Cerebral astroblastoma: analysis of six cases and critical review of treatment options

CLINICAL STUDY - PATIENT STUDY

Cerebral astroblastoma: analysis of six cases and critical reviewof treatment options

Maurizio Salvati Æ Alessandro D’Elia Æ Christian Brogna ÆAlessandro Frati Æ Manila Antonelli Æ Felice Giangaspero ÆAntonino Raco Æ Antonio Santoro Æ Roberto Delfini

Received: 24 August 2008 / Accepted: 30 December 2008 / Published online: 13 February 2009

� Springer Science+Business Media, LLC. 2009

Abstract Astroblastoma is one of the rarest tumors of the

central nervous system (CNS), and its classification, his-

togenesis, diagnosis and therapeutic management are still

being debated. The typical histopathological appearance is

the perivascular, astroblastic pseudorosette, which is

however present in other CNS tumors. To clarify the

clinical, radiological, histopathological, prognostic and

therapeutic characteristics, which have been treated only

recently and are not well established yet due to the rarity of

this tumor, six cases of histologically proven astroblastoma

were retrospectively analyzed in light of more pertinent

literature and paying special attention to therapeutic

remarks. Between 1996 and 2005, six patients with cere-

bral astroblastoma were surgically treated at the

Department of Neurosciences—Neurosurgery of Sapienza

University in Rome. In three cases the lesion was termed

low-grade astroblastoma, and high grade in the other three,

according to current standard parameters. Median age of

the six patients was 36 years. The time to diagnosis ranged

from 1 week to 18 months. The radiological and ana-

tomopathological features of this lesion are described.

Surgical removal was total in four cases and subtotal in

two. All patients received radiotherapy: two also had

chemotherapy with temozolomide (TMZ). The three

patients with low-grade astroblastoma are still alive today

after a follow-up of 2, 5 and 19 years, respectively. Of the

three patients with high-grade lesions, one is still alive after

a 7-year follow-up, while the other two survived for

17 months (progression time 15 months) and 35 months

(progression-reoperation time 23 months), respectively.

Conclusions radical surgical resection is the treatment of

choice for astroblastomas. Radiotherapy may play an

adjuvant role in the treatment of high-grade lesions. The

role of chemotherapy is still very debatable. We propose an

aggressive standardized treatment for those lesions that

meet anaplastic criteria, owing to their postulated glial

origin and the propensity to have aggressive courses, and

we advocate the use of a safe adjuvant chemotherapeutic

regimen with TMZ, used concomitantly and subsequently

to radiotherapy, especially for the high-grade astroblastoma

cases. Multicenter studies, taking into account molecular

biological findings, are necessary to define a common

therapeutic strategy for astroblastomas.

Keywords Astroblastoma � Astroblastic pseudorosette �Low-grade glioma � High-grade glioma �Adjuvant therapy

Introduction

Cerebral astroblastoma is one of the rarest tumors of the

central nervous system (CNS). Its incidence has been cal-

culated to be between 0.45 and 2.8% of all primary brain

tumors [1], occurring most often in infants and young adults.

The nosological and clinical features make astroblastoma a

particularly challenging pathology in terms of both diag-

nosis and definition. The same can be said for the therapeutic

strategy, prognosis and follow-up of this lesion owing to the

M. Salvati (&) � A. D’Elia � C. Brogna � A. Frati �M. Antonelli � F. Giangaspero � A. Raco � A. Santoro �R. Delfini

Department of Neurological Sciences-Neurosurgery, University

of Rome ‘‘Sapienza’’, Via Cardinal Agliardi, 15, 00165 Rome,

e-mail: Salvati.Maurizio@libero.it

M. Salvati � F. Giangaspero

Department of Neurosurgery, INM Neuromed IRCCS,

Pozzilli, IS, Italy

J Neurooncol (2009) 93:369–378

DOI 10.1007/s11060-008-9789-9

fact that over the last 20 years not more than 60 cases have

been described as either series or single case reports.

