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Issue online:
29 Aug 2005

Received 15 December 2004; revised and accepted = 11 April=20 2005.

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Fig. 1 Morphological features of=20 oligodendrogliomas and astrocytomas make a spectrum, with classic=20 as...

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Fig. 2 1p/19q losses and TP53 = mutation=20 are mutually exclusive, thereby clearly dividing the=20 spectrum....

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Neuropathology

Volume 25 Issue 3 Page 247-253, September 2005 =

To cite this article: Keisuke Ueki (2005) = Oligodendroglioma:=20 Impact of molecular biology on its definition, diagnosis and management=20
Neuropathology 25 (3) , 247=E2=80=93253 = doi:10.1111/j.1440-1789.2005.00637.x=20

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Workshop: Modern techniques for the = pathological=20 investigation of brain tumors

Oligodendroglioma: Impact of molecular = biology on its=20 definition, diagnosis and management

Keisuke Ueki¹¹Department of Neurosurgery, = Dokkyo=20 University School of Medicine, Mibu, Tochighi, JapanKeisuke Ueki, md, PhD,=20 Dokkyo University School of Medicine, Kitakobayashi 880, Mibu, = Tochighi=20 321-0293, Japan. Email: = kueki-tky@umin.ac.jp

¹Department of=20 Neurosurgery, Dokkyo University School of Medicine, Mibu, Tochighi,=20 Japan

Keisuke Ueki, md, PhD, Dokkyo University School of Medicine,=20 Kitakobayashi 880, Mibu, Tochighi 321-0293, Japan. Email: kueki-tky@umin.ac.jp

Abstract

Molecular genetics and biology have been having=20 significant influence on the practice of neuro-oncology in recent years, = with=20 oligodendrogliomas being the most prominent example. The majority of=20 oligodendrogliomas show remarkable sensitivity to chemotherapy, and the = finding=20 that the loss of chromosome 1p was tightly associated with the response = opened a=20 new era in which the treatment can be tailored for each tumor patient = based on=20 molecular genetic diagnosis. It has been noticed that histological = features,=20 when closely examined, are also correlated with the molecular genetic = data, such=20 as losses of 1p/19q/10q and TP53 mutation. Furthermore, = expression=20 profiling using microarray technology showed that oligodendrogliomas = with 1p=20 loss express high levels of neuronal genes, suggesting that the = progenitor of=20 those tumors may be shared with neurons. Considering the rapid progress = of the=20 knowledge in neural developmental biology, it is possible that the=20 classification, definition and diagnosis of gliomas will be rewritten = based on=20 such knowledge at the molecular level in the near future, if they = reflect the=20 biological features of each tumor better than the histological diagnosis = based=20 mostly on morphology.

Oligodendroglioma has attracted increasing attention in = recent=20 years, after it was recognized as a special subset of diffuse gliomas = that shows=20 remarkable response to chemotherapy, and probably to radiotherapy as = well.=20 However, the current definition of oligodendrogliomas has a significant = room for=20 subjective judgement, thereby leading to inter-institutional variance on = the=20 diagnosis.¹ This is a = serious=20 problem because discussion on the treatment outcomes of = oligodendrogliomas would=20 not be valid if based on ambiguous diagnosis. To provide optimal = treatment for=20 each patient, we should have a clear definition of oligodendrogliomas = and=20 accurate mothods for the diagnosis. Here I would like to present a brief = overview on how molecular genetics has emerged as a new modality to = improve the=20 diagnosis and management, and I will discuss a possible change in the = way=20 oligodendrogliomas are defined in the future.

HISTOLOGICAL FEATURES OF OLIGODENDROGLIOMAS

Oligodendrogliomas are composed of tumor cells with = rounded,=20 homogeneous nuclei accompanied with clear cytoplasm (perinuclear halo) = on=20 paraffin sections presenting so-called "fried egg" or "honeycomb" = appearances.=20 Dense networks of branching capillaries are also common, demonstrating = the=20 well-known "chicken-wire" pattern. Those histological features are = easily=20 recognizable in typical cases, making the diagnosis relatively = straightforward.=20 However, such typical patterns do not appear in peripheral areas where = tumor=20 cells infiltrate normal brain. Furthermore, the morphology of tumor = cells often=20 display variation even within a single case, showing more astrocytic = features in=20 some areas and oligodendroglial features in others. Among cases showing = various=20 degrees of mixed morphology, drawing a clear line between astrocytomas = and=20 oligodendrogliomas is difficult, and histological diagnosis becomes = subjective.=20 Because there is not a well-defined histological entity of = oligoastrocytomas,=20 many cases showing some histological variations can be put into this = entity, and=20 we occasionally see significant expansion of the range covered by this = diagnosis=20 by some pathologists. However, there has been a trend, especially in the = USA, to=20 make the diagnosis of oligodendrogliomas much more frequently, possibly=20 influenced by psychological pressure from clinicians who are eager not = to miss a=20 favorable tumor. As a result, the number of cases diagnosed as=20 oligodendrogliomas exceeded even that of astrocytic tumors in some = institutions,=20 although oligodendrogliomas used to represent only 10% or less of = gliomas.² In order to organize = such=20 confusion in diagnosis, it would be helpful to schematize the situation = as=20 presented in Figure 1. This = conceptual schema shows that the morphology of oligodendrogliomas and=20 astrocytomas would make a spectrum, having typical oligodendrogliomas on = one end=20 and typical astrocytomas on the other. Where to draw the lines = separating=20 oligodendrogliomas, oligoastrocytomas, and astrocytomas within this = spectrum is=20 difficult, and therefore tends to be arbitrary. Probably, the truth was = that it=20 did not really matter for neurosurgeons or neuro-oncologists whatever = the=20 diagnosis was as long as it was within this spectrum, because the = treatment was=20 not much different anyway. However, this has changed significantly over = the last=20 two decades.

