Assessing and Charting the Future Path : Addressing the Decline of Brain Tumor Specialists in Korea - Insights from the Korea Brain Tumor Society (KBTS) Future Strategy Committee of 2023.

Objective: Although Republic of Korea is an advanced country in medical technology with a successful treatment rate for serious diseases, such as cancer, and has improved technology for highly difficult surgery, many excellent medical doctors and physicians are struggling due to the recent unreasonable medical environment. Specialization in brain tumor surgery also faces challenges in Republic of Korea, including low financial incentives, legal threats, and limited career prospects. In response, the Korea Brain Tumor Society (KBTS) formed the Future Strategy Committee to assess these obstacles and propose solutions. Methods: A survey was conducted among the KBTS members to understand their perceptions and concerns across different career stages. Results: The findings revealed a decline in interest among chief residents in brain tumor surgery, owing to limited job opportunities and income prospects. Neurosurgical fellows expressed neutral satisfaction but highlighted challenges, such as low patient numbers and income. Faculty members with varying levels of experience echoed similar concerns, emphasizing the need for improved financial incentives and job stability. Despite these challenges, the respondents expressed dedication to the field and suggested strategies for improvement. Conclusion: The KBTS outlines a vision that focuses on practical excellence, comprehensive research, professional education, responsibilities, and member satisfaction. Addressing these challenges requires collaborative efforts among healthcare institutions, professional societies, and policymakers to support brain tumor specialists and enhance patient care.

AB051. Multiple meningiomas developed outside the radiation field after cranial irradiation: a case report.

BACKGROUND: Cranial irradiation has well-known long-term side effects, including radiation-induced neoplasms and vasculopathy. This report describes a case of aggressive and rapid-growing multiple meningiomas developed outside the radiation field after the treatment of medulloblastoma. CASE DESCRIPTION: A 6-year-old boy underwent surgery (gross total resection) and radiotherapy (19.8 Gy for posterior fossa only) against medulloblastoma in the 4th ventricle. The patient could not receive further craniospinal irradiation because of ventriculoperitoneal shunt-related complications. Eighteen years after the radiotherapy, the first meningioma developed in the right temporal convexity, without recurrence of medulloblastoma. It was left untreated because it was asymptomatic. Three years later, the meningioma grew from 0.6 to 6.3 cm3 in volume and another large meningioma (22.1 cm3) developed in the left temporal convexity with additional small meningioma in the right frontal convexity. The left large temporal meningioma showed aggressive nature invading the adjacent temporal bone and temporalis muscle. It was completely resected and the histology revealed as transitional meningioma with 2% of Ki-67. Another new meningioma was identified on the right cerebellar convexity three years post-craniotomy. Subsequent follow-up indicated a progressive increase in the tumor size and gamma knife radiosurgery was performed with right frontal convexity small meningioma. The patient is currently under ongoing surveillance through follow-up assessments. CONCLUSIONS: For patients who received radiotherapy at a young age, clinicians should consider the possibility of secondary neoplasm development even outside the radiation field. Careful imaging follow-up and surgical management are warranted because of the aggressive nature of secondary tumors even though benign in histology.

Overview of carboxyl­terminal modulator protein 1 and its importance in various metabolic regulations (Review).

Acyl­coenzyme A thioesterases (ACOTs) are crucial in mediating lipid metabolic functions, including energy expenditure, hepatic gluconeogenesis and neuronal function. The two distinct types are type I and II ACOTs, the latter of which are 'hotdog' fold superfamily members. Type II ACOTs include carboxyl­terminal modulator protein 1 (CTMP1), also termed thioesterase superfamily member 4 (THEM4), and CTMP2, also termed THEM5. Due to their similar structural features and distinct sequence homology, CTMP1 and CTMP2 stand out from other type II ACOTs. CTMP1 was initially known as a protein kinase B (PKB) inhibitor that attenuates PKB phosphorylation. PKB is the central regulator of various cellular functions, including survival, proliferation, growth and metabolism. Therefore, by inhibiting PKB, CTMP1 can affect various cellular processes. Various other functions of CTMP1 have been revealed, including functions in cancer, brain injury, mitochondrial function and lipid metabolism. CTMP2 is a paralog of CTMP1 and was first identified as a cardiolipin remodeling factor involved in the development of fatty liver. As the functions of CTMP1 and CTMP2 were discovered separately, a review to summarize and connect these findings is essential. The current review delineates the intricate complexity of CTMP regulation across different metabolic pathways and encapsulates the principal discoveries concerning CTMP until the present day.