We describe a personal series of six patients with his-

tologically confirmed astroblastomas referred to us

between 1996 and 2005, three with low-grade and three

with high-grade lesions, according to the histological cri-

teria proposed, with the aim of a better characterization of

this tumor entity and the proposal of a safe but aggressive

standardized adjuvant regimen for high-grade cases. The

clinical-radiological, histological and therapeutic charac-

teristics of astroblastoma with the relative follow-up and

prognostic data are discussed, and one of the low-grade

cases with an unusual onset, clinical history, diagnosis and

evolution is described in greater detail.

Materials and methods

Between 1996 and 2005, six patients with histologically

diagnosed cerebral astroblastoma were surgically treated in

the Neurosurgery Division—Neurosciences Department of

Sapienza University of Rome. Table 1 summarizes the

clinical, radiological, therapeutic, follow-up and survival

data of these patients. According to the parameters of Brat

et al. [2], the cases were divided as follows: in three cases

the astroblastoma was low grade, in the other three high

grade. Diagnosis and definition of histotype were carried

out according to the standard international criteria gov-

erning fixation, coloration and interpretation of histological

samples [3]. All six tumor samples from surgical speci-

mens were formalin-fixed and routinely processed, and

each section of 4 lm was stained with hematoxylin and

eosin (Fig. 1a–f). Each slide was reviewed for architectural

and biological characteristics, and mitotic activity was

evaluated by examining ten high-power fields in the region

of high cellularity. All tumors defined as astroblastoma

exhibited variable focal GFAP (Fig. 1g–h) and S-100

immunoreactivity, and monoclonal MIB-1 antibodies were

used to determine the Ki-67 index. For all patients clinical

records were reviewed, and treatment responses were

documented.

Results

Median age in this group of patients was 36 years, with a

range from 27 to 50 years. With respect to epidemiological

studies, this series corresponds to the upper age limit since

there were no pediatric cases. Presenting symptoms

included focal deficits, such as partial seizures (one low-

grade case), aphasia (one low-grade case), hemiparesis

(two cases, one high and one low grade), and right

hemianopsia (one high-grade case). In one high-grade case,

onset consisted of symptoms attributable to intracranial

hypertension. The time from onset to diagnosis ranged

from 1 week (high grade) to 1.5 years (low grade). The

localization of the lesions was as follows: two frontal, two

temporal, one occipital and one parieto-occipital lesion

(see Table 1 for details). At MRI study the lesions

appeared as large, lobulated, peripheral, supratentorial,

solid contrast enhancing, and cystic masses, isointense to

gray matter on T2 signal, sometimes with punctuate

calcifications.

In terms of histopathological characteristics, we point

out the case of a 30-year-old patient who was diagnosed

within a week because his symptoms were those of intra-

cranial hypertension. Surgery brought to light a high-grade

astroblastoma in a right cortical-subcortical temporal

localization. In this patient all the criteria indicating

malignancy were fulfilled: a MIB-1 index of 8%, increased

cellularity, high mytotic index, areas of necrosis and vas-

cular proliferation. Despite the fact that all the predisposing

histopathological features for a worse prognosis were

present, he is still alive 7 years after total removal, whole-

brain radiotherapy (WBRT) and adjuvant chemotherapy

with temozolomide, and the patient presented no signs of

recurrence at follow-up MRI.

The remaining cases, two high grade and three low

grade, were treated by total resection, with radiological

convalidation, with the exception of one low-grade and one

high-grade case in which the extent of resection was

subtotal.

Adjuvant radiotherapy was performed in all cases: four

patients received conformational radiotherapy for a total of

60 Gy, while two patients, one with high grade and one

low grade lesions, received WBRT with Co-60. In only two

cases, one high grade and one low grade, radiotherapy was

followed by adjuvant chemotherapy, employing conven-

tional cycles of temozolomide, according to a protocol

practically identical to the traditional one employed for

high-grade gliomas.

The three patients with a histologically low-grade

astroblastoma are alive today after a follow-up of 2 years,

5 years and 18 years 9 months, respectively. Of the three

patients with a histologically high-grade lesion, one is still

alive at 7-year follow-up, while for the other two, survival

times were 17 months (with progression after 15 months)

and 35 months (with progression and reoperation at

23 months), respectively.

The authors present the case of a patient with low-grade

astroblastoma diagnosed 18 years and 9 months ago.

