Standard neurosurgery for cerebral glioma requires maximal safe tumor resection. For low-grade tumors (WHO Grade II–III), maximal safe resection of the tumor confers an improved outcome without compromising functional outcomes. In the case of glioblastoma, the location of the bulk of the tumor relative to eloquent brain areas dictates the safest and most effective surgical approach.
Brain Tumor Type and WHO Grade | Invasive | Complete Resection Possible | Life Expectancy (Months) Biopsy | Life Expectancy (Months) MR Incomplete Resection | Life Expectancy (Months) MR Complete Resection | Survival Advantage (Months) with MR Complete Resection Compared to Incomplete Resection |
---|---|---|---|---|---|---|
I Neuronal DNET Ganglioglioma Pilocytic astrocytoma |
No | Yes; if outside eloquent structures | Prolonged | Prolonged | Prolonged | Uncertain: residual tumors require additional surgery |
II Low-grade astrocytoma and oligodendroglioma |
Yes | No | 61 | 90.5 | 29.5 | |
III Anaplastic astrocytoma and oligodendroglioma |
Yes | No | 64.9 | 75.2 | 10.3 | |
IV Glioblastoma multiforme |
Yes | No | 11.3 | 14.2 | 2.9 | |
9.4 † | 15.8 † | 6.4 [6] |
Convection-Enhanced Delivery | BBB Opening | Systemic Chemotherapy | |
---|---|---|---|
Drug delivery into brain tissue or lesion | During tissue infusion | During the opening of the BBB | Limited by the intact BBB |
MW of therapeutic agent | Large or small | Large or small | Small |
Brain–Blood Concentration | >100 × systemic concentration | ≤1 × systemic concentration | <1 × systemic concentration |
Hydrophilic compounds | Enters CNS | Enters CNS | <<<1 × systemic concentration |
Hydrophobic compounds | Enters CNS | Enters CNS | <1 × systemic concentration |
Distribution of Compound within CNS | Volume spreads radially from the infusion site | The volume of distribution rests in the arterial distributions injected with mannitol | Entire CNS |
The volume of the brain that can be treated | Large (4–8 cm3) | Large (4–8 cm3) | Large (entire brain) |
Cancer is a cellular disease whose cure requires the lethal treatment of every tumor cell. Substantially prolonged survival in glioblastoma depends on preventing tumor recurrence by eradicating tumor cells in the primary tumor mass and the surrounding and distant brain regions. Conventional surgery and chemoradiation of glioblastoma effectively slow the growth of the tumor by eradicating the fastest dividing tumor cells that create the central mass of the tumor. Chemoradiation targets the fastest dividing cells most amenable to DNA damage, which cannot be repaired between rapid cell divisions. These therapies leave slower-dividing tumor clones to maintain glioblastoma growth. If this theory is correct, the present glioblastoma treatment essentially lengthens survival by eradicating the most rapidly dividing tumor clones. Life expectancy increases after the first wave of therapy because the glioblastoma growth rate falls when slower-dividing tumor clones drive it. If a tumor cure is presently unattainable and radio- and chemotherapy extend life by eliminating the fastest-growing tumor cell clones, therapies that slow the tumor cell cycle through non-DNA toxic treatments may be logical choices for treating recurrent glioblastoma. Future therapies may slow tumor growth by changing the tumor environment, providing time and a more conducive milieu for treatments such as immunotherapy to eradicate glioblastoma.
This entry is adapted from the peer-reviewed paper 10.3390/brainsci12060787