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Adjunct to surgery. However, radiotherapy takes many years to reduce IGF-I and GH concentrations to acceptable levels; thus the use of additional medical therapies to alleviate symptoms may be required in the interim. Dopamine agonists Dopamine agonists e.g. cabergoline and bromocriptine ; bind to D2 receptors in the pituitary and suppress GH secretion in some patients with acromegaly; the exact mechanism of this effect is unclear. Although these agents have been shown to reduce GH concentrations, they rarely do so to acceptable level 14 ; . Review of the literature indicates that less than 10% of patients will experience normalisation of IGF-I and less than 20% of patients will achieve GH concentrations of , 5 mg l 2 ; . Higher doses of cabergoline may be more effective, but future studies are required 15 ; . Somatostatin analogues Octreotide is a long-acting synthetic somatostatin analogue that is administered subcutaneously three times daily and has demonstrated efficacy in the treatment of acromegaly. In two clinical studies, 22% to 40% of patients achieved GH concentrations , 2.5 mg l 16, 17 ; , and in a third study, 45% of patients achieved GH concentrations , 5 mg l 18 ; . IGF-I, which mediates the effects of GH, was normalised in less than half 45% ; of these patients. The use of somatostatin analogues may be limited because of a reduction in gall-bladder motility that may be associated with the development of gallstones. These typically occur in approximately 5% to 20% of patients 19, 20 ; . Long-acting somatostatin analogues are a more effective and convenient means of IGF-I normalisation in patients with acromegaly, and include octreotide LAR and lanreotide. Because these long-acting intramuscular depot preparations allow patients to receive once-monthly injections, they are considerably more convenient than the original octreotide formulation. However, a substantial proportion approximately 35% to 50% ; of patients treated with long-acting somatostatin analogues will still fail to achieve normalisation of IGF-I and GH concentrations, again underscoring the need for more effective treatments 1.
12, 2008 prime newswire ; - hana biosciences nasdaq: hnab ; , a biopharmaceutical company focused on strengthening the foundation of cancer care, today announced that the company has completed patient enrollment in its phase 1 dose-escalation clinical trial of alocrest tm ; vinorelbine liposomes injection, optisome tm.
Causing cystic transformation of the pancreatic duct Review ; S4: 99 mechanical electronically controlled pump for infusion of anticancer agents Short report ; 727 medullary thyroid carcinoma psychosocial impact of genetic testing 87 medulloblastoma in children and the prognostic value of cerebrospinal fluid cytology Short report ; 239 melanoma possible improved survival of patients receiving SRL172 immonotherapy 817 treatment with ET743 against human tumour xenografts 1233 temozolomide and fotemustine 831 MEN1 syndrome in patients with pancreatic endocrine tumors Review ; S4: 170 mesothelioma high-dose paclitaxel plus G-CSF Short report ; 597 meta-analysis of corticosteroids in advanced gynaecological and gastrointestinal cancers Special article ; 1035 survival of chemotherapy in patients with colorectal metastases to the liver 1317 metabolic support during treatment of biliopancreatic malignancy Review ; S4' 273 metabolism of continuous high-dose ifosfamide with Mesna and GM-CSF in advanced sarcoma patients 1087 metalloproteinase in the invasion and metastasis in pancreatic cancer Review ; S4' 46 inhibitor causing cell cycle phase perturbations in ovarian cancer cells Short report ; 589 in the treatment of ovarian cancer Symposium article ; SI: 65 metaplastic breast cancer prognosis and response to systemic therapy 413 metastases detection by laparoscopic staging in biliopancreatic malignancy S4: 33 metastatic bone disease and the use of oral ibandronate 311 breast cancer anthracycline-pretreated patients treated with docetaxel and gemcitabine 211 first-line chemotherapy with epirubicin and cyclophosphamide 795 patients who relapse after stem-cell transplant Letter to the editor ; 1259 phase I study of Doxil and vinorelbine Short report ; 1113 nasopharyngeal carcinoma treatment of Asian patients with a paclitaxel and