Long-term survivor: clinical case

This 50-year-old woman presented 20 years ago with

absence-type comitial seizures. Two years later, after a

370 J Neurooncol (2009) 93:369–378

fronta

ring-s

Long-t

ianopsi

J Neurooncol (2009) 93:369–378 371

generalized seizure, a brain MRI revealed a solid cortical-

subcortical expansive lesion in a right rolandic site

(Fig. 2a–b). The lesion, which had a cystic component and

was well circumscribed with respect to the surrounding

parenchyma, did not display contrast enhancement. The

patient was submitted to surgery, and apparently total

removal of the neoplasm was achieved.

Postoperative neurological assessment showed a residual

spastic paresis in the left leg. Histological analysis of the

surgical sample led to a diagnosis of low-grade tumor with a

mixed oligodendroglial and astrocytic component. Fifteen

years after the first operation, in 2003, a control MRI with

paramagnetic contrast enhancement documented the signs

of the first operation, but no evidence of recurrence (Fig. 3a–

Fig. 1 a–b Hematoxylin and

eosin (HE) stain at 9200

magnification showing

perivascular astroblastic

pseudorosette that shows up as a

perivascular ribbon on

longitudinal images. Vascular

hyalinization is prominent, and

neoplastic cells show round and

ovular nuclei with vesicular

chromatin and a rim of

eosinophilic cytoplasm, and are

orientated around the vascular

channel with marked

hyalinization. c HE stain at

9250 showing the classic

astroblastic pseudorosette: some

areas are completely replaced

by connective tissue. d–f HE-

stained specimens at 9400

magnification. Characteristic

perivascular pseudorosette with

neoplastic cells orientated in

perivascular manner (d) and

with vascular thickening (e).

The characteristic shape of

astroblastoma nuclei are round

with nucleoli and abundant

eosinophilic cytoplasm (f).g–h Cellular processes within

the perivascular rosettes are

immunoreactive for GFAP

(9200 magnification).

(a–h: 27-year-old female

patient; b–d: 39-year-old female

patient; e–g: 50-year-old female

patient; f: 33-year-old male

patient; see Table 1 for details)

372 J Neurooncol (2009) 93:369–378

b). In December 2005, therefore, approximately 18 years

after the first operation, despite the fact the neurological

situation had not varied throughout the years, another MRI

with gadolinium was performed. This time, there were clear

signs of recurrence in a more anterior localization than

before (Fig. 4a–c). Reoperation was performed with the aid

of neuronavigation. Early postoperative MRI with Gd con-

firmed total removal of the recurrence (Fig. 5a–c).

Postoperative neurological assessment did not vary sub-

stantially from the preoperative one. Since histological

diagnosis of the surgical sample was grade III (WHO) ana-

plastic astroblastoma (Fig. 6a–c), the patient was submitted

to adjuvant chemotherapy with temozolomide according to

the protocols for high-grade gliomas. Moreover, a review of

Fig. 3 a–b Long-term survivor case. Post-contrast-enhanced cerebral

MRI (a sagittal; b coronal) performed 15 years after first operation in

2003 showing signs of the past surgery, but no evidence of residual/

recurrent disease

Fig. 2 a–b Long-term survivor case. Cerebral MRI (a coronal;

b sagittal) performed in 1988 (1.5 T) showing the presence of a

neoformation sited in the rolandic-prerolandic cortico-subcortical

area on the right, within the paracentral lobule, apparently well

circumscribed with respect to the cerebral parenchyma

J Neurooncol (2009) 93:369–378 373

the previous histological sample, with the aid of the recent

advances for identification of this lesion, classified the pri-

mary lesion removed 18 years before as a low-grade

astroblastoma: after all these years, it had undergone a

transformation into the malignant form.

Discussion

Astroblastoma is one of the rarest tumors of the CNS, and

its classification, histogenesis, diagnosis and therapeutic

Fig. 4 a–c Long-term survivor case. Post-contrast cerebral MRI

(a coronal; b sagittal; c axial) performed 18 years after the first

operation, demonstrating the presence of a neoformation with a ring-

shaped contrast enhancement anteriorly to the precedent surgical

cavum, sited in correspondence with the posterior part of the superior

frontal gyrus (F1)

Fig. 5 a–b Long-term survivor case. Post-contrast cerebral MRI

(a coronal; b sagittal) performed 24 h after the second operation,

showing the macroscopically total removal of the lesion

374 J Neurooncol (2009) 93:369–378

management are still being debated. In the last WHO

classification of tumors of the nervous system [3], cerebral

astroblastoma was included among the neuroepithelial

tumors other than the astrocytic, oligodendroglial or

ependymal ones.

