As such, it is very important to compile well-described clinical information and patient history. Additionally, when necessary, biomarkers should be used to aid in differential diagnosis and lesions should be reclassified as appropriate. According to Younes et al. However, the fact that this protein remains in the cells of these lesions during the involuted phase implies that its expression is not related to a temporary adaptation caused by a need for glucose to support a high rate of proliferation, and one result is the marker's specificity for identification of HIs.
When VAs previously thought to be HIs exhibit negative immunomarcation for GLUT1, the solution is to reclassify them as other entities, on the basis of clinical and histopathological characteristics described in the literature. Many studies that analyzed GLUT1 expression in samples diagnosed as HIs on the basis of histopathology 20 , 26 , 40 , 42 , 53 - 57 demonstrated that all of the cases analyzed were immunopositive for the protein, providing support for the hypothesis advanced by North et al.
On the other hand, several studies 41 , 43 , 58 - 60 demonstrated that not all specimens diagnosed by histopathology as "hemangiomas" present immunopositivity for the GLUT1 protein and all of these studies considered that only those samples that were GLUT1 positive came from true HIs, showing that over the years this marker has been widely used for the purposes of diagnosis, in addition to confirming its efficacy and reliability as a diagnostic marker.
Patients with VAs continue to be misdiagnosed because of the complexity involved in differentiating these lesions. Many studies are still being conducted without correct parametrization, introducing biases that can compromise the results and return incorrect information. It is therefore important that centers where teaching, research or diagnosis take place should adopt the ISSVA classification when defining new cases, using tools such as GLUT1.
Additionally, older cases should be revisited and, if necessary, reclassified, in order to achieve better communication between professionals and to ensure that research is more trustworthy and better parametrized. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: Plast Reconstr Surg.
Enjolras O, Mulliken JB. Vascular tumors and vascular malformations new issues. Adv Dermatol. Benign cutaneous vascular tumors of infancy: Arch Dermatol. ISSVA classification. New York: Cambridge University Press; [citado abr 23]. Head and neck vascular anomalies in children. Int J Pediatr Otorhinolaryngol. S http: Hemangiomas in children. N Engl J Med. Vascular anomalies. Curr Probl Surg. Hum Pathol. Diagnosis and treatment of infantile hemangioma. An Bras Dermatol. Evaluation of terminology for vascular anomalies in current literature. Vascular malformations: Semin Roentgenol. The use of propranolol in the management of periocular capillary haemangioma--a systematic review.
Eye Lond. Vascular anomalies: Infantile hemangiomas: Proceedings of a research workshop on infantile hemangiomas, april , , Bethesda, Maryland, USA. Pediatr Dermato. Hemangiomas of infancy: Current concepts in the classification, diagnosis and treatment of hemangiomas and vascular malformations of the head and neck.
Eur Arch Otorhinolaryngol. Vascular anomalies in pediatrics. Surg Clin North Am. A unique microvascular phenotype shared by juvenile hemangiomas and human placenta. Curr Probl Diagn Radiol. Guidelines of care for hemangiomas of infancy.
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J Am Acad Dermatol. Infantile hemangioma: J Craniofac Surg. Mesenchymal stem cells and adipogenesis in hemangioma involution. Stem Cells. Mulliken JB, Enjolras O. Congenital hemangiomas and infantile hemangioma: Congenital nonprogressive hemangioma: Functional properties and genomics of glucose transporters. Curr Genomics. Widdas WF. Old and new concepts of the membrane transport for glucose in cells. Biochim Biophys Acta.
Am J Physiol Endocrinol Metab.
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E http: Wright EM, Turk E. Pflugers Arch. Glucose transporters in the metabolic syndrome. Arq Bras Endocrinol Metabol. Wu X, Freeze HH. Joost HG, Thorens B. Mol Membr Biol. Molecular physiology of glucose transporters. Diabetes Care. Regulation of glucose-transporter function. Assuming that the clinical phenotype of this disease is ultimately dictated by biological mechanisms, read-outs of these mechanisms i. More specifically, identifying biomarkers requires knowledge of molecules that contribute to peritoneal dissemination.
Peritoneal dissemination is viewed as a multistep process, in which the establishment of a metastatic lesion ultimately depends on colonisation of cancer cells and the creation of a metastatic niche [ 11 ]. At this step, the formation of a tumour-specific microenvironment is pivotal. Interactions between cancer cells and their surrounding stroma provide growth and survival signals necessary to evade apoptosis, to enable invasion and migration, and to provide oxygen and nutrients through angiogenesis [ 13 — 16 ].
Consequently, angiogenesis influences tumour progression and is associated with higher morbidity and mortality rates in HIPEC patients, as is suggested by several authors [ 19 , 20 ]. Angiogenesis depends on complex interactions between several cell types and extracellular matrix ECM components [ 17 ]. The exact interactions required for this process are not fully understood. Several other studies, however, suggest a role for versican VCAN [ 21 — 24 ]. VCAN is a sulphate proteoglycan overexpressed in a variety of human malignant tumours, including CRC [ 21 , 25 — 31 ].
This complex enhanced endothelial cell adhesion, proliferation and migration, possibly providing the molecular basis by which VCAN promotes angiogenesis [ 33 ]. Complete debulking, stripping of the affected parietal peritoneum, and removal of the omentum and adnexa was performed as described by Sugarbaker et al. When deemed necessary, multi-organ resections were carried out. Specimens of 11 patients were not eligible for analysis due to loss of tissue or technical difficulties, leaving 65 patients eligible for further analysis.