carboplatin combination Short report ; 235 methotrexate 5-fluorouracil combination with Tomudex and leucovorin in first-line chemotherapy of metastatic colorectal cancer Short report ; 985 used for analysis of pharmocokinetic interactions of drugs Rapid publication ; 391 micrometastasis detection in bone marrow of pancreatic cancer patients S4: 111 microsatellite instability MSI ; in gastric MALT lymphomas and associated neoplasms 783 in non-colonic. non-HNPCC tumors Editorial ; 751 microvasculature angiogenesis in breast cancer and upregulation in basic fibroblast growth 707 minimal residual disease variability of PCR detection of the 6c -2-IgH translocation 1349 minimally invasive surgery of advanced pancreatic cancer S4: 278 mismatch repair genes in pancreatic cancer Review ; S4. 4 misunderstanding in cancer patients 39 mitochondrial toxin in chemo-resistant solid tumours 923 mitomycin combined with 5-fluorouracil, epirubicin and cisplatin in recurrent and metastatic UCNT 421 MKTO77 in chemo-resistant solid tumours 923 modulation of 5-fluorouracil and folinic acid with high-dose infusional hydroxyurea in metastatic colorectal carcinoma Short report ; 981 molecular biology developments providing a basis for classification of the endocrine tumours of the gastroenteropancreatic tract Symposium article ; S2: 9 detection of biliopancreatic malignancy Review ; S4: 153 diagnosis of at risk patients with pancreatic cancer Review ; S4: 285 with PCR detection of the bcl-2-\gH translocation 1349 markers as determinants of prognosis for ovarian cancer Symposium article ; SI: 9 its role in the diagnosis of pancreatic cancer Review ; S4: 107, 153 remissions in mantle-cell lymphoma Rapid publication ; 1293 monoclonal antibody cancer therapy Book review ; 750 imaging pancreatic adenocarcinoma Review ; S4: 37 induction of remission in the treatment of germ-cell cancer Letter to the editor ; 1393 therapy as a new approach in cancer treatment Review ; S6: 149 for patients with Waldenstroms macroglobulinemia Short report ; 1525 to detect tumor cells of pancreatic cancer patients in bone marrow S4: 111 monotherapy of patients with refractory recurrent non-Hodgkins lymphoma Short report ; 351 morbidity.
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I writing in regard to the complementary therapies section on page 47 of the December issue of The Hep C Review. I work as a naturopath in North Queensland and as a casual administrative officer at the Cairns NSP. I regard The Hep C Review as an intelligent forum and advocate for the issues surrounding hepatitis C and offer my suggestions as a practitioner to whom this section is referring. This section outlines guidelines and various questions to aid in the selection of complementary therapy practitioners with competence, experience and relevant professional standards. Given the vast array of therapies, the lack of academic standardisation, the maze of available products, I can understand why you have included quite a few questions for the HCV client to put to the practitioner. However, I feel this approach of arming the HCV client with a series of questions is impractical and may pose a conflict of interests. Natural therapists have no professional mentoring or institutionalised training systems such as exists for nurses, interns and registrars. Generally speaking, they must establish mentoring independently. They may or may not do this. They may see a prospective client as an opportunity to gain experience. The practitioner may regard themselves as experienced when they are not. A complementary therapist is generally a sole business trader. They may not wish to turn down a fee by referring on, if it means the difference between paying the rent that day or not. A further suggestion relates to your advice about doctor, specialist and natural therapist being able to consult directly with each other. My attempts to contact GP's and specialists in Far North Queensland have generally met with suspicion and incredulity. They have no idea who I and hence have no reason to trust me. The HCV client is not the person to sort this situation out. We are. My suggestion is that a register of natural therapists who wish to be involved in HCV treatment be formed. Individuals wishing to belong to this could satisfy academic and professional criteria. This register could act to.