Risk factor analyses of contrast leakage and contrast-induced encephalopathy following coil embolization for unruptured intracranial aneurysm.

BACKGROUND: Contrast-induced encephalopathy (CIE) following endovascular interventions is a rare but serious complication. This study aimed to investigate the risk factors of contrast leakage (CL) and CIE in patients who underwent coil embolization of unruptured intracranial aneurysms (UIAs). METHODS: Patients with UIAs who underwent coil embolization at a single tertiary institute between January 2019 and January 2022 were enrolled retrospectively. CL was defined as cortical or subcortical contrast enhancement with effacement of the cortical sulci. CIE was defined as the new onset of neurological deficits associated with CL. Following the procedure, all patients underwent CT scans, and MRI scans were performed on those with symptoms. Patient and procedural risk factors were investigated. RESULTS: In total, 459 patients were analyzed. The median procedure time and contrast dose were 69 min and 96 mL, respectively. CL was evident in 35 patients. In the multivariate analysis, hypertension, large aneurysm, longer procedure time, and greater contrast dose were associated with CL. CIE was diagnosed in 19 patients, and the risk factors included large aneurysm, longer procedure time, and greater contrast dose. The procedure time was predictive of both CL (P<0.001) and CIE (P=0.01). The optimal cut-off value for procedure time was 81.5 min. All CIE patients recovered completely within 8-96 hours. CONCLUSIONS: A large aneurysm and prolonged procedure time may increase the patient's risk of CL and CIE due to increased contrast exposure. Patients who underwent a procedure that exceeded 1.5 hours necessitate post-procedure evaluation and monitoring.

AXL is required for hypoxia-mediated hypoxia-inducible factor-1 alpha function in glioblastoma.

Glioblastoma (GBM) is the most aggressive type of central nervous system tumor. Molecular targeting may be important when developing efficient GBM treatment strategies. Sequencing of GBMs revealed that the receptor tyrosine kinase (RTK)/RAS/phosphatidylinositol-3-kinase pathway was altered in 88% of samples. Interestingly, AXL, a member of RTK, was proposed as a promising target in glioma therapy. However, the molecular mechanism of AXL modulation of GBM genesis and proliferation is still unclear. In this study, we investigated the expression and localization of hypoxia-inducible factor-1 alpha (HIF-1α) by AXL in GBM. Both AXL mRNA and protein are overexpressed in GBM. Short-interfering RNA knockdown of AXL in U251-MG cells reduced viability and migration. However, serum withdrawal reduced AXL expression, abolishing the effect on viability. AXL is also involved in hypoxia regulation. In hypoxic conditions, the reduction of AXL decreased the level and nuclear localization of HIF-1α. The co-expression of HIF-1α and AXL was found in human GBM samples but not normal tissue. This finding suggests a mechanism for GBM proliferation and indicates that targeting AXL may be a potential GBM therapeutic. Supplementary Information: The online version contains supplementary material available at 10.1007/s43188-023-00195-z.

Efficacy of hydroxyapatite-based skull base reconstruction for intraoperative high-flow cerebrospinal fluid leakage performed by less-experienced surgeons.

Cerebrospinal fluid (CSF) leakage after endoscopic skull base surgery remains a challenge despite multilayer reconstruction including nasoseptal flap (NSF) has become a standard technique. Injectable hydroxyapatite (HXA) has shown promising results to prevent CSF leakage. This study aimed to validate the efficacy of HXA-based skull base reconstruction performed by less-experienced neurosurgeons who had short-term clinical experiences as independent surgeons. Between March 2018 and November 2022, 41 patients who experienced intraoperative high-flow CSF leakage following endoscopic endonasal surgery at two independent tertiary institutions were enrolled. Skull base reconstruction was performed using conventional multilayer techniques combined with or without HXA. The primary outcome was postoperative CSF leakage. The surgical steps and nuances were described in detail. The most common pathology was craniopharyngioma. Injectable HXA was used in 22 patients (HXA group) and conventional techniques were performed in 19 patients (control group). The HXA group achieved a significantly lower incidence of postoperative CSF leakage than the control group (0% vs. 26.3%, p = 0.016). No HXA-related complications were observed. The use of injectable HXA in skull base reconstruction was highly effective and safe. This technique and its favorable results might be readily reproduced by less-experienced neurosurgeons.