Resection outcome was determined according to the maximal size of residual tumour tissue. An R1 resection was recorded when no macroscopically visible tumour was left behind, an R2a resection when the residual macroscopic tumour was smaller than 2. Clinicopathological characteristics of 65 colorectal cancer patients with peritoneal metastases. After deparaffinisation and rehydration, endogenous peroxidases were blocked with 0.
Cut-offs were determined that discriminated best between the low and high expressing groups using the Kaplan—Meier method. Staining pattern and the location of protein expression were assessed. VCAN staining was expressed in the cytoplasm of tumour cells and in the stroma surrounding the tumour cells. Hence, both stromal and epithelial VCAN were analysed.
Since VEGF was predominantly seen in the cytoplasm of tumour cells, its intensity was scored in the cytoplasmic compartment. All tissue sections were scored and examined blinded to clinicopathological data. The magnification is shown on the micrographs. Intensities were classified as negative, weak, moderate or strong.
Scoring percentages of all markers are listed next. Stromal VCAN expression: Epithelial VCAN expression: VEGF expression: MVD was determined by automated image analysis of CD31 staining patterns. A computerised morphometric analysis of the CD31 stained slides was executed using ImageJ. The CD31 staining was used to quantify the amount of microvessels per area as the percentage of the field of view that was CD31 positive [ 35 ]. Morphometric measurements were performed without knowledge of sample identity.
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Associations were considered statistically significant for p values smaller than or equal to 0. Overall survival OS was defined as time in months from date of surgery to death from any cause. Patients were censored at date last known to be alive. Variable selection in the Cox model was done using backward selection with a threshold p value of 0.
VCAN was expressed in both the epithelial and the stromal compartment. Stromal VCAN was negative in 1. Epithelial VCAN was negative in In the VCAN positive cells a cytoplasmic staining was seen, sometimes with a highly intense granular pattern, probably depicting the Golgi system [ 37 ]. In The mean and median MVD were MVD correlated to stromal and epithelial VCAN, but did not show associations with other markers or clinicopathological characteristics. Mean OS in the patient cohort was Mean survival in the group patients with low VEGF expression was Mean survival in patients with high epithelial VCAN expression was Furthermore, in patients with low and high stromal VCAN expression a mean survival of Mean survival in patients with low MVD was Kaplan—Meier curves of all patients.
The observation of epithelial VCAN expression being significant in multivariate, but not in univariate analysis, is most probably attributable to the effect of confounding in the univariate analysis. This confounding effect is corrected for in multivariate analysis by including all possibly significant variables. Selection of patients that will benefit most from this treatment is key. Biomarkers could help in patient selection, preventing unnecessary morbidity in patients that will not benefit.
The possible role of VEGF as a predictor of worse outcome corroborates the rationale for neo- adjuvant anti-VEGF based therapy in selected patients [ 20 , 51 , 52 ]. Although a recent study described a twofold increase in morbidity in these patients after administration of bevacizumab [ 54 ], a meta-analysis including more than patients with metastasised CRC reported the amount and severity of treatment with bevacizumab to be acceptable [ 3 ].
The sulphate proteoglycan VCAN is thought to promote tumour development [ 21 , 55 ] by mediating several processes such as proliferation [ 56 — 58 ], drug resistance [ 27 , 56 — 62 ], cell adhesion [ 57 — 60 ], invasion [ 57 , 58 , 63 ] and angiogenesis [ 23 , 24 , 32 , 33 , 64 , 65 ].
MVD is a measure of the number of vessels per high power field. Considering this number of vessels is not only determined by angiogenic factors, such as VEGF, but also by non-angiogenic factors such as oxygen and nutrient consumption rates, one might state that MVD does not necessarily adequately reflect the rate of angiogenesis [ 66 ]. Hence, it is possible that MVD is a marker of a more or less established vessel network, whilst VEGF is produced in the presence of hypoxic stimuli to stimulate angiogenesis [ 67 ].
Once vessels are established and an oxygen-rich environment is created, VEGF is no longer necessary for the formation of new vessels. In the presence of an established vessel network, other molecules, including VCAN, might be required for maintenance -and not creation- of a favourable microenvironment [ 14 , 21 ].
This finding is supported by studies in primary CRC [ 37 ] and serous ovarian cancer [ 68 ]. The mechanism by which epithelial VCAN positively influences patient outcome might be related to tumour cell responses to chemotherapy [ 68 ]. Another study found cells transfected with V1 VCAN to be selectively sensitised to several apoptotic stimuli, for example to the chemotherapeutics etoposide and cisplatin [ 61 ].
The influence of molecules such as VCAN in tumour response to chemotherapy stresses the importance of systematically analysing interactions between cancer cells and their environment in order to identify mechanisms contributing to drug sensitivity. In peritoneal cancer patients, sensitivity of tumour cells to heated MMC might -at least in part- account for good outcome in patients with high epithelial VCAN expression.
Reading 3D Histech digital slides (.mrxs format)
Since identification of sensitivity and resistance mechanisms could lead to mechanism-based therapies and further stratification of HIPEC patients, i. Another interesting finding is that both epithelial and stromal VCAN expression and a granular expression pattern are associated with a better resection outcome. A 'demo version' watermark in the viewer.
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