1. Parker SL, Tong T, Bolden S et al. Cancer Statistics, 1997. CA Cancer J Clin 1997; 47: 5-27. Non-Small-Cell Lung Cancer Collaborators Group. Chemotherapy in non-small cell lung cancer. A meta-analysis using updated data on individual patients from 52 randomized clinical trials. BMJ 1995; 311: 899-909. Chevalier T, Brisgand D, Douillard JYet al. Randomized study of vinorelbine and cisplatin vs. vindesine and cisplatin vs. vinorelbine alone in advanced non-small-cell lung cancer: Results of a European Multicentre Trial Including 612 patients. J Clin Oncol 1994; 12: 360-7. Bonomi P, Kim K, Chang A, Johnson D. Phase III trial comparing etoposide cisplatin versus Taxol with cisplatin-G-CSF versus Taxol-cisplatin in advanced non-small-cell lung cancer. An Eastern Cooperative Oncology Group trial. Proc Soc Clin Oncol 1996; 15: 382 Abstr 1145 ; . 5. Adams DJ. Synergy of Navelbine-Taxol combination treatment in two human breast cancer cell lines. Proc Assoc Cancer Res 1994; 35: 327. Hoffman PC, Masters GA, Drinkard LC et al. Ifosfamide plus and viracept.
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Some of the regimens using vincristine: mopp hodgkin's disease - the letter o for oncovin ; stanford v hodgkin's disease - no letters used ; chop non-hodgkin's - the letter o ; vincristine reference links: information on vincristine from healthtouch us ; information sheet from cancaresa australia ; information sheet from cancerbackup uk ; information from project access hiv ; us ; vincristine-induced fever in children with leukemia and lymphoma - from cancer, feb 15 1988 the pharmacology of vinblastine, vincristine, vindesine, and vinorelbine from cyberbotanica by lucy snyder description and natural history of the periwinkle from cyberbotanica information on alkaloids and microtubule inhibitors from unmc manufacturer eli lilly oncovin ; customer service: 317 ; 276-2000 lilly corporate center indianapolis, indiana 46285 disclaimer: this information is general in nature
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We used sedimentation velocity to obtain thermodynamic parameters for vinca alkaloid interactions with purified tubulin isotypes, apII and aplII, as well as combined apII and III, a, II and I&IV, and aplIl and I&IV. Data were collected at 25C in 10 mM Pipes pH 6.9, 1 mM MgSO4, and 2 mM EGTA in the presence of 50 MM GTP or GDP and were fit with an isodesmic ligand-mediated or ligand-mediated plus -facilitated model to obtain binding affinities. In the presence of vincristine and GTP, K1, drug binding to tubulin heterodimers, is larger for purified apII or aplIl tubulin compared to unfractionated tubulin mean values 4.7 x 105 0.8 vs. 1.1 x 105 0.1 M' ; . Additionally purified apII or aplll tubulin form smaller spirals than unfractionated tubulin as evidenced in K, binding of drug to polymers. For example K, M -' ; from data fit with the ligandmediated model for a4Il is 4.5 x 106 0.8 vs. 1.8 x I0 0.5 for unfractionated tubulin. When apI and III are combined or mixed with other isotypes, association constants approach the unfractionated tubulin values. These differences are not observed in the presence of vinblastine or vinorelbine or GDP. Thus we conclude that vincristine interacts differentially with individual tubulin isotypes, suggesting that tubulin isotype composition may impact drug efficacy and toxicity. Supported by NR00056 S.L. ; and NS21142 A.F.
