 This will be a case-based approach towards supra-tentorial gliomas. Case 1 was a 20-year-old gentleman who had presented with few episodes of seizures and had been on anti-epileptics. And these are the images. So that's the T1 axial, that is a T2 axial flare diffusion ADC, T1 post-contrast gradient and RCVP map. So what we can see on a T2 axial is that we have a homogeneously T2 hyper-intense lesion which is near-completely suppressed on flare with some persistent peripheral rim of flare hyper-intensity. Yes, perfect. So what does that suggest? What does a T2 flare mismatch suggest? A T2 flare mismatch may not indicate aggressiveness of a tumor that would be more suggested by something like necrosis and hemorrhage, anything more that you can suggest. Because the T2 flare mismatch finding which you just mentioned is considered to be quite specific for this entity and can help one make a prospective molecular diagnosis of this neoplasm. It is an IDH mutant astrocytoma. So remember as per the WHO 2021 CNS-5 classification, there is no IDH mutant glioblastoma anymore. It has to be an astrocytoma and it is IDH mutant astrocytoma. Anything more that you would like to add here, any more markers or a molecular landscape that one can prospectively predict on this imaging feature of T2 flare mismatch? That it is a 1P19Q non-co-deleted IDH mutant astrocytoma. So like you all mentioned, this is obviously an IDH mutant astrocytoma, a WHO grade 2 neoplasm. Again, as per the newer classification, the grading has to use Arabic numerals and not the Roman numerals. So what we have is a tumor which is homogeneously hyperintense on T2 gets partially suppressed on flare with a persistence of peripheral rim on flare which doesn't show any post-contrast enhancement without any bleed. So that's the gradient, no blooming. So there is no bleed. And again on RCBV maps, the tumor is ISO2 hypoperfused without any restricted diffusion. In case one encounters some areas of hyperperfusion on RCBV maps, this can be considered a higher grade IDH mutant astrocytoma, something like a WHO grade 3 IDH mutant astrocytoma. So again to quickly summarize, again as per the WHO 2021 classification, the terminologies like anaplastic astrocytoma or IDH mutant glioblastomas don't exist anymore. These are usually WHO grade 2 to grade 4 neoplasms, so grade 4 IDH mutant astrocytoma would be something which would have areas of hemorrhage, necrosis or even irregular heterogeneous post-contrast enhancement. Again, another feature on MRI which one may encounter especially on 3 tesla imaging or higher fission imaging on MR spectroscopy is the presence of 2 hydroxyglutarate peak at 2.25 parts per million, which can be considered to be suggesting an IDH mutant astrocytoma. On histopathology, higher rate tumors can have necrosis and microvascular proliferation and when these tumors or these features are encountered, these tumors would be labeled IDH mutant grade 4 astrocytoma. Another important genetic or molecular marker here is the homozygous deletion of CDKN 2AB gene. So again, even if there is no necrosis present in the tumor or even in the absence of microvascular proliferation, but when this homozygous deletion or this copy number mutation is positive, this tumor would be termed a grade 4 astrocytoma because this is a harbinger of a far worse prognosis than the absence of this mutation. Moving on, next case was a 44-year-old lady who presented with geediness of one month duration and these are the images. So T2 axial first image, that's T1 post contrast, that's a gradient-based or T2 star-based perfusion sequence, RCBB map, again a gradient sequence and RCBB values. One can say that is a fair diagnosis, a GBM, a glioblastoma because we can appreciate that the RCBB values are very high to the tune of 7, but that being said, what one can appreciate here is that this is a cortical-based neoplasm which is heterogeneous in appearance on T2 images, shows heterogeneous post-contrast enhancement. In addition, on gradient images you can see these linear areas of calcification because these are blooming, so these are nothing but the chicken wire calcification which are considered to be a characteristic of this neoplasm and in this case, this neoplasm is nothing but an oligodendroglioma, so if one has a cortical-based neoplasm with linear chicken wire calcifications with elevated RCBB which is by virtue of presence of extensive chicken wire capillary networks and not the new angiogenesis of a glioblastoma, then one should consider a diagnosis of oligodendroglioma which is IDH mutant and in this case, when you say a diagnosis of oligodendroglioma, it is implied that it is associated with 1P19Q co-deletion, so that is oligodendroglioma. Again, a companion case on a CT scan wherein you can appreciate the chicken wire calcification associated with an oligodendroglioma on a CT scan. So, again this is another tumor wherein if you see all these features, one can prospectively make a diagnosis