The clinical onset was the fairly typical one of expansive

brain lesions exerting a mass effect, the most commonly

described symptoms being vomiting, headache, epileptic

seizures and loss of consciousness. Characteristic features

for a diagnostic orientation are the young age and the

localization of the lesion, since astroblastoma almost always

presents as an intra-axial peripheral supratentorial lesion,

more frequently in the vicinity of the convexity, and more

often involves the frontal and parietal lobes of a single

hemisphere, or presents in a medial-sagittal site [4]. Excep-

tionally, other localizations have been reported [4–10].

On CT scan, this lesion may present occasional pointed

calcifications.

On MRI, the typical aspect of astroblastoma is that of a

relatively large mass, from a few millimeters to 8 cm in

diameter [10], that is well circumscribed, lobulated,

peripheral and typically supratentorial. Usually, the mass

consists of a group of solid, cystic lesions. The uneven

‘‘bubbly’’ appearance of the solid component on

T2-weighted sequences is fairly characteristic. Considering

the size of the lesion, the hypointensity on T2-weighted

images is usually noteworthy and is due to the fact that this

lesion is not usually infiltrative and does not cause

important edema (Fig. 2). Contrast enhancement is slight

and heterogeneous, and often includes the capsule/border

of cystic lesions. Usually, there are no substantial differ-

ences between the appearance of high-grade and low-grade

lesions, although the latter may have a very aggressive

natural history.

MR (H?) spectroscopy and diffusion-perfusion

sequences may be helpful in distinguishing high from low

grades [11, 12], but their role in the diagnostic-prognostic

and therapeutic process, while promising, is still not well

established.

The typical histopathological features of astroblastoma

were first described by Bailey and Cushing [13] and Bailey

and Bucy [14]. They consist of a perivascular astroblastic

pseudorosette that shows up as a perivascular ribbon on

longitudinal images and are made up of epithelioid neo-

plastic elements. These structures are characterized by

elongated tumoral cells with abundant eosinophilic cyto-

plasm and a short cytoplasmatic process that is anchored to

the wall of the stromal blood vessels (Fig. 1) [2, 4, 9, 15–

17]. Often there is perivascular hyalination (Fig. 1b), and

the borders of the tumor more commonly compress, rather

than infiltrate, the surrounding tissue [2, 4].

The perivascular pseudorosette is not, in fact, peculiar to

astroblastomas, but may also be a feature of high- and low-

grade astrocytomas, PNET, glioblastomas and ependymo-

mas. However, in astroblastomas this lesion is dominant

and diffuse [4]. As a matter of fact, for a long time before

the discovery of a peculiar genetic and molecular alteration

pattern [2, 18–20], it was doubted that astroblastoma was

really a separate nosological entity [21, 22] because its

features lie halfway between those of astrocytoma and of

ependymoma. In fact, ependymomas are characterized

above all by thin, perivascular fibrillary processes that have

not been observed in astroblastomas, which display a low

fibrillarity (Fig. 1d); furthermore, an astroblastoma is more

frequently hemispheric and more superficial rather than

periventricular like the ependymoma, and the perivascular

hyalinization that often characterizes astroblastomas

(Fig. 1b) is not at all typical of ependymomas. Other

explanations for the confusion surrounding astroblastomas

since they were first described lie in the lack of restrictive

diagnostic criteria prior to 1989 [4] and the ambiguity of

Fig. 6 a–b Long-term survivor case. Hematoxylin and eosin stain

(910) of the high-grade case recurrence specimen, showing a

perivascular pseudorosette and high cellularity (Fig. 5a). The GFAP?

immunostaging (Fig. 5b) results in a focal pattern. Tumor cells show

an epithelial appearance, with plump nuclei, evident nucleoli and

eosinophilic cytoplasm. Neoplastic cells form an astroblastic pseu-

dorosette and are composed of a single cell layer

J Neurooncol (2009) 93:369–378 375

the term ‘‘astroblastoma’’ since this lesion is not clearly

‘‘astrocytic’’ or ‘‘blastic.’’

