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"Now, the eighth in the set returns to the topic of brain tumors, dealing with seven distinct types, astrocytoma, medulloblastoma, retinoblastoma, chordoma, craniopharyngioma, oligodendroglioma, and ependymoma. After updating the classification of medulloblastoma the volume provides an overview of ependymoma as well as describing the delineation of prognosis based on the genetic aberrations of the latter patients. The material offers key insights into the molecular pathways involved in tumor biology, such as the role of E-cadherin gene instability, carbonic anhydrase II, urokinase plasminogen activator, and Wnt signaling in meningioma. Contributors explain the genetic and clinical features associated with recurring meningioma, including the role played by erythropoietin receptor, and examine the way in which OTX2 transcription factor functions as an oncogene in medulloblastoma."

"The most recent developments in diagnostic and therapeutic aspects of gliomas (glioblastoma) in the brain are presented. The importance of personalized medicine and clinical validation for targeted therapy are discussed. The identification of various types of biomarkers (determined by molecular genetics) is included, along with their advantages and limitations as markers in tumor detection and diagnosis. The identification and validation of brain cancer (glioblastoma) genes are discussed. The role of cancer stem cells in the initiation and persistence of malignant gliomas is explained, response of glioblastoma cancer stem cells to various growth factors, such as epidermal growth factor receptor kinase inhibitor, is explained. The use of surgical resection, chemotherapy (e.g., temozolomide), immunotherapy, and radiation therapy for glioblastoma patients is included. Biological impediments for chemotherapy and radiotherapy for malignant glioblastoma are pointed out. Standard (established) as well as newer imaging modalities (proton magnetic resonance spectroscopy) are discussed. Also included are proton magnetic resonance spectroscopy in intracranial gliomas, and the use of proton magnetic spectroscopic imaging in determining the infiltration zone in gliomas. The role of molecular signaling in the CNS cancer development is explained, including cell death signaling in glioblastoma multiforme."

"Various aspects, including diagnosis, therapy, and prognosis, of two brain tumors (meningioma and schwannoma) , of brain tumors are discussed in this volume. Insights on the understanding of molecular pathways involved in brain tumor biology are explained. For example, the role of E-cadherin gene instability, carbonic anhydrase 11, urokinase plasminogen activator, and Wnt signaling is discussed in detail. Such information will lead to the development of effective aniicancer drugs. The role of molecular genetics and epigenetic mechanisms in schwannomas is explained. Also, is explained the role of cyclin D1 in vestibular schwannoma. The determination of subtypes of meningiomas using perfusion magnetic resonance imaging is explained. Diagnosis of incidentally discovered meningioma and cystic papillary meningioma is also included. Diagnosis of facial nerve schwannoma, vestibular schwannoma, and intermediate nerve schwannoma is explained. Treatments for atypical meningioma, oncocytic meneingioma, intracranial meningioma, and cavernous are presented. Therapeutic methods such as neurosurgery, Gamma knife radiosurgery, and adjuvant radiation for this cancer are included. Large number of other treatments, including radiosurgery, retrosigmoidal craniotomy, and immunotherapy, for vestibular schwannoma patients are detailed."

"This volume mainly contains information on the diagnosis, therapy, and prognosis of brain tumors. Insights on the understanding of molecular pathways involved in tumor biology are explained, which should lead to the development of effective drugs. Information on pathways (e.g., hedgehog) facilitates targeted therapies in cancer. Tumor models are also presented, which utilize expression data, pathway sensitivity, and genetic abnormalities, representing targets in cancer. For example, rat model of malignant brain tumors using implantation of doxorubicin with drug eluting beads for delivery is explained. The future of pathway-driven therapies for tumors is summarized. The importance of personalizing cancer care is emphasized. The need for supportive measures for survivors of brain cancer is pointed out, so is the quality of life monitoring. The need of rehabilitation therapy for patients with primary and metastatic brain tumors is also emphasized. Role of MicroRNA in distinguishing primary tumors from metastatic primary tumors is discussed. Advantages and limitations of chemotherapy (e.g., temozolomide and doxorubicin) are discussed. The complexity of tumor to tumor transfer is explained; examples discussed are: brain metastases from breast cancer and brain metastases fro non-small cell lung carcinoma. Identification and characterization of biomarkers, including those for metastatic brain tumors, are presented. Genomic analysis for identifying clinically relevant subtypes of glioblastoma is included. A large number of imaging modalities are detailed to study progression and invasion of gliomas."