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Memory" B cells, meaning that circulating antibodies specific for the antigen circulate in the blood. Most viruses and bacteria activate not just one B cell, but many. For example, Vaccinia virus, used to immunize against smallpox Variola major ; , generates dozens of antibodies to different viral proteins. These help afford long standing protection against infection. T cell receptors, unlike antibodies, are never secreted and undergo their rearrangement and maturation in the thymus. Again, many billions of different T receptors are generated; however, these are edited in the thymus, and only a select subset though still billions ; of T cells successfully graduate from T cell education in the thymus. These T cells do not recognize "self" antigens, but do recognize self major histocompatability molecules, such as HLA-A, B, C, and D families. Unlike B cells, T cells do not recognize tertiary structures of proteins or carbohydrates, but rather recognize small fragments, or peptides of proteins which are bound to HLA molecules on other cells. CD8 + T cells recognize HLA-A, B, and C bound peptides, which CD4 + T cells recognize HLA-D bound peptides. For a T cell to become activated and expand, just being activated by antigen bound to HLA molecule is not enough. Only specialized cells, known as "antigen presenting" cells, can activate T cells. They do so by not only presenting HLA bound antigen, but also stimulating T cells through distinct cell surface receptors, such as CD28. These co-stimulatory molecules are expressed by activated dendritic cells, the most effective antigen presenting cells in the body. Dendritic cells take up antigens by endocytosis, "process" them by cleaving them into right-sized peptides, and then ensure that they bind to HLA molecules that are expressed on the cell surface. When a T cell is activated by a dendritic cell, the two signals one through the T cell receptor, the other through CD28 or similar molecules ; result in clonal expansion; that is, the rapid cell division of a single T cell into thousands of like progeny. These expanded T cells can differentiate along various lines, and some of them will persist as memory T cells, so that upon future encounters with the antigen, many more T cells are available to respond. C. More than one kind of T cell--many different subsets of T cells exist beyond CD4 and CD8 T cells. There are many different ways of classifying T cells. The most fundamental is by whether they have ever been activated by antigen before. If they have not, they are known as nave T cells. Nave T cells have a characteristic phenotype, and circulate between blood and lymphatic tissue, principally lymph nodes. They do not enter peripheral non-lymphoid tissues. On the other hand, T cells that have seen their antigen before, appropriate presented, are known as memory or memory effector T cells. They share in common their previous activation, which has led to clonal expansion. Thus, many memory T cells may share the identical T cell receptor, while every nave T cell has a slightly different T cell receptor. Beyond this common factor, memory effector T cells can differ in many different ways. 1. Cytokine Profile--It has long been appreciated that memory effector T cells can produce unique subsets of cytokines under different influences. So-called Th1 cytokines T helper 1 ; are characterized by the production of interferon gamma IFNg ; , and are generated in response to signals from the dendritic cell such as IL-12 ; . Though still called Th1, because they were originally discovered as being produced by CD4 "T helper" cells, it is clear that CD8 T cells can also produce Th1 cytokines. T cells that produce "type 1" cytokines are thought to have evolved to protect us from intracellular pathogens, such as viruses and mycobacteria. Th2 cells are generated in response to different stimuli from dendritic and other cells, including IL-4. Principal Th2 or "type 2" cytokines, which are produced by both and vivelle.