of its molecular landscape of the tumor. So, again earlier two subtypes of the tumors were described which included well differentiated and anaplastic oligodendroglioma which is no more the case with the WHO-2021 CNS tumor classification. So, oligodendroglioma is an IDH mutant and 1P19Q co-deleted tumor most commonly located in the frontal lobes is cortical based, usually present between age of 4 to 6 decades and all tumors usually present with similar clinical features of seizures or focal neurological deficits especially when these are present in close proximity to the cortex. Again, these have IDH mutation like the IDH mutant astrocytoma, so can demonstrate the two hydroxyglutarate peak on MR spectroscopy at 3 tesla or higher have 1P19Q co-deletion. Median survival is the best amongst any of the diffuse glial neoplasms at about 10 to 12 years and on CT about 70 percent of oligodendrogliomas would demonstrate the chicken wire calcification. On MRI the tumor is classically T1 hypo intense, T2 hyper intense with linear areas of blooming on gradient of or susceptibility weighted images owing to chicken wire calcification. Differential diagnosis would of course include an astrocytoma or even a glioblastoma or an extraventricular neurocytoma. Moving on to next case of 52 years old gentleman who had few episodes of headache and vomiting and short term memory loss and these are the CT scan images on your left these are the non-contrast images and on the right are the contrast enhance CD scan images. So, any takers for this? So, yes, so we have a large tumor which is crossing the midline extending across the corpus callosum from the left side on to the right and showing heterogeneity by virtue of presence of this hyper density which is seconded to hemorrhage. And again this tumor shows this irregular peripheral rind of enhancement which is also a diagnostic clue towards a high grade glioblastom. So, tumor which is crossing midline has areas of necrosis and hemorrhage and it has a so called butterfly appearance of glioma is nothing but a glioblastoma. Again MRI in the same patient on T1 weighted images one can appreciate the T1 hyper intensities because of hemorrhage within the tumor lot of necrotic areas peripheral hemocydrin staining and peripheral irregular thick rind of enhancement which is crossing the midline giving rise to the butterfly glioma appearance. So, this is nothing but an IDH wild type of glioblastoma. So, this is a grade 4 neoplasm another companion case a glioblastoma which is present in the right temporal lobe which shows heterogeneous appearance on T2. So, sorry that is T2 that is the T1 and which has hyper intensities on T1 weighted images because of presence of hemorrhage within and shows heterogeneous post contrast enhancement associated with extensive mass effect effacement of adjacent sulchi, sylvian fissures, midline shift, transcentralization all pointing towards a diagnosis of a high grade glioblastom again elevated RCB values like a glioblastoma multi-form. So, glioblastoma IDH wild type CT scan appearance would be heterogeneous with areas of hemorrhage and necrosis MRI the tumor is usually hyper intense on T1 and hyper intense on T2 with peripheral hemocydrin staining or dark areas on gradient sequences as well as T2 sequences. MR spectroscopy would show elevated choline level which is a marker of cell membrane turnover which would naturally be elevated in any patients with brain tumor undergoing a high cell turnover in a bit like to be elevated in these patients because of presence of necrosis. On histopathology a presence of microvascular proliferation as well as necrosis can be an indicator of IDH wild type of glioma. The genetic mutations in the absence of features like microvascular proliferation could be another indicator of the aggressiveness of this tumor these include the third promoter gene mutation EGFR amplification and chromosome 7 gain or chromosome 10 loss together. So, to summarize the adult type of diffuse gliomas as far as WHO 2021 classification is concerned IDH is the main driver mutation which drives the adult type of diffuse gliomas. So, if there is an IDH mutation one has to look for what is known as ATRX protein on immunohistochemistry or 1P19Q retention or homozygous deletion. So, if there is a homozygous deletion of 1P19Q naturally it is an oligodendroglioma as was discussed earlier. If not then one has to look at CDK and 2AB homozygous deletion or non mutation. So, if there is no mutation then it would be an IDH mutant type of grade 2 or grade 3 astrocytoma. If there is mutation even whether regardless of presence of microvascular proliferation or necrosis it would be an IDH mutant grade 4 astrocytoma. Then if the tumor is not IDH mutant but has features of microvascular proliferation or necrosis or third promoter mutation or EGFR amplification or combined loss of a gain of chromosome 7 and a loss of chromosome 10 that would imply that this is an IDH wild type of glioblastoma.