We report a case of complete remission in anaplastic oligodendroglioma following adoptive cell therapy (ACT) with autologous Wilms tumor 1 (WT-1)-specific CD8+ T cells. A 40-year-old woman referred to our hospital for adjuvant chemotherapy after recurrent anaplastic oligodendroglioma initially presented with a left frontal tumor, diagnosed through seizure onset, and subtotal resection confirmed oligodendroglioma (WHO grade 2). Radiation therapy treated the residual tumor, achieving partial remission until recurrence 2.5 years later when malignant transformation to anaplastic oligodendroglioma (WHO grade 3) occurred following a second craniotomy. After three cycles of procarbazine, lomustine, and vincristine chemotherapy, the residual tumor stabilized for 3 years. However, follow-up MRI identified a new enhancing lesion, prompting a third craniotomy. Recurrent anaplastic oligodendroglioma was confirmed, and adjuvant proton beam therapy and temozolomide chemotherapy were initiated. Two years later, another enhancing lesion appeared on the adjacent medial frontal lobe. Following multidisciplinary review, we introduced WT-1-specific ACT. Although transient swelling was observed 1 month post-therapy, the tumor demonstrated a response within 3–9 months. Continued regression led to complete remission—confirmed via MRI at the 15-month follow-up and sustained for 4.7 years. The patient’s peripheral blood monocyte profiles and immune-associated cytokine analysis indicated T-cell activation following WT-1 sensitization.

This case introduces the differential diagnosis of a well-enhancing lesion in the prepontine cistern of a 55-year-old female patient who was diagnosed with recurrent metastatic breast cancer. The patient was diagnosed with breast cancer 11 years ago and underwent a mastectomy and subsequent adjuvant therapy. Tamoxifen had been given for 5 years, and the treatment was completed. Five years after, she found a lung nodule on her routine chest X-ray examination. Based on her past medical history, systemic cancer work-up was done and it revealed multiple lesions in T10 vertebra, lungs, and mediastinal lymph nodes. Trans-bronchial needle aspiration was performed and the biopsy was a metastatic breast cancer. Brain MRI was taken as she was complaining of headache and it showed a welldefined, ovoid enhancing 0.9-cm nodule in the right prepontine cistern. Neuro-oncology tumor board evaluated the lesion as more likely to be an asymptomatic neurogenic tumor rather than metastasis based on radiological features including brainstem surfaced location, slightly high signal intensity on T2-weighted image and no diffusion restriction. To rule out leptomeningeal metastasis, a serial cerebrospinal fluid cytology examination (×3) was done and negative for malignant cells. Follow-up brain MRIs of 2 and 9 months showed no significant changes in the pre-pontine enhancing lesion.

We report a case of complete remission in anaplastic oligodendroglioma following adoptive cell therapy (ACT) with autologous Wilms tumor 1 (WT-1)-specific CD8+ T cells. A 40-year-old woman referred to our hospital for adjuvant chemotherapy after recurrent anaplastic oligodendroglioma initially presented with a left frontal tumor, diagnosed through seizure onset, and subtotal resection confirmed oligodendroglioma (WHO grade 2). Radiation therapy treated the residual tumor, achieving partial remission until recurrence 2.5 years later when malignant transformation to anaplastic oligodendroglioma (WHO grade 3) occurred following a second craniotomy. After three cycles of procarbazine, lomustine, and vincristine chemotherapy, the residual tumor stabilized for 3 years. However, follow-up MRI identified a new enhancing lesion, prompting a third craniotomy. Recurrent anaplastic oligodendroglioma was confirmed, and adjuvant proton beam therapy and temozolomide chemotherapy were initiated. Two years later, another enhancing lesion appeared on the adjacent medial frontal lobe. Following multidisciplinary review, we introduced WT-1-specific ACT. Although transient swelling was observed 1 month post-therapy, the tumor demonstrated a response within 3–9 months. Continued regression led to complete remission—confirmed via MRI at the 15-month follow-up and sustained for 4.7 years. The patient’s peripheral blood monocyte profiles and immune-associated cytokine analysis indicated T-cell activation following WT-1 sensitization.