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M1' firn inliling of the problcm's actud namrE end dimensions ras Cos; tas'decision collapscthe endre Europcaa o'rganirato tion. Costas bad tbe ciau inforrriag hbr tht be vas collatring Europc. lVhen Uwe Frieseke confronted him with that fast, Costasrcspondedwith a vile, lying ar: ack againstnot onl-l'Uwe, but much of tbc European organization, hindng e\Gn then that he nz's about to unleashmassivelies againn Hdga. I did no grasp ilerr tbcD the enornritl' of thc problcm. I armburcd Cosas' psychoric episode to epmbined phpical and patrhologcal stress in tcrns of kaorn faclors, and coscenmed on calming hisr" reassuring bim that I would raurn immertia'el]'if be judged tbe sinradsn nore tlran hc could carrj'. During that telephoneconycrsation, Costa reponed tc me tha the crux of the problenr as a * 'bole was the threatcnedcollapsc of Computron, which hc reponed as thc result of the "Olympians" blocking of Cornputron's sales.This rcpon b ; ' Costas r?s Dot entirely accuratc, bur I took ir at hb word, and tras$nincd memoranda dsna.oding inmediate countetiaction 4ainst thc "Olympian" Egencicsresponsible. In rcsponseto this Costas rtrd Andy rcaded vioiently. This wasm ; , first inkling thEt Costas'anitude rorerd Cmrputron invohrcd a ncaall, v--abcrranr obsessioD, rarher than objecdvelybased cooccrn as srch. Ir was er tbar Xint that Co * as, for the firsr time, broke off comrnunication * ith me. and tbe firsr occasionhis anacks on the European organizalion focussed on Helga as tbe Erget of his ly"ing, paranoid vitriol. l er, hc did rcleot on collapsing Europc, but the pobhm worscned i! other respocts. Thc fact of the Eranei, as nrbscgue: ltl ; ' conflrmed, ws that CostashaC rmde e Cecisionto colbtse EuropE. aad hed concoctcdthe $ing atrackson Europcan EC memben and orhcrsas a $Dokes6een, a diversionof his onr mincias'a-v from tbe enormity of the immoral decisionhe had made. I also discovcrcC Colomhi3, tha he had actedsimilarll'ln his dedsionto collapne to\ + 'ardLALC, threateningthem if thel' behavingshamelessl!' onceagainattemprei to lobbl' for not uriting-off Colombia. The pcriod, after m]'return, until his pa: znoid gutburst at thc NEC meaing, is rdfirlrl. I tr'zu to rneet * 'ith CostasanC Andl', to revien' the Computron situarion.I rerieu'edthis matter and other mattersof n'ith Costasover severalhours-And1' business organizations waslateby several hoursfor the appointment. Larer, Andl'gave ' a scparate repon, contradicting dircctll'man ; 'thi: rgs had Costas rcported.I no * ' knon' that in somematten Andy'was nrong, n'asmisnken. Both, hou'ever, and in othersCostas u'ereseliing me a bill of goods.Andy', for example, assured that Comme putron's frnancial situationn'asfuUl covered b]'credit-which \A'as e ; gBeration the point of untruth. to Both attempted assure that the business to me endties, espccialll' the Computron, $'ere all in stable condition, and that onl1' werea financialproblem. failuresof the political organization As long asthcy imagined that I w; .sabout to iimit myselfro correfling the nonfeasance the field organization, of no there\ + 'as conflici. Imaginethe enormirl' of it all. Over a siri-moFthjin , weekir'. field incomehad risenin aggregate about S100, 0 CI b ; ' predominantll' field deployments- * ith the field subsidizing on \'?sdrop FEF almostentirely.Although the field pcrformance ping, clearly'a result of mismanagernent from the national performance center, the field organization's $'as nol the problem, could not be the problem.
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8, 12, 14, ; . We found no significant difference in survival between patients 10 years and 10 years of age, or between male and female patients. Bouffet et al. 17 ; , Aragones et al. 21 ; and Silverman and Simpson 28 ; also concluded that age and sex are not prognostic factors in patients with medulloblastoma. Although very young children 2 years ; do have a worse prognosis than older ones, this discrepancy may reflect inadequate treatment of the very young low-dose irradiation without proper chemotherapy ; . With optimal treatment, the difference might be less substantial. The survival difference between tumor size of 90 cm3 and 90 cm3 was not statistically significant in this study. Reports from other authors also suggested prognosis of Chang's T stage to be less important than Chang's M stage 8, 29 ; . In conclusion, we have shown that a delay of radiotherapy after surgery adversely affects the outcome of patients with medulloblastoma. Age, sex, and tumor size are not prognostic factors when modern therapy is given and voriconazole
