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Introduction: Prognosis is a forecast of the likely course of a disease and its future implications on treatment outcomes. The significance of periodontal prognosis in clinical practice is evident by its influence on treatment planning, communication, and in the retrospective evaluation of treatment results. While there are multiple well-known prognosis systems reported in the periodontal dental literature, there is an absence of data on the actual use of prognosis assignment among practicing clinicians. The purpose of this study was to survey military periodontists regarding their utilization of periodontal prognosis and associated systems and to evaluate prognosis' influence on treatment planning as well as its implications on operational dental readiness., Methods: A 19-question internet survey was disseminated to military periodontists in the U.S. Air Force, Army, and Navy via their respective Periodontal Consultants to the Surgeon Generals. The survey inquired on provider-specific demographic information, the provider's favored periodontal prognosis system, when and how prognosis is applied, and on the relationship between prognosis and operational dental readiness., Results: Fifty-five percent (n = 65 out of 120) of eligible survey participants completed the survey. Army (94.4%, n = 17) and Air Force (72.2%, n = 13) respondents preferred utilizing the Kwok and Caton periodontal prognosis system compared to 37.9% (n = 11) of Navy periodontists. Most respondents assigned prognosis at multiple time points in a patient's overall course of treatment (68%, n = 44), identified the severity of the periodontal presentation and the predictability of treatment outcomes as the most important factors involved in assigning a prognosis (82%, n = 55), and indicated that periodontal prognosis did not influence their dental readiness classification and vice versa., Conclusions: Kwok and Caton and McGuire periodontal prognosis systems were utilized by the majority of respondents but differed in utilization by military service branch. Respondents considered periodontal presentation severity and treatment outcome predictability the most important factors when assigning a prognosis. There was minimal influence between operational dental readiness and periodontal prognosis. Future research will evaluate prognosis system utilization in a broader population and will assess the impact of system standardization in education and clinical practice., (Published by Oxford University Press on behalf of the Association of Military Surgeons of the United States 2024. This work is written by (a) US Government employee(s) and is in the public domain in the US.)

With improvements in survival for patients with metastatic cancer, long-term local control of brain metastases has become an increasingly important clinical priority. While consensus guidelines recommend surgery followed by stereotactic radiosurgery (SRS) for lesions >3 cm, smaller lesions (≤3 cm) treated with SRS alone elicit variable responses. To determine factors influencing this variable response to SRS, we analyzed outcomes of brain metastases ≤3 cm diameter in patients with no prior systemic therapy treated with frame-based single-fraction SRS. Following SRS, 259 out of 1733 (15%) treated lesions demonstrated MRI findings concerning for local treatment failure (LTF), of which 202 /1733 (12%) demonstrated LTF and 54/1733 (3%) had an adverse radiation effect. Multivariate analysis demonstrated tumor size (>1.5 cm) and melanoma histology were associated with higher LTF rates. Our results demonstrate that brain metastases ≤3 cm are not uniformly responsive to SRS and suggest that prospective studies to evaluate the effect of SRS alone or in combination with surgery on brain metastases ≤3 cm matched by tumor size and histology are warranted. These studies will help establish multi-disciplinary treatment guidelines that improve local control while minimizing radiation necrosis during treatment of brain metastasis ≤3 cm., (© 2024. The Author(s).)

The development of neurosurgery at Baylor College of Medicine began with the medical school's relocation to the new Texas Medical Center in Houston in 1943. An academic service was organized in 1949 as a section of neurosurgery within Baylor's Department of Surgery. Soon the practice, led by Dr. George Ehni, evolved to include clinical services at Methodist, Jefferson Davis (forerunner of Ben Taub), Texas Children's, the Veterans Affairs, and the University of Texas MD Anderson Cancer Center hospitals. A neurosurgery residency program was established in 1954. As the clinical practice expanded, neurosurgery was upgraded from a section to a division and then to a department. It has been led by four chiefs/chairs over the past 60 years-Dr. George Ehni (1959-1979), Dr. Robert Grossman (1980-2004), Dr. Raymond Sawaya (2005-2014), and Dr. Daniel Yoshor (2015-2020). Since the 1950s, the department has drawn strength from its robust residency program, its research base in the medical school, and its five major hospital affiliates, which have largely remained unchanged (with the exception of Baylor St. Luke's Medical Center replacing Methodist in 2004). The recent expansion of the residency program to 25 accredited positions and the growing strength of relationships with the "Baylor five" hospitals affiliated with Baylor College of Medicine portend a bright future.