OLIGODENDROGLIOMAS AS A CHEMOSENSITIVE = TUMOR

In 1988, Cairncross and Macdonald reported that anaplastic = oligodendrogliomas=20 (World Health Organization (WHO) grade III) showed remarkable response = to a=20 chemotherapy regimen using procarbazine, CCNU, and vincristin (PCV = therapy).³ Those tumors often = showed=20 complete response to the chemotherapy administered alone, even at = recurrence=20 from successful initial treatment including radiation therapy. This = turned out=20 to be true for WHO grade II oligodendrogliomas, and oligodendroglioma = has since=20 been recognized as one of the most chemosensitive solid tumors.^4,5 In addition, it was, = of=20 course, good news for a patient that his/her tumor was likely to predict = a=20 better prognosis. It would not be surprising that such a situation has = led to=20 the increased diagnosis of oligodendrogliomas, as described earlier.

However, it was also true that not all = oligodendrogliomas=20 responded to chemotherapy; the response rate was in the range of = 40=E2=80=9370%, and the=20 next question to be asked was: which oligodendrogliomas were the good = ones=20 responding to chemotherapy, and how could we tell that?

MOLECULAR GENETIC FEATURES OF = OLIGODENDROGLIOMAS

Molecular genetic analysis on brain tumors was started on schwannomas = by=20 Seizinger et al. in the late 1980s, and was then applied to=20 gliomas.⁶ Since then, = a flood=20 of knowledge has accumulated over the last two decades, and gene = mutations, gene=20 amplifications, and chromosomal losses of various locations have been=20 identified. Among those were mutations of TP53 (p53), = CDKN2=20 (p16ARF), PTEN, gene amplifications of EGFR and=20 MDM2, and chromosomal losses of 10q, 1p, 19q, 11p, and 22q. Those = genetic=20 alterations were found in various incidences in various = grades/histological=20 subtypes of gliomas. However, how those genetic alterations would affect = the=20 clinical practice was not clear at the beginning. In 1993, von Deimling=20 et al. reported that, in glioblastomas, there was a mutual=20 exclusiveness between TP53 mutation/17p loss and EGFR=20 amplification, thereby dividing the glioblastomas into two separate = subsets=20 based on molecular genetic analysis. An important finding was that = tumors with=20 TP53 mutations tended to occur in a younger population who fared = better,=20 whereas tumors with EGFR amplification were found in older = patients whose=20 prognosis was worse, in general.⁷ This notion was soon = confirmed=20 by other groups as well, and it was also demonstrated that so-called = primary=20 glioblastomas (glioblastomas at the initial diagnosis) were more likely = to=20 harbor EGFR amplifications, whereas secondary glioblastomas=20 (glioblastomas as a result of progression from lower grade gliomas) more = commonly harbor TP53 mutations.⁸ This was the first = example of=20 the notion that molecular genetic analysis in neuro-oncology could = provide=20 clinically relevant information which histological diagnosis alone could = not.=20 With time, various positive and negative associations among genetic = alterations=20 were found in glioblastomas, and the current textbook of WHO = classification on=20 CNS tumors has integrated this knowledge, presenting genetic subsets of=20 glioblastomas in a neat figure. The idea of genetic subsets, then, may = be=20 applicable to oligodendrogliomas.

In oligodendrogliomas, it has been known that losses of = chromosome=20 1p and 19q were frequently observed, up to 40=E2=80=9370%, and those two = genetic=20 alterations most commonly appear simultaneously in oligodendrogliomas.⁹ In contrast, the = incidence of=20 TP53 mutations was not as frequent as in astrocytomas, remaining = within=20 the range of 10=E2=80=9320%. However, it was not until 1998 that those = genetic=20 alterations were linked to the clinical outcome, when Cairncross=20 et al. analyzed a series of anaplastic oligodendrogliomas = treated by=20 PCV chemotherapy as a major modality. Their study found that losses of=20 chromosome 1p and 19q, especially the former, was closely associated = with the=20 chemosensitivity of oligodendrogliomas.¹⁰ Therefore, = oligodendrogliomas=20 can be divided into a better-prognosis subset and a worse-prognosis = subset by=20 chromosomal 1p loss. This was an important achievement in neuro-oncology = in=20 which they first demonstrated that molecular genetic analysis would = influence=20 the management of patients with gliomas. Several studies followed to = confirm and=20 supplement the notion.¹¹ For=20 instance, it was noted that TP53 mutations were almost = exclusively found=20 in oligodendrogliomas without 1p loss, and that loss of 10q indicated a=20 prognosis similar to glioblastomas.^12,13 All of those = results=20 indicated that examination of chromosome 1p/19q loss was essential in = glioma=20 cases when oligodendroglioma was suspected. Then, many others started to = ask=20 further questions: what was oligodendroglioma, and what was the meaning = of=20 1p/19q loss in gliomas in general?