"This volume contains information on the diagnosis, therapy, and prognosis of spinal tumors. Various aspects of different major types of spinal tumors (astrocytomas, ependymomas, and oligodendroglioma) are discussed. Insights into the understanding of molecular pathways involved in tumor biology are explained. Classification of intradural spinal tumors, including the percentages of each of the three major types, is detailed. Symptoms, radiological features, and clinicopathological parameters of spinal cord tumors are explained. Diagnosis, outcome, and prognosis of primary spinal cord and oligodendroglioma are discussed. Diagnosis of some other spinal tumors (e.g., pilomyxoid and chordomas) is also explained. The useful role of neuroimaging in diagnosing spinal teratoid/rhabdoid and gangliogliomas is included. A wide variety of treatments of a number of spinal cord tumor types are presented in detail. Therapies discussed include chemotherapy, surgery, radiosurgery, stereotactic radiosurgery, Cyberknife stereotactic radiotherapy, standard radiation alone, and rhenium-186 intracavity radiation. Also are duiscussed embolozation and spondylectomy. The usefulness of transplantation of human embryonic stem cells-derived oligodendrocyte progenitors and motoneuron progenitors in the repair of injured spinal cord is emphasized. Symptoms of the advent of spinal tumors are pointed out. Introduction to new technologies and their applications to spinal cord tumor diagnosis, treatment, and therapy assessment are explained."

"Latar Belakang: Tumor sistem saraf pusat (SSP) merupakan salah satu penyebab utama morbiditas di seluruh dunia yang menyebabkan disabilitas dan penurunan kualitas hidup. Tumor SSP menyebabkan defisit neurologis dan berisiko terjadinya kaheksia. Kaheksia dihubungkan dengan penurunan respons pengobatan dan penurunan kesintasan. Peradangan sistemik merupakan ciri khas kaheksia. Rasio neutrofil limfosit (RNL) merupakan penanda inflamasi sistemik yang mudah dan rutin diperiksa dengan harga yang tidak mahal. Belum diketahui hubungan antara RNL dengan kejadian kaheksia pada tumor SSP.Metode: Studi potong lintang ini dilakukan pada subjek berusia 18–65 tahun di RSUPN Dr. Cipto Mangunkusumo, yang dirawat dengan diagnosis tumor SSP pada bulan November hingga Desember 2023. Nilai RNL diambil dari pemeriksaan darah perifer lengkap dan dilakukan penegakan diagnosis kaheksia berdasarkan kriteria Evans. Dilakukan analisis hubungan RNL dengan kejadian kaheksia.Hasil: Terdapat 50 subjek dengan diagnosis tumor SSP. Median RNL adalah 4,13 (1,26; 23,22). Nilai RNL secara signifikan lebih tinggi pada kelompok subjek yang mengalami kaheksia (median RNL 7,19 (1,26; 23,22)) dibandingkan tanpa kaheksia (median RNL 3,10 (1,40; 8,48)) (p<0,001).Simpulan: RNL berhubungan dengan kejadian kaheksia pada tumor SSP. Subjek yang mengalami kaheksia memiliki RNL yang lebih tinggi dibandingkan dengan yang tidak kaheksia.

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Background: Central nervous system (CNS) tumors are one of the leading causes of morbidity worldwide, causing disability and decreased quality of life. Central nervous system tumors cause neurological deficits and are at risk of developing cachexia. Cachexia is associated with decreased treatment response and reduced survival. Systemic inflammation is the hallmark of cachexia. Neutrophil lymphocyte ratio (NLR) is a systemic inflammation that included in routine laboratory examination and inexpensive. The association between NLR and the incidence of cachexia in CNS tumors remain unknown.

Methods: This cross-sectional study was conducted on subjects aged 18–65 years old at RSUPN Dr. Cipto Mangunkusumo Hospital, who were admitted with CNS tumor diagnosis from November to December 2023. The NLR value was taken from the complete peripheral blood examination and the diagnosis of cachexia was based on Evans criteria. The relationship between NLR and the incidence of cachexia was analyzed.

Results: There were 50 subjects with CNS tumor diagnosis. The median NLR was 4,13 (1,26; 23,22). The mean NLR was significantly higher in the group of subjects with cachexia (median NLR 7,19 (1,26; 23,22)) than without cachexia (median NLR 3,10 (1,40; 8,48)) (p<0,001).

Conclusion: NLR is associated with the incidence of cachexia in CNS tumors. Subjects with cachexia had higher NLR compared to those withoit cachexia."