Purpose: Approximately 12,000 glioblastomas are diagnosed annually in the United States. The median survival rate for this disease is 12 months, but individual survival rates can vary with patient-specific factors, including extent of surgical resection (EOR). The goal of our investigation is to develop a reliable strategy for personalized survival prediction and for quantifying the relationship between survival, EOR, and adjuvant chemoradiotherapy., Patients and Methods: We used accelerated failure time (AFT) modeling using data from 721 newly diagnosed patients with glioblastoma (from 1993 to 2010) to model the factors affecting individualized survival after surgical resection, and we used the model to construct probabilistic, patient-specific tools for survival prediction. We validated this model with independent data from 109 patients from a second institution., Results: AFT modeling using age, Karnofsky performance score, EOR, and adjuvant chemoradiotherapy produced a continuous, nonlinear, multivariable survival model for glioblastoma. The median personalized predictive error was 4.37 months, representing a more than 20% improvement over current methods. Subsequent model-based calculations yield patient-specific predictions of the incremental effects of EOR and adjuvant therapy on survival., Conclusion: Nonlinear, multivariable AFT modeling outperforms current methods for estimating individual survival after glioblastoma resection. The model produces personalized survival curves and quantifies the relationship between variables modulating patient-specific survival. This approach provides comprehensive, personalized, probabilistic, and clinically relevant information regarding the anticipated course of disease, the overall prognosis, and the patient-specific influence of EOR and adjuvant chemoradiotherapy. The continuous, nonlinear relationship identified between expected median survival and EOR argues against a surgical management strategy based on rigid EOR thresholds and instead provides the first explicit evidence supporting a maximum safe resection approach to glioblastoma surgery.

Object: Medical student exposure to neurosurgery is limited. To improve the educational interactions between neurosurgeons and medical students as well as neurosurgical medical student rotations or clerkships (NSCs) we must first understand the current status., Methods: Two questionnaires were sent, one to every neurosurgery course coordinator or director at each US neurosurgery residency program (99 questionnaires) and one to the associated parent medical school dean's office (91 questionnaires), to assess the current status of NSCs and the involvement of neurosurgeons at their respective institutions., Results: We received responses from 86 (87%) of 99 neurosurgery course coordinators or directors and 64 (70%) of 91 medical school deans' offices. Most NSCs do not have didactic lectures (53 [62%] of 86 NSCs), provide their medical students with a syllabus or educational handouts (53 [62%] of 86), or have a recommended/required textbook (77 [90%] of 86). The most common method of evaluating students in NSCs is a subjective performance evaluation. Of 64 medical school deans, 38 (59%) felt that neurosurgery should not be a required rotation. Neurosurgical rotations or clerkships are primarily offered to students in their 4th year of medical school, which may be too late for appropriate timing of residency applications. Only 21 (33%) of 64 NSCs offer neurosurgery rotations to 3rd-year students., Conclusions: There is significant room for improvement in the neurosurgeon-to-medical student interactions in both the NSCs and during the didactic years of medical school.