CORRELATION OF HISTOLOGY AND MOLECULAR = GENETICS

To the eyes of experienced neuropathologists, there were = noticeable differences in the histological features between = oligodendrogliomas=20 with 1p/19q loss and those without. Burger et al. examined = the=20 1p/19q status of 18 gliomas which were referred to them as possible=20 oligodendrogliomas, and found the combination of 1p/19q loss in six = cases. After=20 reviewing the sections, all cases with 1p/19q loss were confirmed to be=20 oligodendrogliomas by their standard, whereas the remaining 12 cases = were=20 diagnosed as astrocytomas, oligoastrocytomas, or glioblastomas.¹⁴ Sasaki = et al.=20 reviewed 44 cases of pure low-grade oligodendrogliomas, and divided = those into=20 two groups: classical oligodendrogliomas and oligodendrogliomas with = more=20 astrocytic features. 1p loss was found in 19 of 22 (86%) classical=20 oligodendrogliomas, and 16 of 22 (73%) oligodendrogliomas with = astrocytic=20 features maintained both 1p alleles.¹⁵ Ueki = et al.=20 performed a molecular genetic examination on 91 gliomas including 33=20 oligodendrogliomas and oligoastrocytomas, and compared the results with = the=20 histological diagnoses by four independent neuropathologists. There were = eight=20 cases unanimously diagnosed as pure oligodendroglioma or anaplastic=20 oligodendrogliomas by all four neuropathologists, and all of those had = 1p/19q=20 loss except for one with non-informative 1p status. TP53 mutation = was=20 detected much more frequently in cases with astrocytic features, and 1p = loss and=20 TP53 mutations were mutually exclusive in general.¹² Those studies = confirmed that,=20 although not clear-cut, there were histological features closely = associated with=20 the 1p/19q status and TP53 mutations. If histological variance in = astrocytic and oligodendroglial tumors makes a spectrum as was shown in = Figure 1, 1p/19q losers should = aggregate=20 at the oligodendroglial end, whereas TP53 mutators mostly be = located at=20 the other end (Fig. 2). = What is=20 important here is that molecular genetic data are clear-cut; "digital" = data=20 compared to the "analog" nature of histological diagnosis and drawing = lines is=20 much easier when based on molecular analysis.

INFLUENCE OF RECENT PROGRESS IN BIOLOGY

Developmental biology has been one of the most exciting fields in = molecular=20 cell biology in recent years, and neural developmental biology is = certainly a=20 part of it. Identification of neural stem cells made an epoch, followed = by rapid=20 discovery of serial molecular events leading to the formation of various = cell=20 types constituting the nervous system.¹⁶ Considering that all = glioma=20 classification and nomenclature refer to presumed origins of the tumor, = it would=20 be reasonable to expect that those new findings may advance the = knowledge of=20 glioma biology, and could provide new markers for the glioma = classification and=20 diagnosis. In oligodendroglioma, the expression of OLIG1/OLIG2,=20 helix-loop-helix transcription factors specifically expressed in cells = of=20 oligodendroglial lineage, was investigated as a potential molecular = marker for=20 oligodendrogliomas.^17,18=20 Despite the promising early reports, many laboratories demonstrated that = the=20 OLIG1/2 genes were expressed in a wide range of gliomas including = astrocytomas, and the initial excitement seems to have diminished.^{19=E2=80=9321} However, such=20 investigations are still in their early phase, and further studies along = this=20 line may well be able to identify new molecular markers for=20 oligodendroglioma.

Novel technologies have been shedding a new light on glioma biology = as well.=20 The invention of microarray technology has enabled the examination of=20 comprehensive gene expression in a relatively short period, which has = been=20 applied to investigate oligodendrogliomas. Mukasa et al. = used the=20 GeneChip (Affimetrix, Santa Clara, CA, USA) system to see the expression = profile=20 of more than 20 000 genes in gliomas including oligodendrogliomas,=20 astrocytomas and glioblastomas. Genes showing significantly lower = expression in=20 oligodendrogliomas with 1p/19q loss included numerous genes on = chromosome 1p and=20 19q, most likely reflecting the loss of whole arms of 1p and 19q.²² When they examined = genes=20 expressed significantly higher in oligodendrogliomas with 1p/19q loss, = many such=20 genes were also highly expressed in normal neurons, but not in=20 oligodendrogliomas without 1p/19q loss or other gliomas.²³ In line with this = observation,=20 recent studies demonstrated that there are indeed common precursor cells = differentiating both into neurons and oligodendroglia, and histological=20 observations also revealed that there are cases of oligodendrogliomas = showing=20 partial differentiation to neuronal cells.²⁴ Those data suggest = the=20 possibility of new markers for oligodendrogliomas with 1p/19 loss = related to=20 neuronal cells.

Invsetigating the origin of gliomas and the mechanism of = tumorigenesis in=20 humans is not an easy task because we can almost never follow the = time-course of=20 the initial tumor formation in patients. For such purposes, animal = models=20 reproducing the glioma formation process should be one of the best = tools. For=20 examle, Dai et al. created a mouse brain tumor = histologically=20 compatible with oligodendroglioma by overexpressing the PDGF gene = in=20 nestin-expressing neural progenitor cells, suggesting that those cells = could be=20 the origin of oligodendrogliomas.²⁵ At the same time, = however,=20 they also indicated that GFAP-positive astrocytes could also give rise = to=20 oligodendroglial tumors in the mouse when PDGF was overexpressed, = leaving=20 the conclusion on the origin of oligodendrogliomas still unsettled. = Although=20 many questions remain to be answered, similar efforts in the near future = may=20 resolve, at least in the mouse, which cells are the most likely origin = of=20 gliomas.