81. Haider K, Kornek GV, Kwasny W, Weinlander G, Valencak J, Lang F, et al. Treatment of advanced breast cancer with gemcitabine and vinorelbine plus human granulocyte colony-stimulating factor. Breast Cancer Res Treat 1999; 55: 20311. Leone BA, Vallejo CT, Romero AO, Perez JE, Cuevas MA, Lacava JA, et al. Ifosfamide and vinorelbine as first-line chemotherapy for metastatic breast cancer. J Clin Oncol 1996; 14: 29939. Kornek GV, Haider K, Kwasny W, Hejna M, Raderer M, Meghdadi S, et al. Effective treatment of advanced breast cancer with vinorelbine, mitomycin C plus human granulocyte colonystimulating factor. Br J Cancer 1996; 74: 166873. Burstein HJ, Kuter I, Campos SM, Gelman RS, Tribou L, Parker LM, et al. Clinical activity of trastuzumab and vinorelbine in women with HER2-overexpressing metastatic breast cancer. J Clin Oncol 2001; 19: 272230. Nole F, Munzone E, Mandala M, Catania C, Orlando L, Zampino MG, et al. Vinorelbine, cisplatin and continuous infusion of 5-fluorouracil ViFuP ; in metastatic breast cancer patients: a Phase II study. Ann Oncol 2001; 12: 95100. Guler N, Yucel I, Ozet A, Bilkay BC, Erkisi M, Onur H, et al. Vinorelbine N ; , epirubicin E ; and 5-fluorouracil F ; combination in the first-line treatment of metastatic breast carcinoma MBC ; [meeting abstract]. Proceedings of the 2nd European Breast Cancer Conference; 2000 Sept 2630; Brussels, Belgium. Brussels: Federation of European Cancer Societies; 2001. S90. 87. Kakolyris S, Kourousis C, Koukourakis M, Androulakis N, Vamvakas L, Agelaki S, et al. First-line treatment of metastatic breast cancer with mitoxantrone, vinorelbine, and carboplatin. J Clin Oncol 1999; 22: 56872. Wendling JL, Nouyrigat P, Vallicioni D, Cals L. Cisplatin CDDP ; -mitoxantrone MTZ ; -vinorelbine VNR ; as first line chemotherapy CT ; for metastatic breast cancer: a pilot study [meeting abstract]. Proceedings of the 31st Annual Meeting of the American Society of Clinical Oncology; 1995 Mar 2023; Los Angeles, CA, USA. Alexandria, VA: ASCO; 1995. A266. 89. Subramanyan S, Abeloff MD, Bond SE, Davidson NE, Fetting JH, Gordon GB, et al. A Phase I II study of vinorelbine, doxorubicin, and methotrexate with leucovorin rescue as firstline treatment for metastatic breast cancer. Cancer Chemother Pharmacol 1999; 43: 497502.
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O17. corticAl cereBrAl neurons: tArgets for cytotoxic t cells in Anti-yo AssociAted PArAneoPlAstic syndrome Pns ; F. Aboul-Enein, 1 R. Hftberger, 2 T. Voigtlnder, 2 V. Buxhofer, 3 H. Budka, 2 and W. Kristoferitsch1; 1SMZ-Ost Donauspital, Department of Neurology, Vienna, Austria, 2Institute of Neurology, Medical University of Vienna, Vienna, Austria, and 3SMZ-Ost Donauspital, Department of Medicine, Division of Oncology, Vienna, Austria A 66-year-old man was admitted to our department because of progressive gait ataxia, acute vertigo, and incipient slurred speech and language disturbance. Three weeks earlier, the patient, who had smoked heavily for 40 years, underwent biopsy of enlarged bronchial lymph nodes. Invasion of non-small-cell lung cancer cells was found. The results of physical and neurological examination were normal except for mild tetraspasticity, gait ataxia, and dysarthria and mild aphasia. Computed tomography and MRI investigation of the brain, both performed with contrast media, showed normal results. While gait ataxia declined progressively, dysarthria and aphasia were fluctuating, thus seeming to change "from day to day." The results of radiographic follow-up investigations were repeatedly negative. PnS was suspected and then confirmed by antineuronal antibodies -- anti-Yo -- in the patient's serum. Although chemotherapy with cisplatin vinorelbine was started immediately, the patient's general condition and neurological symptoms deteriorated rapidly, and he died of septic complications five months after onset of neurological symptoms. Autopsy revealed an adenocarcinoma of the lung with infiltration of mediastinal lymph nodes only. Further detailed examination confirmed paraneoplastic cerebellar degeneration with complete loss of Purkinje cells, but also loss of cerebral cortical neurons. These changes were accompanied by infiltration of cytotoxic T lymphocytes and gliosis. In conclusion, we provide further evidence for the occurrence of anti-Yo PnS in male and in nongynecological tumors. In addition, besides already well-described cerebellar cortical degeneration, we found cortical cerebral degeneration. Our data suggest that highly