It has been suggested that this tumor might originate from

the tanicyte, a glial precursor whose characteristics lie

between those of astrocytes and ependymocytes [23].

Another important aspect is the appearance of the interface

between the tumor and the healthy tissue, because the bor-

ders of the lesion more often compress rather than infiltrate

the brain parenchyma [2, 4, 9, 19]. This observation is fun-

damentally important for understanding the behavior of this

tumor and, in particular, allows its radical surgical excision.

In fact, infiltrative foci via tumoral tongues/fibrils into the

adjacent tissue were reported in very few cases [2].

For establishing the glial nature of this tumor, immu-

nohistochemical studies have shown a variable but strong

positivity for GFAP, especially perivascular, and a more

uniform positivity for vimentine and protein S-100. The

positivity generally displayed for neuron-specific enolase

(NSE) and cytocheratin was less marked, whereas reac-

tivity for the epithelial membrane antigen (EMA) was only

minimal: all these findings were similar to those found in

the literature [1, 17, 24–26].

Anyway, it appears more interesting to understand the

natural history and prognosis of this type of tumor. Three

recent series [2, 4, 15], comprising a total of 50 cases,

showed that astroblastomas could be roughly divided into

two prognostic groups on the strength of histopathological

and biological criteria as either low grade/well-differenti-

ated or high grade/malignant. For the high-grade variety,

these parameters include: (1) areas of high cellularity, (2)

anaplastic nuclear pattern, (3) high mycotic index ([5/10

HPF, high power fields), (3) vascular proliferation, (5)

necrosis, eventually with pseudopalisades and (6) MIB-1

proliferative index between 6 and 22%. Of the 21 low-grade

cases available to follow-up, considering all the three above-

mentioned series together, only 4 (19%) presented a recur-

rence after total removal. In three of these the lesion had

undergone a transformation into a more aggressive type

(glioblastoma and gliosarcoma), while in the remaining

case, which recurred after 6 months, the patient is still alive

at 3-year follow-up. In the rest of the low-grade cases, there

were patients who presented a disease-free interval of up to

20 years. All the recurrences were treated by surgery plus

radiotherapy. Of the 18 high-grade cases available to follow-

up, only 6 had not recurred after surgery (recurrence rate

67%). Follow-up varied from 15 to 64 months, and all

patients but two had been given adjuvant radiotherapy.

In these three series, the number of long-term survivors

varied considerably, probably owing to several factors,

such as the localization of the tumor, the extent of resection

and the response to adjuvant treatment [2]. The interval

before recurrence of the lesion after total removal varied

from 6 months to 8.5 years.

Actually, given the rarity of this pathology, the prognostic

criteria available were not always reliable, and there were

some cases of an unforeseeable or unusual progression of the

illness. In fact, in our cases, a 30-year-old male with high-

grade astroblastoma who received a total resection and was

treated with adjuvant radiotherapy and chemotherapy is still

alive at 7 years of follow-up, whereas the other two patients

with high-grade astroblastoma died after 17 and 34 months,

respectively, from the diagnosis. Concerning the literature,

Yunten et al. [27] reported a case in which a low-grade

astroblastoma was difficult to diagnose because its features

were those of an extra-axial lesion, and Lau et al. [28]

reported a case in which a low-grade astroblastoma recurred

12 months after apparently total resection.

The natural history of this pathology can be summed up

by two main considerations: (1) the duration of symptoms

before diagnosis, often between 1 and 5 months, but pos-

sibly as long as 2–4 years; (2) the high number of long-

term survivors after total removal of the lesion. Generally

speaking, these features point to astroblastoma being a

slow-growing tumoral pathology; however, we do not

know to what extent this is due to the real propensity of this

lesion to become more aggressive and to what extent to the

diagnostic difficulties that could lead to pathologies in

which astroblastoma only represents the focal lesion of a

low-grade disease [4].

However, there can be no doubt regarding the value of

surgical treatment that can be validated by both theoretical

and practical considerations. In fact, one theoretical factor

leading to longer survival and absence of disease, in other

words a better prognosis, is the non-infiltrative nature of this

tumor, whose growth is almost always expansive, com-

pressing the surrounding tissues and allowing cleavage and

total removal even in high-grade lesions [4, 9, 19]. There-

fore, in practical terms, total resection of astroblastoma may

be curative [2], although a longer period of follow-up

observation is necessary in such cases, like in our low-grade

case, which recurred 18 years after total resection (Fig. 2).