Another recent progress in cancer research related to=20 developmental biology is the emergence of cancer stem cell theory. This = theory=20 proposes that cancer cells showing heteogeneous characteristics are born = through=20 assymmetric division of cancer stem cells, a small fraction of cells = within the=20 tumor which reproduce unlimittedly, like stem cells in normal = development. A few=20 laboratories reported isolation of glioma stem cells from human gliomas, = suggesting that this theory might hold in gliomas as well. However, so = far, such=20 glioma stem cells are isolated only from highly malignant tumors, and = whether=20 low-grade gliomas also contain similar components remains to be=20 investigated.^26,27 An=20 interesting question would be whether such glioma stem cells, if they = exist,=20 arise from neural stem cells or through de-differenciation of more=20 differentiated cells like astrocytes and oligodendrocytes. Animal = models, again,=20 would be the most promising tool to answer this important = question.

LOCATION=E2=80=93GENETIC CORRELATION IN = OLIGODENDROGLIOMAS

There was one more surprising observation related to=20 oligodendroglioma: the close association between location and genetic = profile.=20 When Zlatescu et al. compared the location of their series = of=20 oligodendrogliomas with genetic analysis results, they noticed that = tumors with=20 1p/19q loss, which were practically 100% chemosensitive, were mostly = located in=20 the frontal, parietal and occipital lobes, whereas tumors with intact = 1p/19q=20 were found in the temporal lobe, insula and diencephalon. Statistic = significance=20 (P < 0.001) was unequivocal.²⁸ There seems to be = two=20 viewpoints from which this unexpected finding could be explained. One is = from=20 the environment: the specific environment in each location may provide a = growth=20 advantage to a specific genetic alteration. The other is from the tumor = origin:=20 there may be two groups of precursor cells, one giving rise to = oligodendroglioma=20 with 1p/19q loss and the other to the tumors without, and those = precursor cells=20 are distributed unevenly within the brain. Each of the two explanations = would be=20 possible, but I would prefer the latter considering the expression = profiling=20 data suggesting the different precursor cells. Either way, further = studies to=20 solve this mystery are awaited, which should shed new light on = oligodendroglioma=20 biology.

MECHANISM OF CHEMOSENSITIVITY: ANOTHER UNSOLVED=20 QUESTION

An important question is what is the molecular basis for = the=20 chemosensitivity in 1p/19q-losing oligodendrogliomas? If this question = is=20 answered, that could be extrapolated to other types of gliomas and = greatly=20 advance the knowledge on glioma chemosensitivity. Expression of = MGMT was=20 proposed to be a major factor asociated with the chemosensitivity in = gliomas,=20 and comparison between MGMT expression and 1p/19q status in=20 oligodendrogliomas found some postive association.^29,30 At this point, = however, no=20 specific molecules or genes mapped to 1p or 19q are linked to the=20 chemosensitivity observed in 1p/19q losing oligodendrogliomas. = Microarray=20 studies did not come up with specific suspects possibly affecting the=20 chemosensitivity either. Therefore, 1p/19q should be understood as a = marker at=20 this point, rather than the chromosomal location of genes involved in = the=20 chemosensitivity. We need further advancement in this front as well to = improve=20 patient care.

TOWARD A BETTER DEFINITION OF = OLIGODENDROGLIOMAS

With all those new findings accumulating, it seems to be a good time = to start=20 considering what is the best way to define and diagnose = oligodendrogliomas.

Good definition and classification should have several features: (i) = they=20 should be based on feasible and simple methods; (ii) they should = correlate well=20 with clinical characteristics; and (iii) they should be objective to = minimize=20 inter-institutional variance. Histological diagnosis has maintained all = those=20 features well over the last several decades, and it is unlikely that = molecular=20 diagnosis of the current standard would replace it completely, although = it may=20 in the future. In the management of oligodendrogliomas, however, many=20 neuro-oncologists now consider that examination of 1p/19q status is = almost a=20 "must" to provide optimal treatment for each patient if = oligodendroglioma is=20 suspected. Objectiveness is the obvious strength of molecular diagnosis, = and the=20 clinical course, such as chemosensitivity and prognosis, seems to be = well=20 predicted by molecular genetics. Furthermore, these molecular genetic = tests now=20 can be done in a relatively small laboratory in a short period, even = more=20 quickly than histological examination. Therefore, it would be reasonable = to=20 consider incorporating 1p/19q status and TP53 mutation in the = definition=20 of oligodendroglial tumors. For instance, it would be a possibility to = use=20 1p/19q status to draw the line between oligodendroglioma and = oligoastrocytoma.=20 TP53 mutation would be a strong indicator for astrocytoma, by=20 contrast.

As for the general classification of gliomas, it may = need to be=20 rewritten along the context of neural developmental biology in the near = future,=20 in a way analogous to the classification of leukemia. Hemato-oncology is = arguably the most successful field in oncology, and many leukemia = patients are=20 now practically cured by aggressive treatment. The introduction of = potent=20 chemotherapeutic agents and the advancement in bone marrow = transplantation=20 should be counted as the major factors for such success, but another = factor was=20 the establishment of a detailed classification based on the knowledge of = hematopoiesis, identifying which stage of hematopoiesis the precursor = cells=20 giving rise to the specific subtype of leukemia were at the molecular = level.=20 Progress in neuro-oncology may be achieved through a similar path, and=20 oligodendroglioma may well be a gateway to that goal.