specialized neurons other than Purkinje cells may serve as targets for direct cytotoxic T-cell attack. o19. csf Protein Profiling: A PotentiAl new diAgnostic And Prognostic tool for PAtients w ith lePtomeningeAl metAstAses D. Brandsma, 1 E.E. Voest, 2 W. de Jager, 3 H. Bonfrer, 4 A. Algra, 5 W. Boogerd, 6 T. Korse, 4 J.C. Reijneveld, 7 M.M. Verbeek, 8 and M.J.B. Taphoorn 9; 1Department of Neurology, University Medical Center Utrecht, Utrecht, The Netherlands, 2Laboratory of Medical Oncology, Department of Medical Oncology, University Medical Center Utrecht, Utrecht, The Netherlands, 3Department of Pediatric Immunology, Wilhelmina Children's Hospital, University Medical Center Utrecht IACOPO Institute for Translational Medicine, Utrecht, The Netherlands, 4 Department of Clinical Chemistry, Antoni van Leeuwenhoek Hospital, Amsterdam, The Netherlands, 5Department of Clinical Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands, 6Department of Neurology, Antoni van Leeuwenhoek Hospital, Amsterdam, The Netherlands, 7 Department of Neurology, VU University Medical Center, Amsterdam, The Netherlands, 8Department of Neurology, University Medical Center Nijmegen, Nijmegen, The Netherlands, and 9Department of Neurology, Medical Center Haaglanden, Den Haag, The Netherlands Background: Leptomeningeal metastases LM ; occur in 0.8% to 8% of cancer patients and are associated with a poor prognosis. The diagnosis of LM is based on clinical symptoms, MRI of brain and spine, and cytological analysis of CSF. The clinical picture of LM is highly variable, and both cytological CSF analysis and contrast-enhanced MRI are limited in sensitivity. More sensitive tools are welcomed to diagnose LM. Furthermore, to make a better estimation of the survival of LM patients so as to decide on treatment, additional prognostic indicators are needed. Methods: Using multiplex immunoassay, we measured a profile of nine proteins involved in adhesion and inflammation in the CSF of LM n and control patients systemic malignancy [n 5 20], aseptic viral meningitis [n 5 11], and other neurological diseases [n 5 19] ; and determined their potential diagnostic and prognostic value. Results: We found high CSF levels of soluble vascular cell adhesion molecule 1 sVCAM-1 ; , soluble intercellular adhesion molecule 1 sICAM-1 ; , interleukin 8 IL-8 ; , pulmonary and activation regulated chemokine PARC ; , interleukin 18 IL-18 ; , and interferon inducible protein IP-10 ; in patients with LM. The CSF protein profile in patients with LM differed significantly from the profile found in control patients. Multivariate logistic regression and ROC analysis showed that the MIA-measured CSF protein profile has an additive discriminating value for LM above standard CSF parameters. A combination of total protein, glucose, IL-8, PARC, and IP-10 CSF levels proved to be most discriminative between LM and non-LM patients. Multivariate Cox proportional hazard regression analysis further demonstrated that high IL-8 CSF levels in patients with LM predicted shortterm survival. Conclusions: Our data indicate a potential diagnostic and prognostic value of CSF protein profiling for patients with LM. The results need to be confirmed in a prospective setup before they can have clinical implications and vortex.
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Toxicity was graded and reported according to expanded criteria of the National Cancer Institute of Canada Clinical Trials Group.15, 16 The percent denotes the percentage of the 231 patients who received at least one dose of the protocol treatment. Six percent had febrile neutropenia after the dose of vinorelbine was reduced. ALT denotes alanine aminotransferase and vinorelbine.
1 Edwards JG. Long term pharmacotherapy of depression. BMJ 1998; 316: 1180-1. April. ; 2 Anderson IM, Tomenson BM. Treatment discontinuation with selective serotonin reuptake inhibitors compared with tricyclic antidepressants: a meta-analysis. BMJ 1995; 310: 1433-8. Department of Health. The health of the nation. London: HMSO, 1992. 4 Marzuk PM, Leon AC, Tardiff K, Morgan EB, Stajic M, Mann JJ. The effect of access to lethal methods of injury on suicide rates. Arch Gen Psychiatry 1992; 49: 451-8. Croft R, Gilis P. Economic comparisons of the pharmacotherapy of depression: an overview. Acta Psychiatr Scand 1998; 9: 241-52 and vytorin.
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