Object: Stereotactic radiosurgery (SRS) is commonly used to treat brain metastases. Complications associated with this treatment are underreported. The authors reviewed a large series of patients who underwent SRS for brain metastases to identify complications and factors predicting their occurrence., Methods: Prospectively collected clinical data from 273 patients undergoing SRS for 1 or 2 brain metastases at The University of Texas M. D. Anderson Cancer Center between June 1993 and December 2004 were reviewed. Patients who had received prior treatment for their tumor, including whole-brain radiation, SRS, or surgery, were excluded from the study. Data on adverse neurological and nonneurological outcomes following treatment were collected., Results: Three hundred sixteen lesions were treated. Complications were associated with 127 (40%) of 316 treated lesions. New neurological complications were associated with 101 (32%) of 316 lesions. The onset of seizure was the most common complication, occurring in 41 (13%) of 316 SRS cases. On multivariate analysis, progressing primary cancer (hazard ratio [HR]=2.4, 95% CI 1.6-3.6, p<0.001), tumor location in eloquent cortex (HR=2.3, 95% CI 1.6-3.4, p<0.001), and lower (<15 Gy) SRS dose (HR=2.1, 95% CI 1.1-4.2, p=0.04) were significantly associated with new complications. On multivariate analysis, a tumor location in the eloquent cortex (HR=2.5, 95% CI 1.6-3.8, p<0.001) and progressing primary cancer (HR=1.6, 95% CI 1.1-2.5, p=0.03) were significantly associated with new neurological complications., Conclusions: The authors showed that new neurological and nonneurological complications were associated with 40% of SRS treatments for brain metastases. Patients with lesions in functional brain regions have a significantly increased risk of treatment-related complications.

Purpose: Population-based estimates of the incidence of brain metastases are not generally available. The purpose of this study was to calculate population-based incidence proportions (IPs) of brain metastases from single primary lung, melanoma, breast, renal, or colorectal cancer., Patients and Methods: Patients diagnosed with single primary lung, melanoma, breast, renal, or colorectal cancer (1973 to 2001) in the Metropolitan Detroit Cancer Surveillance System (MDCSS) were used for analysis. IP of brain metastases by primary site and variable of interest (race, sex, age at diagnosis of primary cancer, and Surveillance, Epidemiology, and End Results [SEER] stage of primary cancer) was calculated with 95% CIs., Results: Total IP percentage (IP%) of brain metastases was 9.6% for all primary sites combined, and highest for lung (19.9%), followed by melanoma (6.9%), renal (6.5%), breast (5.1%), and colorectal (1.8%) cancers. Racial differences were seen with African Americans demonstrating higher IP% of brain metastases compared with other racial groups for most primary sites. IP% was significantly higher for female patients with lung cancer, and significantly higher for male patients with melanoma. The highest IP% of brain metastases occurred at different ages at diagnoses: age 40 to 49 years for primary lung cancer; age 50 to 59 years for primary melanoma, renal, or colorectal cancers; and age 20 to 39 for primary breast cancer. IP% significantly increased as SEER stage of primary cancer advanced for all primary sites., Conclusion: Total IP% of brain metastases was lower than previously reported, and it varied by primary site, race, sex, age at diagnosis of primary cancer, and SEER stage of primary cancer.

Purpose: To evaluate the outcome for elderly or younger poor prognosis glioblastoma patients treated with hypofractionated radiotherapy (HypoRT)., Methods and Materials: Retrospective review at The University of Texas M. D. Anderson Cancer Center identified 59 glioblastoma patients (median age 65 years) treated with HypoRT between 1988 and 2001 with 50 Gy given at 2.5 Gy/fraction/day in 20 fractions within 4 weeks. Classification was according to the Radiation Therapy Oncology Group recursive partitioning analysis and was Class IV in 11, V in 29, and VI in 19. Surgery consisted of gross total resection (n = 16), subtotal resection (n = 28), and biopsy only (n = 13). Two patients were treated presumptively on the basis of radiographic findings. Chemotherapy was given either as part of the initial treatment (n = 15) or for progression (n = 9)., Results: The median survival time for the entire study population was 7 months, and the median progression-free survival was 3.9 months. The median survival time for patients with Class IV, V, and VI was 11, 7, and 5 months, respectively. Concordance was found with Radiation Therapy Oncology Group-established recursive partitioning analysis class survival. Steroid requirements were not increased during RT compared with preoperatively and immediately postoperatively. Late complications of HypoRT were limited to 3 cases of radiation necrosis suggested by MRI, 2 of which were pathologically confirmed., Conclusion: HypoRT consisting of 50 Gy in 4 weeks can be used for selected GBM patients to reduce the overall treatment time of conventional RT by 33-39% without apparent increased toxicity or decrement in survival.