This case introduces the differential diagnosis of a well-enhancing lesion in the prepontine cistern of a 55-year-old female patient who was diagnosed with recurrent metastatic breast cancer. The patient was diagnosed with breast cancer 11 years ago and underwent a mastectomy and subsequent adjuvant therapy. Tamoxifen had been given for 5 years, and the treatment was completed. Five years after, she found a lung nodule on her routine chest X-ray examination. Based on her past medical history, systemic cancer work-up was done and it revealed multiple lesions in T10 vertebra, lungs, and mediastinal lymph nodes. Trans-bronchial needle aspiration was performed and the biopsy was a metastatic breast cancer. Brain MRI was taken as she was complaining of headache and it showed a welldefined, ovoid enhancing 0.9-cm nodule in the right prepontine cistern. Neuro-oncology tumor board evaluated the lesion as more likely to be an asymptomatic neurogenic tumor rather than metastasis based on radiological features including brainstem surfaced location, slightly high signal intensity on T2-weighted image and no diffusion restriction. To rule out leptomeningeal metastasis, a serial cerebrospinal fluid cytology examination (×3) was done and negative for malignant cells. Follow-up brain MRIs of 2 and 9 months showed no significant changes in the pre-pontine enhancing lesion.

We report a case of complete remission in anaplastic oligodendroglioma following adoptive cell therapy (ACT) with autologous Wilms tumor 1 (WT-1)-specific CD8+ T cells. A 40-year-old woman referred to our hospital for adjuvant chemotherapy after recurrent anaplastic oligodendroglioma initially presented with a left frontal tumor, diagnosed through seizure onset, and subtotal resection confirmed oligodendroglioma (WHO grade 2). Radiation therapy treated the residual tumor, achieving partial remission until recurrence 2.5 years later when malignant transformation to anaplastic oligodendroglioma (WHO grade 3) occurred following a second craniotomy. After three cycles of procarbazine, lomustine, and vincristine chemotherapy, the residual tumor stabilized for 3 years. However, follow-up MRI identified a new enhancing lesion, prompting a third craniotomy. Recurrent anaplastic oligodendroglioma was confirmed, and adjuvant proton beam therapy and temozolomide chemotherapy were initiated. Two years later, another enhancing lesion appeared on the adjacent medial frontal lobe. Following multidisciplinary review, we introduced WT-1-specific ACT. Although transient swelling was observed 1 month post-therapy, the tumor demonstrated a response within 3–9 months. Continued regression led to complete remission—confirmed via MRI at the 15-month follow-up and sustained for 4.7 years. The patient’s peripheral blood monocyte profiles and immune-associated cytokine analysis indicated T-cell activation following WT-1 sensitization.

This case introduces the differential diagnosis of a well-enhancing lesion in the prepontine cistern of a 55-year-old female patient who was diagnosed with recurrent metastatic breast cancer. The patient was diagnosed with breast cancer 11 years ago and underwent a mastectomy and subsequent adjuvant therapy. Tamoxifen had been given for 5 years, and the treatment was completed. Five years after, she found a lung nodule on her routine chest X-ray examination. Based on her past medical history, systemic cancer work-up was done and it revealed multiple lesions in T10 vertebra, lungs, and mediastinal lymph nodes. Trans-bronchial needle aspiration was performed and the biopsy was a metastatic breast cancer. Brain MRI was taken as she was complaining of headache and it showed a welldefined, ovoid enhancing 0.9-cm nodule in the right prepontine cistern. Neuro-oncology tumor board evaluated the lesion as more likely to be an asymptomatic neurogenic tumor rather than metastasis based on radiological features including brainstem surfaced location, slightly high signal intensity on T2-weighted image and no diffusion restriction. To rule out leptomeningeal metastasis, a serial cerebrospinal fluid cytology examination (×3) was done and negative for malignant cells. Follow-up brain MRIs of 2 and 9 months showed no significant changes in the pre-pontine enhancing lesion.