ACKNOWLEDGEMENT

This work was supported in part by grant-in-aide to = Keisuke Ueki=20 for scientific research from the Japan Society for the Promotion of = Science no.=20 16390419.

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Dong SM, Pang JC, Poon WS et = al.=20 Concurrent hypermethylation of multiple genes is associated with grade = of=20 oligodendroglial tumors. J Neuropathol Exp=20 Neurol 2001; 60: 808=E2=80=93 816.

Medline,=20 ISI,=20 CSA

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url(/templates/jsp/_synergy.2/images/content/synergy_house/header_registe= r.gif); BACKGROUND-REPEAT: no-repeat; HEIGHT: 64px } DIV#page DIV.mySynergy { BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/content/synergy_house/header_my_syne= rgy.gif); BACKGROUND-REPEAT: no-repeat; HEIGHT: 64px } ------=_NextPart_000_007F_01C87ACC.55440FA0 Content-Type: text/css; charset="iso-8859-1" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/_synergy.2/css/print.css #page { WIDTH: 640px! important } #main_content { PADDING-RIGHT: 0px; PADDING-LEFT: 17.8em; PADDING-BOTTOM: 0px; = PADDING-TOP: 0px } .homepage #main_content { PADDING-RIGHT: 0px; PADDING-LEFT: 280px; PADDING-BOTTOM: 0px; = PADDING-TOP: 0px } #right_column { POSITION: relative } ------=_NextPart_000_007F_01C87ACC.55440FA0 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/_synergy.2/scripts/add_load_event.js function addLoadEvent(func) {=0A= var oldonload =3D window.onload;=0A= if (typeof window.onload !=3D 'function') {=0A= window.onload =3D func;=0A= } else {=0A= window.onload =3D function() {=0A= oldonload();=0A= func();=0A= }=0A= }=0A= } ------=_NextPart_000_007F_01C87ACC.55440FA0 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/_synergy.2/scripts/column_size.js /* =0A= Fix for 3 column layout in the event of left_column or right_column = being longer than main_content=0A= If a page's lh or rh columns are taller than content (so far none = encountered), this script should be included to ensure correct heights.=0A= */=0A= function matchColumns() {=0A= if (! document.getElementById("left_column")) {=0A= return;=0A= }=0A= var h =3D 280; // min height=0A= h =3D Math.max(h, = document.getElementById("left_column").offsetHeight);=0A= h =3D Math.max(h, = document.getElementById("right_column").offsetHeight);=0A= h =3D h + 20; // make main content little longer than side = regions=0A= var m =3D document.getElementById("main_content");=0A= if (m.offsetHeight < h) m.style.height =3D h + "px";=0A= }=0A= // add to the onload queue...=0A= addLoadEvent(matchColumns);=0A= =0A= function fixHeaderHeight() {=0A= var headerHeight =3D 5;=0A= for (var headerhack =3D document.getElementById("headerHack"); = headerhack; headerhack =3D headerhack.offsetParent) headerHeight +=3D = headerhack.offsetTop;=0A= if (headerHeight && (headerHeight > 90 || document.headerHeightSet)) = {=0A= document.getElementById("header").style.height =3D headerHeight = + "px";=0A= document.headerHeightSet =3D true;=0A= }=0A= }=0A= if (window.attachEvent) {=0A= /* for IE */=0A= window.attachEvent("onload", fixHeaderHeight);=0A= window.attachEvent("onresize", fixHeaderHeight);=0A= } else if (window.addEventListener) {=0A= /* for modern browsers */=0A= window.addEventListener("load", fixHeaderHeight, true);=0A= window.addEventListener("resize", fixHeaderHeight, true);=0A= } ------=_NextPart_000_007F_01C87ACC.55440FA0 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/script.js /* function that will be called from document.onload event=0A= * main event handling, for all pages */=0A= function preload() {=0A= load();=0A= }=0A= function preunload() {=0A= unload();=0A= }=0A= =0A= /* function that will be called from document.onload event=0A= * override this function to do individual onload event */=0A= function load()=0A= {=0A= }=0A= function unload()=0A= {=0A= }=0A= =0A= /**=0A= * Change the forecolor of the element with id eid=0A= * to the color specified by color=0A= */=0A= function changeForegroundColor(eid, color) {=0A= if(document.getElementById && (elem=3Ddocument.getElementById(eid)))=0A= elem.style.color=3Dcolor;=0A= }=0A= =0A= /**=0A= * Shorthand for id'ing elements=0A= */=0A= if (typeof $ =3D=3D "undefined") $ =3D function(id) { return = document.getElementById(id); } // do not override if already defined = by prototype=0A= =0A= /** ccc rights link */=0A= function RightslinkPopUp(aPublisher, aPublication, aTitle, aDate, = aAuthor, aContentId, aCopyright, aVolume, aIssue, aStartPage, aEndPage, = aIssn, aOrderBeanReset, aColor)=0A= {=0A= var location =3D=0A= "?publisherName=3D" + aPublisher=0A= + "&publication=3D" + aPublication=0A= + "&title=3D" + aTitle=0A= + "&publicationDate=3D" + aDate=0A= + "&author=3D" + aAuthor=0A= + "&contentID=3D" + aContentId=0A= + "©right=3D" + aCopyright=0A= + "&startPage=3D" + aStartPage=0A= + "&endPage=3D" + aEndPage;=0A= if (aVolume !