Exploring scavenger receptor class F member 2 and the importance of scavenger receptor family in prediagnostic diseases.

Scavenger Receptor Class F Member 2 (SCARF2), also known as the Type F Scavenger Receptor Family gene, encodes for Scavenger Receptor Expressed by Endothelial Cells 2 (SREC-II). This protein is a crucial component of the scavenger receptor family and is vital in protecting mammals from infectious diseases. Although research on SCARF2 is limited, mutations in this protein have been shown to cause skeletal abnormalities in both SCARF2-deficient mice and individuals with Van den Ende-Gupta syndrome (VDEGS), which is also associated with SCARF2 mutations. In contrast, other scavenger receptors have demonstrated versatile responses and have been found to aid in pathogen elimination, lipid transportation, intracellular cargo transportation, and work in tandem with various coreceptors. This review will concentrate on recent progress in comprehending SCARF2 and the functions played by members of the Scavenger Receptor Family in pre-diagnostic diseases.

Role of Adjunctive Tranexamic Acid in Facilitating Resolution of Chronic Subdural Hematoma after Surgery.

OBJECTIVE: Chronic subdural hematoma (CSDH) is a common neurosurgical disease and generally treated with burr-hole surgery alone. Tranexamic acid (TXA) is an antifibrinolytic agent that potentially reduces recurrence rates and the residual hematoma volume. However, the role of postoperative TXA medication remains unclear to date. This study aimed to verify the effectiveness of adjunctive TXA in the view of early hematoma resolution. METHODS: Between January 2018 and September 2021, patients with CSDH who underwent burr-hole trephination in a single tertiary institute were reviewed. The study population was divided into three groups, TXA, non-TXA, and antithrombotics (AT) groups, according to the medical history of cardio-cerebrovascular disease and TXA administration. The primary endpoint was CSDH recurrence, defined as re-appearance or re-accumulation of CSDH requiring neurosurgical interventions. The secondary outcome was CSDH resolution, defined as complete or near-complete resorption of the CSDH. The CSDH resolution time and serial changes of hematoma thickness were also investigated. RESULTS: A total of 240 patients was included in the analysis consisting of 185 male and 55 female, with a median age of 74 years. During the median imaging follow-up period of 75 days, 222 patients were reached to the primary or secondary endpoint. TXA was administered as an adjunctive therapy in 41 patients (TXA group, 16.9%) while 114 patients were included in the non-TXA group (47.9%) and 85 were in the AT group. The recurrence rate was the lowest in the TXA group (2.4%), followed by non-TXA (7.0%) and AT (8.2%) groups. However, there was no statistical significance due to the small number of patients with recurrence. CSDH resolution was achieved in 206 patients, and the median estimated time to resolution was significantly faster in the TXA group (p<0.001). Adjunctive TXA administration was a significant positive factor for achieving CSDH resolution (p<0.001). The hematoma thickness was comparable among the three groups at the initial time and after surgery. However, CSDH thickness in the TXA group decreased abruptly in a month and showed a significant difference from that in the other groups (p<0.001). There was no TXA-related adverse event. CONCLUSION: The adjunctive use of TXA after CSDH surgery significantly facilitated the resorption of residual CSDH and resulted in the early CSDH resolution. Adjunctive TXA may be an effective treatment option to reduce recurrence by enhancing CSDH resolution in the selective patients.

A Huge Radiation-Induced Cavernous Hemangioma Following Stereotactic Radiosurgery for Meningioma: A Case Report.

Radiation-induced cavernous hemangiomas (RICHs) have been increasingly reported as a late complication after conventional radiotherapy. RICH after stereotactic radiosurgery (SRS) is extremely rare and the few cases have been reported to demonstrate their properties. A 72-year-old female patient presented with progressive neurologic deficits. She underwent tumor surgery for meningioma 13 years ago and two times of SRS for treating a residual tumor. Newly-developed mass was 4.3 cm-sized heterogeneously enhancing mass with severe cerebral edema. She underwent surgical resection and the histologic examinations revealed organized hematoma. Finally, it was diagnosed as a RICH following SRS based on radiological and histological findings and a history of multiple radiosurgeries. Clinical, radiological, and histological features of a RICH following SRS were discussed in this report.