"Latar Belakang: Kanker primer tahap lanjut dapat bermetastasis ke sistem saraf pusat (SSP) yaitu otak dan spinal, maupun ke selain SSP. Perbedaan gejala klinis antara metastasis SSP dan tanpa keterlibatan SSP adalah defisit neurologis pada metastasis SSP. Kedua metastasis tersebut dapat berisiko menyebabkan indeks massa otot skeletal yang rendah akibat gejala klinis dan peningkatan metabolisme akibat kanker. Namun, belum diketahui perbedaan di antara keduanya. Tujuan penelitian ini untuk mengetahui perbedaan appendicular skeletal muscle index (ASMI) pada pasien metastasis dengan dan tanpa keterlibatan SSP. Metode: Penelitian ini adalah studi potong lintang pada subjek berusia 18-65 tahun. Karakteristik subjek berupa usia, jenis kelamin, indeks massa tubuh, status gizi berdasarkan ASPEN, lokasi tumor primer, lokasi metastasis, waktu terdiagnosis metastasis, defisit neurologis, asupan energi dan protein, Karnofsky Performance Scale, kemoterapi, terapi glukokortikoid, dan nilai ASMI. Analisis bivariat digunakan untuk menilai perbedaan nilai ASMI antara metastasis SSP dan tanpa keterlibatan SSP. Hasil: Terdapat 59 subjek dengan nilai ASMI rendah. Rerata nilai ASMI pada metastasis SSP lebih rendah (3,81±1,19 kg/m2) dibandingkan dengan metastasis tanpa keterlibatan SSP (3,97±0,93 kg/m2) dengan perbedaan tidak signifikan pada kedua kelompok (p = 0,568). Terdapat perbedaan bermakna antara ASMI rendah dengan jenis kelamin (p=0,000), asupan energi (p=0,012), disfagia (p=0,027), nyeri kepala (p=0,033), dan gangguan kognitif (p=0,032). Kesimpulan: Tidak ditemukan perbedaan bermakna antara subjek yang memiliki ASMI rendah pada metastasis SSP dan tanpa keterlibatan SSP. Perbedaan bermakna ditemukan antara ASMI dengan karakteristik subjek yaitu jenis kelamin, asupan energi, disfagia, nyeri kepala, dan gangguan kognitif.

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Background: Advanced primary cancer can metastasize to the central nervous system (CNS), namely the brain and spinal cord, or to other than the CNS. The difference in clinical symptoms between CNS metastases and those without CNS involvement is the neurological deficit in CNS metastases. Both metastases may be at risk for low skeletal muscle mass index due to clinical symptoms and increased metabolism due to cancer. However, the differences between them are unknown. The aim of this study was to determine the difference of appendicular skeletal muscle index in metastatic patients with and without CNS involvement. Methods: This study was a cross-sectional study on subjects aged 18-65 years. Subject characteristics included age, gender, body mass index, nutritional status based on ASPEN, primary tumor location, metastasis location, time of metastasis diagnosis, neurological deficits, energy and protein intake, Karnofsky Performance Scale, chemotherapy, glucocorticoid therapy, and ASMI value. Bivariate analysis was used to assess the difference in ASMI value between CNS metastasis and without CNS involvement Results: There were 59 subjects with low ASMI values. The mean ASMI value in CNS metastasis was lower (3,81±1,19 kg/m2) compared to metastasis without CNS involvement (3,97±0,93 kg/m2) without significant difference in both groups (p=0,568). There was a significant difference between low ASMI and gender (p=0,000), energy intake (p=0,012), dysphagia (p=0,027), headache (p=0,033), and cognitive impairment (p=0,032). Conclusion: No significant difference was found between subjects who had low ASMI in CNS metastasis and without CNS involvement. Significant differences were found between ASMI and subject characteristics such as gender, energy intake, dysphagia, headache, and cognitive impairment."

""This new book carries on a strong tradition of diagnostically oriented texts established by the Biopsy Interpretation Series, in the present case focused on lesions of the Central Nervous System. Our purpose is to provide a practical guide and concise reference that can be a companion text for the general surgical pathologist, trainees in pathology and neuropathology, and clinicians who treat patients with neurological diseases that require surgical sampling. Given the heavy orientation of the Biopsy Interpretation Series to the busy and serious-minded diagnostician, we have taken this opportunity to create something new and, we think, useful. While there are certainly several excellent books on neuropathology and surgical neuropathology, the majority are reference texts that are comprehensive and encyclopedic, making them less than optimal on a daily basis to assist with interpretation. Because the central concern here is with establishing the correct diagnosis, the content is aimed at anticipating difficult diagnostic decisions and providing concise and reliable guide to their resolution"--Provided by publisher."