Purpose: To describe both the common and less frequently encountered magnetic resonance (MR) imaging features of radiation therapy- and chemotherapy-induced brain injury, with particular emphasis on radiation necrosis., Materials and Methods: A cohort of 148 adult patients underwent surgical resection of malignant brain (glial) tumors and were subsequently entered into a research protocol that consisted of accelerated radiation therapy with carboplatin followed by chemotherapy with procarbazine, lomustine, and vincristine. Patients typically underwent sequential MR imaging at 6-8-week intervals during the 1st year and at 3-6-month intervals during subsequent years. In all patients, histopathologic confirmation of lesion composition was performed by board-certified neuropathologists., Results: The patients exhibited different types of MR imaging-detected abnormalities of the brain: pure radiation necrosis in 20 patients, a mixture of predominantly radiation necrosis with limited recurrent and/or residual tumor (less than 20% of resected tissue) in 16 patients, radiation necrosis of the cranial nerves and/or their pathways in two patients, radiation-induced enhancement of the white matter in 52 patients, and radiation-induced enhancement of the cortex in nine patients., Conclusion: The frequent diagnostic dilemma of recurrent neoplasm versus radiation necrosis is addressed in this study through a description of the varying spatial and temporal patterns of radiation necrosis at MR imaging.

As many as 100,000 new cases of brain tumor are diagnosed each year in the United States. About half of these are primary gliomas and the remaining half are metastatic tumors and non-glial primary tumors. Currently, gliomas are classified based on phenotypic characteristics. Recent progress in the elucidation of genetic alterations found in gliomas have raised the exciting possibility of using genetic and molecular analyses to resolve some of the problematic issues currently associated with the histological approach to glioma classification. Recently, immunohistochemical studies using novel proliferation markers have significantly advanced the assessment of tumor growth potential and the grading criteria of some tumor subtypes. Preliminary studies using cDNA array technologies suggest that the profiling of gene expression patterns may provide a novel and meaningful approach to glioma classification and subclassification. Furthermore, cDNA array technologies may also be used to identify candidate genes involved in glioma tumor development, invasion, and progression. This review summarizes current glioma classification schemes that are based on histopathological characteristics and discusses the potential for using cDNA array technology in the molecular classification of gliomas.

Gliomas are the most common primary malignant brain tumours and are classified into four clinical grades, with the most aggressive tumours being grade 4 astrocytomas (also known as glioblastoma multiforme; GBM). Frequent genetic alterations in GBMs (refs 2-5) result in stimulation of common signal transduction pathways involving Ras, Akt and other proteins. It is not known which of these pathways, if any, are sufficient to induce GBM formation. Here we transfer, in a tissue-specific manner, genes encoding activated forms of Ras and Akt to astrocytes and neural progenitors in mice. We found that although neither activated Ras nor Akt alone is sufficient to induce GBM formation, the combination of activated Ras and Akt induces high-grade gliomas with the histological features of human GBMs. These tumours appear to arise after gene transfer to neural progenitors, but not after transfer to differentiated astrocytes. Increased activity of RAS is found in many human GBMs (ref. 11), and we show here that Akt activity is increased in most of these tumours, implying that combined activation of these two pathways accurately models the biology of this disease.