Functional characteristics and research trends of PDE11A in human diseases (Review).

cAMP and cGMP are important secondary messengers involved in cell regulation and metabolism driven by the G protein­coupled receptor. cAMP is converted via adenylyl cyclase (AC) and activates protein kinase A to phosphorylate intracellular proteins that mediate specific responses. cAMP signaling serves a role at multiple steps in tumorigenesis. The level of cAMP is increased in association with cancer cell formation through activation of AC­stimulatory G protein by mutation. Phosphodiesterases (PDEs) hydrolyze cAMP and cGMP to AMP and GMP. PDEs are composed of 11 families, and each can hydrolyze cAMP and cGMP or both cAMP and cGMP. PDEs perform various roles depending on their location and expression site, and are involved in several diseases, including male erectile dysfunction, pulmonary hypertension, Alzheimer's disease and schizophrenia. PDE11A is the 11th member of the PDE family and is characterized by four splice variants with varying tissue expression and N­terminal regulatory regions. Among tissues, the expression of PDE11A was highest in the prostate, and it was also expressed in hepatic skeletal muscle, pituitary, pancreas and kidney. PDE11A is the first PDE associated with an adrenocortical tumor associated genetic condition. In several studies, three PDE11A mutations have been reported in patients with Cushing syndrome with primary pigmented nodular adrenocortical disease or isolated micronodular adrenocortical disease without other genetic defects. It has been reported that an increase in PDE11A expression affects the proliferation of glioblastoma and worsens patient prognosis. The present mini­review summarizes the location of PDE11A expression, the impact of structural differences and disease relevance.

Phosphodiesterase 11 A (PDE11A), a potential biomarker for glioblastoma.

Phosphodiesterase 11A (PDE11A), a 3',5'-cyclic nucleotide phosphodiesterase, is a key regulator of intracellular signaling that functions by degrading cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). However, the function of PDE11A in brain tumors is currently unclear. In this study, we found that PDE11A may be involved in glioblastoma development. The protein and mRNA levels of PDE11A were significantly higher in U87-MG, U251-MG and U343-MG glioblastoma cell lines. Gene expression analyses by deep-sequencing revealed that PDE11A mRNA levels were higher in U87-MG and U251-MG cells compared to other cells in the cerebral cortex. A comprehensive analysis of The Cancer Genome Atlas (TCGA) data revealed that PDE11A expression was also elevated in glioblastoma patients. Taken together, these data indicate that PDE11A expression was increased in glioblastoma cell lines and glioma patients, suggesting that PDE11A could be a putative diagnostic marker and therapeutic target for glioma.

Emerging role of LETM1/GRP78 axis in lung cancer.

The selective autophagy of damaged mitochondria is called mitophagy. Mitochondrial dysfunction, mitophagy, and apoptosis have been suggested to be interrelated in various human lung carcinomas. Leucine zipper EF-hand-containing transmembrane protein-1 (LETM1) was cloned in an attempt to identify candidate genes for Wolf-Hirschhorn syndrome. LETM1 plays a role in mitochondrial morphology, ion homeostasis, and cell viability. LETM1 has also been shown to be overexpressed in different human cancer tissues, including lung cancer. In the current study, we have provided clear evidence that LETM1 acts as an anchoring protein for the mitochondria-associated ER membrane (MAM). Fragmented mitochondria have been found in lung cancer cells with LETM1 overexpression. In addition, a reduction of mitochondrial membrane potential and significant accumulation of microtubule-associated protein 1 A/1B-light chain 3 punctate, which localizes with Red-Mito, was found in LETM1-overexpressed cells, suggesting that mitophagy is upregulated in these cells. Interestingly, glucose-regulated protein 78 kDa (GRP78; an ER chaperon protein) and glucose-regulated protein 75 kDa (GRP75) were posited to interact with LETM1 in the immunoprecipitated LETM1 of H460 cells. This interaction was enhanced in cells treated with carbonyl cyanide m-chlorophenylhydrazone, a chemical mitophagy inducer. Treatment of cells with honokiol (a GRP78 inhibitor) blocked LETM1-mediated mitophagy, and CRISPR/Cas9-mediated GRP75 knockout inhibited LETM1-induced autophagy. Thus, GRP78 interacts with LETM1. Taken together, these observations support the notion that the complex formation of LETM1/GRP75/GRP78 might be an important step in MAM formation and mitophagy, thus regulating mitochondrial quality control in lung cancer.