"Latar Belakang: Tumor sistem saraf pusat (SSP) meningkatkan tekanan intrakranial dan menyebabkan berbagai gangguan neurologis yang dapat memengaruhi status gizi pasien. Status gizi memengaruhi imunitas bawaan dan adaptif. Pada hampir semua jenis keganasan kadar asam amino rantai cabang (AARC) didapatkan rendah. Asam amino rantai cabang meningkatkan imunitas dengan meningkatkan fagositik neutrofil, proliferasi limfosit, sintesis protein, menjaga jalur pensinyalan yang sensitif terhadap nutrisi. Rasio neutrofil limfosit (RNL) menggambarkan keseimbangan sistem imunitas dengan inflamasi. Peningkatan RNL dihubungkan dengan penurunan respon imun tubuh, terapi, harapan hidup dan prognosis. Penelitian ini dilakukan untuk mengetahui hubungan asupan AARC terhadap RNL pada pasien tumor SSP.Metode: Penelitian ini merupakan studi potong lintang pada pasien tumor SSP yang dirawat di RSCM. Karakteristik subjek berupa usia, jenis kelamin, jenis tumor, defisit neurologis, status performa karnofsky, indeks massa tubuh (IMT), status gizi berdasarkan ASPEN, penyakit komorbid, status infeksi, kemoterapi, radiasi, dan atau kemoradiasi, terapi glukokortikoid, asupan energi dan protein, asupan AARC, serta nilai RNL. Dilakukan analisis hubungan antara dua kelompok asupan AARC yang dibagi sesuai median populasi penelitian terhadap RNL.Hasil: Terdapat 66 subjek penelitian dengan median usia 48 tahun, mayoritas subjek perempuan (56,1%), dengan jenis tumor sekunder sebanyak 38 subjek (57,6%). Defisit neurologis tertinggi berupa nyeri kepala (60,6%), proporsi status performa karnofsky terganggu sedang-berat (60,6%). Proporsi IMT estimasi normal sebanyak 34,8%, rerata IMT 23,46 ± 4,95 kg/m2, dengan mayoritas malnutrisi (54,5%) berdasarkan kriteria ASPEN. Mayoritas subjek tidak memiliki komorbid (65,2%), tidak infeksi (80,3%), tidak menjalani kemoterapi, radiasi dan atau kemoradiasi (84,8%), serta tidak mendapat glukokortikoid (71,2%). Rerata asupan energi 1519 kkal, protein 65 g/hari, median AARC 9 g/hari. Terdapat perbedaan bermakna nilai RNL (p=0,047) pada kelompok asupan AARC <9 g/hari (median RNL 4,9); pada kelompok asupan AARC ≥9 g/hari (median RNL 3,1).

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Background: Central nervous system (CNS) tumors increase intracranial pressure and cause various neurological disorders that can affect the nutritional status of patients. Nutritional status influences both innate and adaptive immunity. In almost all malignancies, low levels of branched-chain amino acids (BCAA) are observed. Branched-chain amino acids enhance immunity by increasing neutrophil phagocytosis, lymphocyte proliferation, protein synthesis, and maintaining nutrient-sensitive signaling pathways. The neutrophil lymphocyte ratio (NLR) reflects the balance of the immune system with inflammation. An elevated NLR is associated with decreased body immune response, therapy outcomes, life expectancy, and prognosis. This study aims to determine the relationship between BCAA intake and NLR in CNS tumor patients.

Method: This is a cross-sectional study on CNS tumor patients treated at RSCM. Subject characteristics include age, gender, tumor type, neurological deficits, Karnofsky performance status, body mass index (BMI), nutrition status based on ASPEN, comorbidities, infection status, chemotherapy, radiation, and/or chemoradiation, glucocorticoid therapy, energy, and protein intake, BCAA intake, and NLR values. The analysis examines the relationship between two groups of BCAA intake divided according to the study population's median with NLR.

Results: There were 66 study subjects with a median age of 48 years, mostly female subjects (56,1%), with 38 subjects (57,6%) having secondary tumors. The highest neurological deficit was headache (60,6%), and the majority have a moderately to severely impaired Karnofsky performance status (60,6%). The proportion of estimated normal Body Mass Index (BMI) was 34.8%, with a mean BMI of 23,46 ± 4,95 kg/m2, and the majority were malnourished (54,5%) based on ASPEN criteria. Most subjects had no comorbidities (65,2%), no infections (80,3%), did not undergo chemotherapy, radiation, and/or chemoradiation (84,8%), and did not receive glucocorticoids (71.2%). The mean energy intake was 1519 kcal, protein intake 65 g/day, and the median BCAA was 9 g/day. There was a significant difference in the NLR values (p=0,047) between the group with BCAA intake <9 g/day (median NLR 4,9) and the group with BCAA intake ≥9 g/day (median NLR 3,1).

Conclusion: BCAA intake is related to NLR values in CNS tumor patients. Higher BCAA intake is associated with lower NLR values."