Purpose: To conduct a Phase II study to evaluate the long-term efficacy and safety of high-dose 5'-bromodeoxyuridine (BrdU) and accelerated radiotherapy followed by procarbazine, lomustine (CCNU), and vincristine (PCV) chemotherapy in patients with glioblastoma multiforme., Methods and Materials: Between 1994 and 1996, 88 patients were enrolled to receive 1.9 Gy of radiation three times a day for two 5-day cycles separated by 2 weeks; each 5-day cycle was preceded by a continuous 96-hour infusion of BrdU at a dose of 2.1 g/m2/day. After radiotherapy, patients received PCV chemotherapy., Results: Median survival for all 88 patients was 50 weeks. Seventy (79.5 %) received one or more courses of PCV; their median survival was 57 weeks. Covariates predictive of improved survival were gross total versus subtotal resection or biopsy (p = 0.0048) and radiation dose > or = 56 Gy (p = 0.019). While receiving BrdU, 47 patients (53%) suffered grade 3 or 4 thrombocytopenia or leukopenia; 22 patients (25%) suffered grade 3 or 4 dermatologic toxicity., Conclusion: Survival was not extended in patients with glioblastoma or gliosarcoma who received BrdU at the dose and administration schedule used in this study. The BrdU dose used in this study resulted in substantial myelosuppressive and dermatologic toxicity.

Background: Patients whose brain metastases from breast cancer are treated nonsurgically have a median length of survival ranging from 2.5 to 7.5 months, and a median time to recurrence ranging from 2 to 5 months. Patients treated with radiotherapy have a median length of survival ranging from 3 to 4 months. Those treated with chemotherapy have a median length of survival ranging from 5.5 to 7.5 months., Methods: We conducted a retrospective analysis on 63 patients treated over a 10-year period. Only patients who underwent surgery for nonrecurrent brain metastases were studied. Sixty-one patients (97%) underwent surgery within 2 weeks of diagnosis of the brain metastases., Results: The median length of survival was 16 months (95% confidence interval [CI] 11 to 22 months), and the 5-year survival rate was 17% (CI 9% to 29%). Brain metastases recurred in 27 patients at a median interval of 15 months (CI 12 to 24 months). Eleven patients had local recurrence, 10 had distal recurrence, and seven developed leptomeningeal disease. Significant prognosticators of length of survival were age (p = 0.011), menopause status (p = 0.10), postoperative radiotherapy (p = 0.054), preoperative neurologic status (p = 0.011), and preoperative systemic disease status (p = 0.0003). Systemic disease status had a significant effect on the length of survival but not on the time to recurrence.

Laser-induced autofluorescence measurement of the brain was performed to assess its spectroscopic properties and to distinguish brain tumors from the normal tissues. The excitation-induced emission spectra were plotted on a 2-dimensional map, the excitation-emission matrix, to determine the excitation wavelengths most sensitive for the spectroscopic identification of brain tumors. The excitation-emission matrices of various types of human brain tumors and normal brain samples lead to the selection of three fluorescence peaks at 470, 520, and 630 nm, corresponding excitation light at 360, 440, and 490 nm, respectively for comparing the autofluorescence signatures of brain tissue. The fluorophores most likely related to each of these peaks are NAD(P)H, various flavins, and porphyrins, respectively. In vivo studies of rat gliomas showed that "NAD(P)H", "flavin", and "porphyrin" fluorescence were lower in gliomas than in normal brain. This finding suggests that there are certain relationship between brain tissue autofluorescence intensity and metabolic activity. In vitro human normal brain tissue fluorescence signals were lower in gray matter than in white matter and "NAD(P)H" fluorescence were lower in all measured human brain tumors than in normal brain. "Flavin" and "porphyrin" fluorescence in the neoplastic tissues was lower or higher than normal tissue depending on their nature. In conclusion, the fluorescence spectroscopic diagnostic system might be able to distinguish brain tumors from the normal brain tissue. The results of this study need to be verified and the investigation extended to human brain tumors in the operating room.

Background: Brain metastases account for 20-54% of reported deaths from melanoma. Duration and quality of survival depend on the extent of metastatic disease and response to treatment. Treatment goals are palliation of symptoms and prolongation of life. No studies have directly compared surgery alone and surgery with adjunctive cranial irradiation in patients with solitary brain metastases., Methods: We evaluated postoperative adjunctive cranial irradiation in 34 patients with solitary brain metastases., Results: Overall survival was significantly improved in the 22 patients who received adjunctive cranial irradiation versus that in the 12 patients who had surgery alone. Twenty-eight patients subsequently relapsed. Nine of 10 patients with surgery alone had brain recurrence as a component of failure. Six of 10 patients not receiving irradiation had brain recurrences as a component of relapse at multiple sites whereas only 1 of 18 patients receiving irradiation relapsed with the brain., Conclusions: Adjunctive cranial irradiation is justified for melanoma patients who undergo surgical therapy for solitary brain metastases. Survival in patients presenting with solitary brain metastases was improved by a reduction of relapse in the brain as a component of failure by combined surgery and irradiation.

