left behind.

It matters because, um, less tumor means less radiation field and hopefully also less neurological dysfunction as, as, um, uh, long as it's done safely.

And to achieve that, there's plenty of intraoperative techniques, um, as well as, like, topography, functional MRIs, intraoperative monitoring.

All of these are used to maximize that ability to recognize tumor intraoperatively to be able to get more of that tumor, um, safely.

And of course, there's always the question, um, of supramaximal resection.

You know, this remains a controversy, and some people, um, will reside to supramaximal resections as long as it's done safely.

Um, as some studies have shown, some delayed recurrences, delayed malignant transformation, as well as seizure control, um, it, it can affect, um, those outcomes as well.

Um, and radiotherapy, um, which had been, uh, the first step that we usually get after, after surgery, especially in what we used to think of as high-risk patients in low-grade gliomas, those who had a large residual going back to the first slide of, you know, we want the most of the tumor out.

We also used, um, age cutoff, so patients who were older than 40 we used to be, uh, thought of as high risk, and people who had neurological dysfunction besides seizures.

So these people used to go directly into radiotherapy after surgery, um, although the patients who were-- did not have those high-risk features could wait and not get radiation till recurrence.

Obviously, all of this has changed, um, in the era of IDH inhibitors, which we're gonna touch upon in, in, in the next slides.

Radiation modalities have also changed in the recent years.

Back in the day, everybody used to get r- you know, conventional radiation, and the-- of course, the, the elephant in the room with that was the fear of cognitive impairment for these usually young patients still in their func- uh, in their functional year, in their, in their prime years.

And, uh, doing radiation could affect their, um, cognition, um, in the, in the next, uh, in the following years.

Adjuvant therapy, again, the classic teachings we're just touching upon, whether with temozolomide or procarbazine, CCNU, and vincristine.

And as we know, the choice of temozolomide in astrocytic tumors versus PCV in oligodendrogliomas.

And this brings us to the targeted therapy shift, um, that happened at the, in the recent years.

And we have to touch upon the INDIGO trial and vorasidenib.

Of course, when we talk about vorasidenib, we're talking about a dual oral inhibitor targeting mutant IDH1 and two enzymes.

And this was studied on a large scale in a phase three trial, the INDIGO trial, that randomized three hundred and thirty-one patients to receiving, um, vorasidenib versus not.

Today we're gonna talk about the treatment options for first-line treatment of, uh, low-grade gliomas in adults.

So we cannot start without talking about the surgical management of these tumors.

It remains the mainstay of management, and we always aim for maximal safe resection while preserving the neurological function.

Of course, we talk about the extent of resection.

This matters.

It matters because we want less of the tumor left behind.

It matters because, um, less tumor means less radiation field and hopefully also less neurological dysfunction as, as, um, uh, long as it's done safely.

And to achieve that, there's plenty of intraoperative techniques, um, as well as, like, topography, functional MRIs, intraoperative monitoring.

All of these are used to maximize that ability to recognize tumor intraoperatively to be able to get more of that tumor, um, safely.

And of course, there's always the question, um, of supramaximal resection.

You know, this remains a controversy, and some people, um, will reside to supramaximal resections as long as it's done safely.

Um, as some studies have shown, some delayed recurrences, delayed malignant transformation, as well as seizure control, um, it, it can affect, um, those outcomes as well.

Um, and radiotherapy, um, which had been, uh, the first step that we usually get after, after surgery, especially in what we used to think of as high-risk patients in low-grade gliomas, those who had a large residual going back to the first slide of, you know, we want the most of the tumor out.

We also used, um, age cutoff, so patients who were older than 40 we used to be, uh, thought of as high risk, and people who had neurological dysfunction besides seizures.

So these people used to go directly into radiotherapy after surgery, um, although the patients who were-- did not have those high-risk features could wait and not get radiation till recurrence.

Obviously, all of this has changed, um, in the era of IDH inhibitors, which we're gonna touch upon in, in, in the next slides.

Radiation modalities have also changed in the recent years.

Back in the day, everybody used to get r- you know, conventional radiation, and the-- of course, the, the elephant in the room with that was the fear of cognitive impairment for these usually young patients still in their func- uh, in their functional year, in their, in their prime years.

And, uh, doing radiation could affect their, um, cognition, um, in the, in the next, uh, in the following years.

Adjuvant therapy, again, the classic teachings we're just touching upon, whether with temozolomide or procarbazine, CCNU, and vincristine.

And as we know, the choice of temozolomide in astrocytic tumors versus PCV in oligodendrogliomas.

And this brings us to the targeted therapy shift, um, that happened at the, in the recent years.

And we have to touch upon the INDIGO trial and vorasidenib.

Of course, when we talk about vorasidenib, we're talking about a dual oral inhibitor targeting mutant IDH1 and two enzymes.

And this was studied on a large scale in a phase three trial, the INDIGO trial, that randomized three hundred and thirty-one patients to receiving, um, vorasidenib versus not.