=3D null) {=0A= location +=3D "&volumeNum=3D" + aVolume;=0A= }=0A= if (aIssue !=3D null) {=0A= location +=3D "&issueNum=3D" + aIssue;=0A= }=0A= if (aIssn !=3D null) {=0A= location +=3D "&issn=3D" + aIssn;=0A= }=0A= if (aOrderBeanReset !=3D null) {=0A= location +=3D "&orderBeanReset=3D" + aOrderBeanReset;=0A= }=0A= if (aColor !=3D null){=0A= location +=3D "&color=3D" + aColor;=0A= }=0A= =0A= var link =3D "/servlet/linkout?type=3Drightslink&url=3D" + = escape(location);=0A= var winprops =3D = "location=3Dno,toolbar=3Dno,directories=3Dno,status=3Dno,menubar=3Dno,scr= ollbars=3Dyes,resizable=3Dyes,width=3D650,height=3D550";=0A= PopUp =3D window.open(link, 'Rightslink', winprops);=0A= }=0A= =0A= =0A= /* Function to load images.=0A= * note: make this empty method so that=0A= * 1) mininize code changes; 2) for future integration; 3) easier to = take the feature back=0A= */=0A= function MM_preloadImages() {=0A= }=0A= =0A= function MM_swapImgRestore() {=0A= }=0A= =0A= function MM_findObj(n, d) {=0A= }=0A= =0A= function MM_swapImage() {=0A= }=0A= =0A= function menuMouseOver(type, actualType) {=0A= = document.getElementById('MenuItem_'+type).className=3D'MenuItemOver_'+(ty= pe =3D=3D actualType);=0A= }=0A= function menuMouseOut(type, actualType) {=0A= = document.getElementById('MenuItem_'+type).className=3D'MenuItem_'+(type = =3D=3D actualType);=0A= }=0A= function menuClick(type) {=0A= document.getElementById('MenuLink_'+type).click();=0A= }=0A= =0A= // browser detection=0A= function browserCheck() {=0A= this.ns4 =3D (document.layers)? true:false;=0A= this.ie =3D (document.all&&(!window.opera))? true:false;=0A= this.dom =3D (document.getElementById)? true:false;=0A= this.ns6 =3D (window.sidebar)? true:false;=0A= this.moz =3D = (window.sidebar||navigator.userAgent.indexOf('Gecko')!=3D-1)? true:false;=0A= this.opera =3D (window.opera)? true:false;=0A= this.mac =3D (navigator.userAgent.indexOf('Mac')!=3D-1)? true:false;=0A= }=0A= browser =3D new browserCheck();=0A= var Obj;=0A= =0A= // multibrowser get object by id, in NN4 you cannot access all object = (test it first)=0A= function getObjectByName(nameOfObject){=0A= Obj =3D null;=0A= if (browser.ie) Obj =3D document.all[nameOfObject]=0A= else if (browser.dom) Obj =3D findDOMObject(nameOfObject)=0A= else if (browser.ns4) findLayer(window,nameOfObject);=0A= return (!Obj || ( browser.ns4 && Obj =3D=3D window ) ) ? "Object not = found" : Obj;=0A= }=0A= // helper function=0A= function findDOMObject(nameOfObject) {=0A= for (var i =3D 0; i < document.images.length; i++) {=0A= if (document.images[i].name=3D=3DnameOfObject) return = document.images[i]=0A= }=0A= return document.getElementById(nameOfObject)=0A= }=0A= // helper function=0A= function findLayer(node,nameOfObject) {=0A= if ( node.name =3D=3D nameOfObject ) Obj =3D node;=0A= for ( var counter =3D 0; counter < node.document.images.length; = counter++ ) {=0A= if (node.document.images[counter].name=3D=3DnameOfObject) Obj =3D = node.document.images[counter];=0A= }=0A= for ( var i =3D 0; i < node.document.layers.length; i++ ) {=0A= findLayer(node.document.layers[i],nameOfObject);=0A= }=0A= }=0A= =0A= function toggleVisibility(id) {=0A= obj =3D getObjectByName(id);=0A= if (obj) {=0A= v =3D obj.style.display;=0A= obj.style.display =3D (v =3D=3D 'none') ? 'block' : 'none';=0A= i =3D getObjectByName('hiddenImage');=0A= if(i) i.src =3D '/page/imageHack.jsp?object=3D' + id + = '&display=3D' + obj.style.display + '&dummy=3D' + (new Date()).getTime();=0A= }=0A= }=0A= =0A= /** CSS class support */=0A= /** return true if removed, false if not found */=0A= function removeClass(el, className) {=0A= if (!(el && el.className)) return false;=0A= var cls =3D el.className.split(" ");=0A= var ar =3D new Array();=0A= for (var i =3D cls.length; i > 0;) if (cls[--i] !=3D className) = ar[ar.length] =3D cls[i];=0A= el.className =3D ar.join(" ");=0A= return cls.length !=3D ar.length;=0A= }=0A= /** return true if element has that class */=0A= function hasClass(el, className) {=0A= if (!