We report complete remission of dural-based leptomeningeal metastasis (LM) in an 80-year-old female patient with non-small cell lung cancer (NSCLC) by osimertinib. She was diagnosed with NSCLC (adenocarcinoma, T4N3M1a) 8 years ago. Mutation analysis of biopsied tissue revealed exon 19 deletion positive, and gefitinib was prescribed. Follow-up chest CT showed a radiological response, and wholebody positron emission tomography 3 years later revealed the disappearance of the previous high-uptake lesions. The medication was continued for maintenance but stopped 4 years later due to intolerable dermatitis. Two years after discontinuing chemotherapy, the patient had a gait disturbance, and brain MRI revealed a right cerebellar mass (diameter [d]=3 cm) with peritumoral edema, compatible with solitary brain metastasis. Retromastoid suboccipital craniotomy and gross total removal of the dura-attached lesion were performed. As the systemic cancer status evaluation revealed no radiological cancer lesion, only tumor bed radiation therapy was given (4,000 cGy/10 fractions) without re-introducing gefitinib. She was followed with a brain MRI at 6-month intervals, and a brain MRI 2 years postoperatively revealed a dural-based extra-axial mass in the left prepontine cistern (d=2.2 cm). Serial cerebrospinal fluid (CSF) cytology was positive for cancer cells. Upon LM diagnosis, the third-generation receptor tyrosine kinase inhibitor osimertinib was given. Two-month follow-up CSF cytology and five consecutive tests over 14 months demonstrated negative conversion. Five-month follow-up brain MRI revealed near complete remission of dural-based LM, and the response was maintained until the 13-month follow-up brain MRI.

Delayed cerebral necrosis is a well-known complication of radiation therapy (RT). Because of its irreversible nature, it should be avoided if possible, but avoidance occurs at the expense of potentially compromised tumor control, despite the use of the modern advanced technique of conformal RT that minimizes radiation to normal brain tissue. Risk factors for radiation-induced cerebral necrosis include a higher dose per fraction, larger treatment volume, higher cumulative dose, and shorter time interval (for re-irradiation). The same principle can be applied to proton beam therapy (PBT) to avoid delayed cerebral necrosis. However, conversion of PBT radiation energy into conventional RT is still short of clinical support, compared to conventional RT. Herein, we describe two patients with excessively delayed cerebral necrosis after PBT, in whom follow-up MRI showed no RT-induced changes prior to 3 years after treatment. One patient developed radiation necrosis at 4 years after PBT to the resection cavity of an astroblastoma, and the other developed brainstem necrosis that became symptomatic 6 months after its first appearance on the 3-year follow-up brain MRI. We also discuss possible differences between radiation changes after PBT versus conventional RT.

Differential diagnosis of focal brainstem lesions detected on MRI is challenging, especially in young children. Formerly, brainstem gliomas were classified mainly based on MRI features and location. However, since 2016, the World Health Organization’s brainstem lesion classification requires tissue biopsy to reveal molecular characteristics. Although modern techniques of stereotactic or navigation-guided biopsy ensure accurate biopsy of the lesion with safety, biopsy of brainstem lesions is still generally not performed. Here, we report a focal brainstem lesion mimicking brainstem glioma in a 9-year-old girl. Initial MRI, MR spectroscopy, and 11 C-methionine positron emission tomography (PET) features suggested low-grade glioma or diffuse intrinsic pontine glioma. However, repeated MR spectroscopy, perfusion MRI, and 18 fluorodeoxyglucose PET findings suggested that it was more likely a non-tumorous lesion. As the patient presented not with a neurological manifestation but with precocious puberty, the attending oncologist chose to observe with regular follow-up MRI. The pontine lesion with high signal intensity on T2-weighted MRI regressed from the 6-month follow-up and became invisible on the 1.5-year follow-up MRI. We reviewed brainstem glioma–mimicking lesions in the literature and discussed the key points of differential diagnosis.

High-grade transformation of low-grade gliomas has long been a poor prognostic factor during therapy. In 2016, the World Health Organization (WHO) Classification of Tumors of the Central Nervous System (CNS) adopted isocitrate dehydrogenase (IDH) mutation status in the classification of diffuse astrocytomas. The 2021 classification denoted glioblastomas as IDH-wildtype and graded IDH-mutant astrocytomas as 2, 3, or 4. Gemistocytic morphology, a large proportion of residual tumor, the patient’s age, and recurrence after radiotherapy were previously mentioned as risk factors for high-grade transformation of low-grade gliomas. We report a 34-year-old male patient initially diagnosed with IDH-mutant grade 2 astrocytoma according to the 2021 WHO classification of CNS tumors. As the first surgical resection achieved gross total resection on postoperative MRI, no adjuvant therapy was given and regular follow-up was planned. On 1-year follow-up MRI, two new enhancing nodular lesions appeared at the ipsilateral brain parenchyma abutting the surgical resection cavity. Salvage craniotomy achieved gross total resection, and the pathologic diagnosis was IDH-mutant WHO grade 4 astrocytoma. We describe this tumor in terms of the previous WHO classification to evaluate the risk of high-grade transformation and discuss possible risk factors leading to high-grade transformation of low-grade astrocytoma.