Another controversial point regards the effectiveness of

adjuvant therapy. In some selected cases, the efficacy of

radiotherapy has been widely demonstrated [4, 27], but

mainly with reference to high-grade cases. In fact, the only

patient who had been submitted to radiotherapy after

biopsy alone was still alive 12 years after diagnosis.

Moreover, the only patient with a high-grade astroblastoma

who had not been submitted to adjuvant radiotherapy

presented the worst prognosis, with a survival time of

1.5 years, and Cabello et al. [25] reported the case of a

patient who was not treated with adjuvant radiotherapy and

had a recurrence after just 6 months. More recently, Lau

et al. [28] described the case of a patient with a low-grade

lesion removed totally, but not treated by adjuvant radio-

therapy, who presented a recurrence 12 months after

376 J Neurooncol (2009) 93:369–378

surgery. Subtotal removal of the recurrence was followed

by radiotherapy and, although follow-up MRI showed the

tumor residue, the disease appeared to be under control.

It therefore appears evident that adjuvant radiotherapy is

effective and undoubtedly advisable for high-grade lesions

that warrant a more aggressive approach; for low-grade

lesions, the therapeutic strategy with reference to radio-

therapy still has to be clearly defined [4, 15, 28, 29]. Our

strategy consisted of treating the three low-grade astrocy-

tomas by adjuvant radiotherapy, too, given their probable

radio-sensitivity and unpredictable evolution, but our results

will only be assessable in due time by a comparison with a

larger number of cases and in light of wider experience.

Even more controversial is the situation regarding che-

motherapy. In the series described by Bonnin and

Rubinstein [4], five patients (two with high-grade lesions,

two with low grade, and one uncertain) were given adju-

vant chemotherapy, but the poor results obtained did not

make it possible to draw any conclusions. On the other

hand, Thiessen et al. [15] described four high-grade

patients who were treated by adjuvant chemotherapy after

surgery and radiotherapy. This consisted of an induction

phase based on cisplatin, cyclophosphamide, etoposide and

vincristine and a consolidation phase by means of myelo-

suppressive treatment based on carboplatin, thiothepa and

etoposide, the entire protocol carried out with the aid of

ABMT (autologous bone marrow transplantation). The

aggressiveness of this protocol is implicit, and one patient

died after 3 months of treatment. However, one patient

made a complete recovery, suggesting that at the very least

these tumors are chemo-sensitive. Kubota et al. [16]

described the case of a patient treated with bleomycin

without radiotherapy in whom the disease remained under

control for at least 3.5 years. Further radiological evidence

of a response to chemotherapy, consisting of vincristine,

etoposide and carboplatin, was described by Pizer et al. [1]

in a case of congenital astroblastoma.

In our series, two cases (one high- and one low-grade

lesion) were treated by adjuvant chemotherapy based on

temozolomide. This drug was used both for its excellent

tolerability and, in one case [29], for an initial diagnosis of

glioblastoma (the high-grade case treated by TMZ, see

Table 1). In summary, it is necessary to define a standard

efficacy-based protocol to be adopted principally for high-

grade cases or those at risk of a malignant transformation as

well as for cases susceptible to more aggressive treatment.

Conclusion

Surgical resection is the approach of choice for treatment

of astroblastoma. Radiotherapy plays a very important role

in the adjuvant treatment of high-grade astroblastomas.

However, the need for and the benefits of adjuvant che-

motherapy are not well defined, but the glial nature and the

possibility of transformation to a more aggressive tumor

lead us to treat astroblastoma patients with a well-tolerated

TMZ regimen, especially the anaplastic variants, which are

more prone to an anaplastic transformation. Given the

rarity of this tumor, multicenter studies are required to

define the best therapeutic strategy in this tumor in light of

the recent discoveries in the field of molecular biology.

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Cerebral astroblastoma: analysis of six cases and critical review of treatment options

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Transcript of Cerebral astroblastoma: analysis of six cases and critical review of treatment options

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