Sabato 27 ottobre 2012 - Pacini Editore

COmuNiCaziONi ORali
Fig. 4. tCRGd+cells/100 EC were significantly different between il
with normal and abnormal serology.
TCRGD+ IELs were significantly higher in CD (21.4±11.7) (Figure
1B), IL-GFD (16.2±8.7) and IL (9.9±6.6) (Figure 2B) compared
to CTR (3.4±1.0) (p < 0.0001, p = 0.0004 and p = 0.0046,
respectively) (Figure 3B).
In contrast to CD3+ IELs, TCRGD+ IELs were significantly
higher in CD and IL-GFD compared with IL (p = 0.0010 and
p = 0.0126 respectively).
Furthermore, TCRGD+ IELs discriminated between IL with
normal (6.7±2.9) and abnormal (14.2±8) serology (p = 0.02)
(Figure 4).
Discussion . TCRGD+IELs can be identified on FFPE samples;
their evaluation adds useful information for the workup of small
bowel biopsies and GSE diagnosis. They may recognize IL cases
with abnormal serology, possibly representing early GSE stages.
references
1 Brown I, et al. Arch Pathol Lab Med 2006;130:1020-5.
2 Arranz E, et al. Gut 1994;35:476-82.
3 Järvinen TT, et al. Am J Gastroenterol 2003;98:1332-7.
Apoptosis related biomarkers in advanced
colorectal cancer: chemotherapy outcome
and carcinogenesis
F. Melotti, F. Pietrantonio, A. Pellegrinelli, L. Battaglia, A. Cesa
Bianchi, G. Pelosi, F. de Braud, E. Leo, M. Milione
Fondazione IRCCS Istituto Nazionale Dei Tumori, Department of pathology
and Laboratory Medicine, Milan
Background. Apoptosis-related biomarkers may predict chemosensitivity
of advanced gastrointestinal cancers in vivo 1 2 . TP53
gene usually remains wild type throughout the progression from
normal mucosa to adenoma development and an alteration of the
p53 gene appears to be a late step in the progression of colorectal
tumorigenesis 3 . Despite the considerable body of evidence in support
of the adenoma-carcinoma sequence, the de novo theory still
has some support and may be mediated by alternative mechanisms.
Materials and methods. Forty-nine patients, affected by synchronous
or metachronous metastatic colorectal cancer, were
enrolled from August 2002 to October 2004 at the coordinator
center “Istituto Nazionale dei Tumori” of Milan and treated
within a randomized phase II trial with first-line UFT/leucovorin
(LV) plus irinotecan (TEGAFIRI) versus UFT/LV plus oxaliplatin
(TEGAFOX) (4). ERCC1, Bax and TP53 expression was
assessed by immunohistochemistry on paraffin sections. The
samples were scored positive if more than 5% of tumor cells
showed specific staining. Tissue blocks of primary resected tumors
were also evaluated in a subset of thirty-nine pts for residual
adenomatous component.
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Results. ERCC1 and TP53 failed to show any correlation with
outcome in terms of response to chemotherapy and progressionfree/overall
survival. Responses significantly lower in Baxpositive
vs Bax-negative (Odds Ratio [OR] = 0.26; p = 0.03 by
logistic regression): 25% (6/24) vs 56% (14/25). No significant
differences in terms of outcome in TEGAFOX-treated pts, while
Bax-positive pts in TEGAFIRI subgroup had lower response rate
as compared to Bax-negative (OR = 0.11; p = 0.03 by logistic
regression): 18% (2/11) vs 67% (8/12). Residual adenoma component
in primary colorectal cancer specimens was < 10% in
27 (69%) cases and was > 10% in 12 (31%). TP53 expression
was significantly higher in the group without residual adenoma
vs the one with adenomatous component: 15/27, 56% vs 2/12,
17%, P = 0.03 by Fisher’s exact test), while Bax and ERCC1
were not associated with morphological characteristics. Notably,
one patient with TP53 expression and residual adenoma showed
microsatellite instability.
Conclusions. TP53 alteration may accelerate the progression of
adenoma-carcinoma sequence or even allow a de novo colorectal
carcinogenesis. However, TP53 expression does not seem to affect
chemotherapy outcome, while Bax positivity may identify a
subset of patients with particular sensitivity to irinotecan-based
regimens.
refereces
1 Benhattar J, Cerottini JP, Saraga E, et al. P53 mutations as a possible
predictor of response to chemotherapy in metastatic colorectal carcinomas.
Int J Cancer 1996; 69:190-2.
2 Pietrantonio F, Biondani P, de Braud F, et al. Bax espression in predictive
of favorable clinical outcome in chemonaive advanced gastric
cancer patients trated with capecitabine, oxaliplatin and irinotecan
regimen. Transl Oncol. 2012;5:155-9.
3 Baker SJ, Preisinger AC, Jessup JM, et al. P53 gene mutations occur
in combination with 17p allelic deletions as late events in colorectal
tumorigenesis. Cancer Res 1990;50:7717-22.
4 Bajetta E, Celio L, Ferrario E, et al. Capecitabine plus oxaliplatin and
irinotecan regimen every other week: a phase I/II study in first-line
treatment of metastasic colorectal cancer. Ann Oncol 2007;18:1810-6.
Cutaneous melanoma metastatic to the gallbladder:
an additional case
V. Mourmouras1 , M.R. Ambrosio2 , B.J. Rocca2 , S. Giunti1 ,
A. Amorosi1 1 2 Centro Oncologico Fiorentino, Sesto Fiorentino and Departement of
Human Pathology and Oncology, Anatomic Pathology Section, University
of Siena, Italy
Background. Malignant cutaneous melanoma can metastasize to
virtually any organ. The most common sites of distant metastases
are lungs, liver and brain. Only 2% to 4% of patients with melanoma
will be diagnosed with gastrointestinal metastasis during
the course of the disease, the most common sites being the small
bowel, colon and stomach. Metastatic melanoma to the gallbladder
is extremely rare and it is associated with a poor prognosis.
Material and methods. A 27 year-old woman was admitted to
our clinic with abdominal pain in her right upper quadrant, and
associated nausea and vomiting. Laboratory tests were within
normal limits. On ultrasound examination of the abdomen a
polypoid lesion within the gallbladder wall was demonstrated.
A clinical diagnosis of chronic cholecystitis was made and the
patient underwent laparotomy and cholecystectomy. Two years
earlier, she underwent surgical removal of a primary cutaneous
melanoma.
Results. The surgical specimen consisted of a 7 cm-long gallbladder
which macroscopically showed an ulcerated, polypoid,
black lesion in the fundus. The lumen was filled with bile. At
pathological examination, the wall of the gallbladder was diffusely
infiltrated by epithelioid and spindle, pigmented cells
forming a nodule. The superficial epithelium was focally eroded