A Deep Neural Network-Based Model Predicting Peritumoral Edema After Radiosurgery for Meningioma.

BACKGROUND: Gamma Knife radiosurgery (GKS) is a promising treatment option for meningioma. However, the incidence of peritumoral edema (PTE) following GKS has been reported to be 7%-38%. This study aimed to develop a predictive model for post-GKS PTE using a deep neural network (DNN) algorithm. METHODS: Patients treated with GKS for meningioma between November 2012 and February 2020 at a single tertiary center were reviewed. The primary outcome was newly developed or aggravated PTE after GKS. Clinical data, including radiosurgical parameters, were collected, and imaging data obtained at the time of GKS were incorporated into the model using a 50-layered residual neural network, ResNet50. Consequently, the model efficiency was evaluated considering the accuracy and area under the receiver operating curve (AUC) values. RESULTS: A total of 202 patients were included in this study. The median tumor volume was 2.3 mL, and the median prescription dose was 13 Gy. PTE was observed before GKS in 22 patients. Post-GKS PTE was evident in 28 patients (13.9%), which further evolved to radiation necrosis in 5 patients. The accuracy and AUC values of the hybrid data model based on both clinical and imaging data were 0.725 and 0.701, respectively. The performance of the hybrid data model was superior to that of the other models based on clinical or image data only. CONCLUSIONS: The DNN-based model using both clinical and imaging data exhibited fair results in predicting post-GKS PTE in meningioma treatment. Predictive models using imaging data may be helpful in prognostic research.

Scavenger receptor class F member 2 (SCARF2) as a novel therapeutic target in glioblastoma.

Scavenger receptor class F member 2 (SCARF2) is expressed by endothelial cells with very large cytoplasmic domains and is the second isotype, also known as scavenger receptor expressed by endothelial cells 2 (SREC-2). SREC-1 plays an important role in the binding and endocytosis of various endogenous and exogenous ligands. Many studies have been carried out on modified low-density lipoprotein internalization activity, but there have been few studies on SCARF2. Higher expression of SCARF2 has been found in glioblastoma (GBM) than normal brain tissue. Through analysis of The Cancer Genome Atlas database, it was confirmed that SCARF2 is widely expressed in GBM, and increased SCARF2 expression correlated with a poor prognosis in patients with glioma. The results of this study showed that the expression of SCARF2 is increased in GBM cell lines and patients, suggesting that SCARF2 may be a potential diagnostic marker and therapeutic molecule for cancers including glioma.

Reverse Trans-Sellar Neuroendoscopic Management of a Large Rathke's Cleft Cyst Causing Obstructive Hydrocephalus: A Case Report.

Symptomatic Rathke's cleft cysts (RCCs) can be treated by surgical procedures, usually through an endonasal transsphenoidal corridor using either a microscope or an endoscope. We report a large suprasellar extended RCC causing obstructive hydrocephalus, which was efficiently managed by a novel surgical route named "reverse" trans-sellar approach using transventricular neuroendoscopy. A 48-year-old woman complained of persistent headache and a tendency to fall that had begun 6 months previously. The images obtained from MRI scan showed intra- and supra-sellar cystic masses occupying the third ventricle with obstruction of the foramina of Monro and the aqueduct of Sylvius. The cystic wall showed a slight enhancement, and the cystic contents showed iso-signal intensity on T1-and T2-weighted images. Instead of trans-nasal trans-sellar surgery, we decided to operate using a conventional transventricular endoscope. A thin cystic capsule, which blocked the foramina of Monro and the aqueduct of Sylvius, was fenestrated and removed and a third ventriculostomy was performed. The defect in the infundibulum between sellar and suprasellar cysts was widened and used as a corridor to drain cystic contents (reverse trans-sellar route). The final pathological finding revealed an RCC with focal metaplasia. We efficiently managed a large RCC by transventricular neuroendoscopic surgery with cyst fenestration and third ventriculostomy and simultaneously drained the sellar contents using a novel surgical route. Reverse trans-sellar neuroendoscopic surgery is a relevant treatment option for selective patients with large suprasellar extensions of RCCs.