Matrix metalloproteinases play an important regulatory role in tissue morphogenesis, cell differentiation and motility, and tumor cell invasiveness. We have recently demonstrated elevated activity of the 92 kDa type IV collagenase (MMP-9) in human glioblastoma and in the present study examine the relative amounts of MMP-9 protein and mRNA in human gliomas and as well as the distribution of MMP-9 in human glioma tumors in vivo. Using an enzyme-linked immunosorbent assay for the quantitative determination of MMP-9 protein, we found that levels were significantly higher in malignant astrocytomas, especially in glioblastoma multiforme, than in normal brain tissues and low-grade gliomas. In addition, the amount of MMP-9 mRNA, as determined by northern blot analysis was higher in anaplastic astrocytomas and glioblastoma multiforme than in normal brain tissue and low-grade gliomas. Immunocytochemical staining for MMP-9 showed strong cytoplasmic immunoreactivity in the tumor cells and the proliferating endothelial cells of glioblastoma multiforme and anaplastic astrocytomas. The staining intensity was lowe in low-grade astrocytomas, and was undetectable or very low in normal brain astrocytes. The results indicate that expression of MMP-9 is dramatically upregulated in highly malignant gliomas and correlates with the highly malignant progression of human gliomas in vivo, and support a role for the MMP-9 in facilitating the invasiveness seen in malignant gliomas in vivo.

The 72 kDa type IV collagenase (gelatinase), a matrix metalloproteinase (MMP-2), has been proposed to potentiate the invasion and metastasis of malignant tumors. To determine the potential role of the MMP-2 in human gliomas and normal brain tissue, we examined the relative amounts of protein, mRNA, and distribution. Using gelatin zymography, densitometry, and an enzyme-linked immunosorbent assay for the quantitative determination of the MMP-2, we found that the enzyme's activity was significantly elevated in malignant astrocytomas, especially in glioblastoma multiforme, compared to low-grade glioma and normal brain tissues. As determined by Northern blot analysis, the amount of MMP-2 mRNA transcript was higher in anaplastic astrocytomas and glioblastoma multiforme tumors than in normal brain tissues or low-grade gliomas, a finding that was consistent with the amounts of MMP-2 protein detected in these tissues. Immunohistochemical studies demonstrated that MMP-2 was localized in tumor cells and vasculature cells of malignant astrocytomas. Staining intensity was clearly lower in low-grade astrocytomas, and immunoreactivity was very low or undetectable in normal brain astrocytes. The results suggest that expression of the MMP-2 is dramatically upregulated in malignant gliomas, correlating with the malignant progression of human gliomas in vivo.

The cell-surface receptor for hyaluronic acid, CD44, is expressed by both normal and malignant cells. Numerous CD44 isoforms have recently been identified that are derived by alternative ribonucleic acid splicing. The expression of some CD44 isoforms has been shown to be involved in tumor progression and metastatic spread in a rat carcinoma model and in human carcinomas. In the present study, CD44 isoform expression was evaluated by reverse transcriptase-polymerase chain reaction (PCR) analysis in frozen sections derived from three samples of normal brain tissue and from 40 brain tumors, including samples of glioblastoma multiforme, anaplastic astrocytoma, low-grade astrocytoma, cerebral primitive neuroectodermal tumor, medulloblastoma, metastatic colon carcinoma, and metastatic melanoma. Normal brain tissue adjacent to the tumors was also examined in 14 of 18 glioblastomas. In all normal brain and tumor samples, with the exception of metastases from colon carcinoma, PCR analysis demonstrated one prominent product that corresponded to the CD44H hematopoietic form of CD44. Metastases from colon carcinoma demonstrated two prominent PCR amplification products corresponding to CD44H and CD44R1. These results suggest that CD44H is the predominant isoform of this protein in normal human brain tissue and in human neuroectodermal tumors of varying degrees of malignancy. The ability of CD44H to mediate tumor cell motility and invasiveness (in contrast to CD44R1) suggests that the CD44 alternative splicing pattern of neuroectoderm-derived tumors may enhance their local biological aggressiveness and intracerebral spread. The lack of expression of larger molecular weight CD44 variants by primary brain tumors may also partially explain why these tumors rarely metastasize to distant sites.