(el && el.className)) return false;=0A= var cls =3D el.className.split(" ");=0A= for (var i =3D cls.length; i > 0;) if (cls[--i] =3D=3D className) = return true;=0A= return false;=0A= }=0A= /** add class to element, if element already had that class - does = nothink */=0A= function addClass(el, className) {=0A= if (!el || hasClass(el, className)) return;=0A= if (el.className) el.className +=3D " " + className;=0A= else el.className =3D className;=0A= }=0A= /** Add CSS rule as last rule in last stylesheet - override all previous = definitions=0A= removing is harder - not implemented, use it with caution */=0A= function addCssRule(selector, rule) {=0A= if (document.styleSheets) {=0A= var css =3D document.styleSheets[document.styleSheets.length-1]; = // get last css=0A= if (css.addRule) css.addRule(selector, rule); // IE=0A= else if (css.insertRule) css.insertRule(selector + "{" + rule + = "}", css.cssRules.length); // W3C=0A= }=0A= }=0A= /** get CSS style of the document */=0A= function getCssText() {=0A= var imports =3D "";=0A= var cssText =3D "\n";=0A= var styleSheets =3D document.styleSheets;=0A= for (var i =3D 0; i < styleSheets.length; i++) {=0A= var css =3D styleSheets.item(i);=0A= var mediaText =3D typeof css.media =3D=3D "string" ? css.media : = css.media.mediaText;=0A= if (!mediaText || mediaText.indexOf("all") !=3D -1 || = mediaText.indexOf("screen") !=3D -1) {=0A= if (css.imports) {=0A= // IE imports=0A= for (var j =3D 0; j < css.imports.length; j++) {=0A= var href =3D css.imports[j].href;=0A= var lastQuote =3D href.lastIndexOf('"');=0A= if (lastQuote !=3D -1) {=0A= // href contains media - "url" media=0A= mediaText =3D href.substr(lastQuote + 1);=0A= if (mediaText.indexOf("all") =3D=3D -1 && = mediaText.indexOf("screen") =3D=3D -1) continue;=0A= href =3D href.substr(1, lastQuote - 1);=0A= }=0A= imports +=3D '@import url("' + href + '");\n';=0A= }=0A= }=0A= if (css.rules) {=0A= // IE rules=0A= for (var j =3D 0; j < css.rules.length; j++) {=0A= // How to filter media rules ???=0A= cssText +=3D css.rules[j].selectorText + " { " + = css.rules[j].style.cssText + " }\n";=0A= }=0A= } else if (css.cssRules) {=0A= // W3C compliant browser=0A= for (var j =3D 0; j < css.cssRules.length; j++) {=0A= var rule =3D css.cssRules.item(j);=0A= if (rule.type =3D=3D rule.IMPORT_RULE || rule.type =3D=3D = rule.MEDIA_RULE) {=0A= mediaText =3D rule.media.mediaText;=0A= if (mediaText && mediaText.indexOf("all") =3D=3D -1 && = mediaText.indexOf("screen") =3D=3D -1) continue;=0A= if (rule.type =3D=3D rule.IMPORT_RULE) imports +=3D = rule.cssText;=0A= else cssText +=3D rule.cssText + "\n";=0A= } else {=0A= cssText +=3D rule.cssText + "\n";=0A= }=0A= }=0A= }=0A= }=0A= }=0A= return imports + cssText;=0A= }=0A= =0A= function loadCss(url, title, media) {=0A= var el =3D document.createElement('link');=0A= el.type =3D 'text/css';=0A= el.rel =3D 'stylesheet';=0A= el.href =3D url;=0A= el.media =3D media || 'screen';=0A= el.title =3D title || 'dynamicLoadedSheet';=0A= document.getElementsByTagName("head")[0].appendChild(el);=0A= }=0A= =0A= function loadJs(url) { =0A= var el =3D document.createElement("script");=0A= el.type =3D "text/javascript";=0A= el.src =3D url;=0A= document.getElementsByTagName("head")[0].appendChild(el);=0A= }=0A= =0A= /** DOM Event support */=0A= /** addEventListener method may already exist, it's not trivial = implement it and not break it, use other mame 'addListener' is simple */=0A= function addListener(el, evname, func) {=0A= if (el.attachEvent) el.attachEvent("on" + evname, func);=0A= else if(el.addEventListener) el.addEventListener(evname, func, true);=0A= }=0A= /** removeEventListener */=0A= function removeListener(el, evname, func) {=0A= if (el.detachEvent) el.detachEvent("on" + evname, func);=0A= else if (el.removeEventListener) el.removeEventListener(evname, func, = true);=0A= }=0A= =0A= /** Server session access */=0A= /** helper method to access session object */=0A= function _getSession() {=0A= return window.session ? window.session : (window.session =3D new = Array());=0A= }=0A= /** send request to server to preserve some value between different = requests, value is accessible using getSessionAttribute */=0A= function setSessionAttribute(name, value) {=0A= /* just to test callback */=0A= function test(doc) {=0A= // alert("Server returned: " + doc.body.innerHTML);=0A= }=0A= = sendServerMsg("/action/sessionAccess?action=3DsetJavaScriptAttribute&name= =3D" + name + "&value=3D" + value, test);=0A= _getSession()[name] =3D value;=0A= }=0A= /** see setSessionAttribute */=0A= function getSessionAttribute(name) {=0A= return _getSession()[name];=0A= }=0A= =0A= /** send request - url - to the server, response is accessible in = document passed to callback function=0A= DO NOT Send anything before page is loaded!