Corrigendum: Current Knowledge on the Function of α-Methyl Acyl-CoA Racemase in Human Diseases.

[This corrects the article DOI: 10.3389/fmolb.2020.00153.].

Alpha-Methylacyl-CoA Racemase (AMACR), a Potential New Biomarker for Glioblastoma.

Alpha-Methylacyl-CoA racemase (AMACR), which was initially discovered as a prostate cancer marker, is critical for the chiral inversion mechanism of branched-chain fatty acids. However, the function of AMACR in brain tumors has not been investigated. In this study, AMACR appeared to be involved in glioblastoma. The protein and mRNA levels of AMACR were highly elevated in glioblastoma. Downregulation of AMACR inhibited cell proliferation. Comprehensive analysis of the public REMBRANDT GBM dataset also confirmed that the level of AMACR expression was correlated with the clinical prognosis of glioma patients. In summary, these findings indicate that AMACR expression is increased in a glioblastoma cell line and glioma patients, suggesting that AMACR might be a potential diagnostic marker and therapeutic target for cancer, including glioma.

How to Find Dural Defect of Spinal Extradural Arachnoid Cyst.

Spinal extradural arachnoid cysts (SEACs) are rare and usually asymptomatic, and they usually do not require surgical treatment. If symptoms manifest, however, surgical treatment is required. A 25-year-old male patient complained of impotence upon admission. Magnetic resonance images (MRIs) of his lumbar spine showed a SEAC located longitudinally from the T11 to L3, which was accompanied by thecal sac compression. Verifying the location of the dural defect is crucial for minimizing surgical treatments. Cystography, myelography, and lumbar spine MRI were conducted to locate the leak in real-time; however, it was not found. Hence, the location of the cerebrospinal fluid leak was estimated based on cystography, computed tomography, myelography, and MRI findings. We suggest that the region with the earliest contrast-filling, as well as the middle and widest area of the cyst, may correspond to the location of the dural defect.

Endovascular coil embolization for unruptured intracranial aneurysms in patients over 80 years of age.

OBJECTIVE: As the average life span in modern society continues to increase, much interest is focused on high-risk procedures in elderly patients, including major surgical operations. We investigated the results of endovascular coiling of unruptured intracranial aneurysms (UIA) in patients over 80 years of age. METHODS: We retrospectively analyzed 39 patients aged over 80 years who underwent coil embolization for UIA between April 2007 and April 2019 at our hospital. RESULTS: Complete occlusion on digital subtraction angiography (DSA) immediately after surgery was performed in 44 (84.6%) of 52 cases of cerebral aneurysms. Four patients (7.7%) had residual aneurysmal necks, and four (7.7%) had contrast flow in the aneurysmal sac. Follow-up magnetic resonance angiography (mean: 8.2 months) was performed in 37 aneurysms in 24 patients. There was evidence of blood flow in the neck in seven cases (18.9%) and aneurysm in two cases (5.4%). Follow-up DSA (mean: 20.5 months) was performed in 14 aneurysms in 11 patients, and 11 aneurysms (78.6%) had complete occlusion, 1 aneurysm (7.1%) had an aneurysmal neck, and 2 aneurysms (14.3%) had contrast filling into the aneurysmal sac. Coil embolization procedure-related complications occurred in 3 patients (7.7%). Cerebral infarction occurred in 1 (2.6%), arterial dissection in 1 (2.6%), and hypoesthesia in 1 (2.6%). CONCLUSIONS: Active treatment of UIA in elderly patients over 80 years of age through endovascular coil embolization can be considered.

Revisiting the Warburg Effect: Diet-Based Strategies for Cancer Prevention.

It is widely acknowledged that cancer cell energy metabolism relies mainly on anaerobic glycolysis; this phenomenon is described as the Warburg effect. However, whether the Warburg effect is caused by genetic dysregulation in cancer or is the cause of cancer remains unknown. The exact reasons and physiology of this abnormal metabolism are unclear; therefore, many researchers have attempted to reduce malignant cell growth in tumors in preclinical and clinical studies. Anticancer strategies based on the Warburg effect have involved the use of drug compounds and dietary changes. We recently reviewed applications of the Warburg effect to understand the benefits of this unusual cancer-related metabolism. In the current article, we summarize diet strategies for cancer treatment based on the Warburg effect.