We report on 21 patients surgically treated for intraparenchymal brain metastasis from sarcoma, including six osteosarcomas, four leiomyosarcomas, three malignant fibrous histiocytomas, two alveolar soft-part sarcomas, two Ewing's bone sarcomas, one extraskeletal osteosarcoma, one extraskeletal Ewing's sarcoma, and two unclassified sarcomas. Median survival after craniotomy was 11.8 months. Patients with a preoperative Karnofsky performance score of > 70 survived for 15.7 versus 6.6 months for those with a Karnofsky performance score < or = 70. Patients. undergoing complete resection survived 14.0 versus 6.2 months for patients undergoing incomplete resection. Patients with evidence of lung metastases at the time of surgery survived 11.8 months, which was similar to the 10.5-month survival for patients with disease limited to the brain. The two patients with alveolar soft-part sarcoma are alive at 16 and 25 months after surgery. We conclude that surgery is effective in treating selected patients with sarcoma metastatic to the brain and that patients with metastasis from alveolar soft-part sarcoma may have a relatively good prognosis if they are surgically treated. The complete removal of all brain metastases and a Karnofsky performance score > 70 are associated with a favorable prognosis, whereas the presence of concurrent lung metastases is not a contraindication to surgery.

Thromboembolic complications are the second most common cause of death in hospitalized cancer patients; they are caused by alterations of hemostasis and include hypercoagulable states, acute and chronic disseminated intravascular coagulation, and primary fibrinolysis. The fibrinolytic system is comprised of several serine protease enzymes and their inhibitors and is associated in various biological systems with physiological and pathological events such as tissue development, remodeling, invasiveness, and migratory potentials of both normal and malignant cells. It also plays a key role in the dissolution of fibrin strands. Defective fibrinolysis, which is often associated with the pathogenesis of venous thrombosis and other thromboembolic complications, occurs when the balance is disrupted, resulting in either inhibition or enhancement of fibrinolysis. The association between thromboembolic complications and neoplastic disease has been well-established since Trousseau in 1865 first reported a high incidence of venous thrombosis in a series of patients with gastric carcinoma. In this article, we discuss the factors that have been shown to be associated with thromboembolic complications in patients who harbor brain tumors, namely, hemostatic alterations caused by the tumors themselves or through interactions with neural tissue around the tumors, pre-operative hemostatic alterations in certain patients, and defective fibrinolysis associated with specific tumor types and/or tumor locations.

The cellular receptor for urokinase-type plasminogen activator (uPAR) in glioblastoma cell lines has been identified and found to be similar to the uPAR expressed by other tumor cell lines. Increased levels of uPAR have been found in primary malignant brain tumor tissues, especially highly malignant glioblastoma, and, to a lesser degree, in malignant astrocytomas, suggesting that this receptor might be involved in efficient activation of pro-uPA and confinement of uPA activity on the cell surface of invading brain tumors. The cell surface uPARs in gliomas could constitute an optimum environment for the generation and activity of plasmin, which is known to play a crucial role in the dissolution of the extracellular matrix during tumor cell invasion. In situ hybridization studies have shown that uPAR mRNA is expressed abundantly in tumor cells and is consistently present at the invasive edges of malignant gliomas. These results imply that uPAR is involved in plasmin-catalyzed proteolysis during glioma invasion and that interference with the uPA:uPAR interactions could constitute a novel approach for developing therapeutic strategies to counteract invasion of brain tumors.