=0A= */=0A= function sendServerMsg(url, callBack) {=0A= /* called when frame is loaded */=0A= function _receiveServerResponse(ev) {=0A= var iFrame =3D window.event ? window.event.srcElement : = ev.currentTarget; // IE : W3C=0A= var doc =3D iFrame.contentDocument ? iFrame.contentDocument : = document.frames(iFrame.id).document; // W3C : IE=0A= if (iFrame.callBack) iFrame.callBack(doc);=0A= document.body.removeChild(document.getElementById(iFrame.id));=0A= }=0A= =0A= var iFrame =3D document.createElement('iframe');=0A= addListener(iFrame, "load", _receiveServerResponse);=0A= iFrame.setAttribute("id", "msgFrame" + new Date().getTime()); // = so IE can retrive document=0A= iFrame.setAttribute("src", url);=0A= iFrame.setAttribute("style", "display:none");=0A= if (callBack) iFrame.callBack =3D callBack;=0A= document.body.appendChild(iFrame);=0A= }=0A= =0A= /**=0A= copy innerHTML of src element to innerHTML of target element=0A= */=0A= function copyInnerHtml(src, target) {=0A= var domSupported =3D document.getElementById ? true : false;=0A= var se =3D (domSupported && typeof src =3D=3D "string") ? = document.getElementById(src) : src;=0A= var te =3D (domSupported && typeof target =3D=3D "string") ? = document.getElementById(target) : target;=0A= if (se.innerHTML && te.innerHTML) te.innerHTML =3D se.innerHTML;=0A= }=0A= /**=0A= filter select options, options that do not contain filter text are = removed=0A= in first use, original select options are backed up as attribute = optionsCopy=0A= */=0A= function filterSelect(selectId, value) {=0A= var select;=0A= if (document.getElementById && (select =3D = document.getElementById(selectId)) && select.options) {=0A= if (!select.optionsCopy) {=0A= select.optionsCopy =3D new Array();=0A= select.optionTexts =3D new Array();=0A= for (var i=3D0; i'+document.title+'');=0A= tmp.writeln(el.innerHTML);=0A= tmp.writeln('');=0A= tmp.close();=0A= }=0A= if (anchor) {=0A= var target =3D (tmp.getElementById) ? = tmp.getElementById(anchor) :=0A= (tmp.all) ? tmp.all[anchor] : false;=0A= if (target) {=0A= if (target.scrollIntoView) target.scrollIntoView();=0A= else if (window.scroll && target.offsetTop) = el.popupWindow.scroll(0, target.offsetTop);=0A= }=0A= }=0A= }=0A= }=0A= =0A= /** marks all check box */=0A= function markAllCheckboxes(aForm, aNamePrefix, aChecked)=0A= {=0A= var elmts =3D aForm.elements;=0A= for (var i=3D0; i 0);=0A= if (addElmt)=0A= url +=3D "&" + elmts[i].name + "=3D" + elmts[i].value;=0A= }=0A= window.location =3D url;=0A= }=0A= }=0A= =0A= /**=0A= * @param aAuthorArray array stores all authors=0A= * @param aKeywordArray array stores all keywords=0A= */=0A= function getAuthorsAndKeywords(aForm, aAuthorArray, aKeywordArray, = aForceAdd)=0A= {=0A= setCheckWhenDefine(aForm.sauthusercbx, true);=0A= setCheckWhenDefine(aForm.keyusercbx, true);=0A= =0A= var elements =3D aForm.elements;=0A= var cntAuthor =3D -1;=0A= var cntKeyword =3D -1;=0A= for (var i=3D0; i0) || (aKeywords.length>0))=0A= {=0A= pmurl =3D = "http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?dopt=3DDocSum&cmd=3DSearch= &db=3DPubMed&term=3D";=0A= =0A= for (var i=3D0; i0) && (aKeywords.length>0)) {=0A= pmurl +=3D "+OR+";=0A= }=0A= =0A= for (var i=3D0; i0) || (aKeywords.length>0))=0A= {=0A= adsurl =3D=0A= "http://adsabs.harvard.edu/cgi-bin/nph-abs_connect?db_key=3DAST" +=0A= "&sort=3DSCORE&ttl_syn=3DYES&version=3D1" +=0A= "&txt_syn=3DYES&txt_logic=3DAND" +=0A= "&aut_syn=3DYES&aut_logic=3DAND";=0A= =0A= if (aAuthors.length > 0) {=0A= adsurl +=3D "&author=3D";=0A= for (var i=3D0; i 0) {=0A= adsurl +=3D "&text=3D";=0A= for (var i=3D0; i0) || (aKeywords.length>0))=0A= {=0A= var array =3D [aAuthors, aKeywords];=0A= for (var i=3D0; i]+>/g,"");=0A= }=0A= =0A= // go through page and check for h3 elements within div#main_content=0A= function createJumpers() {=0A= // Browser detect used here to isolate IE Mac - DOM implementation is = too buggy for this script=0A= if (navigator.userAgent.indexOf('MSIE') !=3D -1 && = navigator.userAgent.indexOf('Mac') !=3D -1) return false;=0A= // compatibility tests=0A= if(!document.getElementsByTagName) return false;=0A= if(!document.getElementById("main_content")) return false;=0A= // main function -=0A= // go through the main_content area and get an array of the div tags = present=0A= var divs_arr =3D = document.getElementById("main_content").getElementsByTagName("DIV");=0A= var selected_arr =3D new Array();=0A= var options_arr =3D new Array();=0A= for (var i=3D0; i element=0A= var container_span =3D document.createElement("span");=0A= //container_span.setAttribute("class","select_bg");=0A= container_span.className =3D "select_bg";=0A= // create the