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Journal of Analytical Oncology

Inflammation and Urothelial Bladder Cancer: What we Need to Known? (Review)
Pages 75-80
Tommaso Cai, Gabriella Nesi, Sandra Mazzoli, Francesca Meacci, Galliano Tinacci, Cesare Selli and Riccardo Bartoletti
DOI:
http://dx.doi.org/10.6000/1927-7229.2015.04.02.3
Published: 13 May 2015


Abstract: The association between inflammation and bladder cancer has been debated in several studies, highlighting that inflammation may be a crucial component both in tumor development or progression. On the other hand, several authors suggest that the presence of an inflammatory cell infiltrate within the urothelial bladder cancer is a good prognostic predictor in terms of recurrence-free survival time. The question is: What is the prognostic role of inflammation in patients affected by urothelial bladder cancer? On one hand, chronic inflammation should be considered a risk factor in developing bladder cancer, as demonstrated by Schistosoma haematobium infection and, on the other hand, the inflammation induced by the Bacillus Calmette-Guérin intravesical therapy has a protective effect on cancer recurrence. Recently, some authors highlight that the presence of an inflammatory cell infiltrate within the urothelial bladder cancer is a good prognostic predictor in terms of recurrence-free survival time, due to the host generating angiogenic stimulation of a local inflammatory reaction against cancer. This is probably due to the angiogenetic stimulation of a local inflammatory reaction generated by the host against superficial bladder cancer. However, the debate is still open. This review will summarize recent data regarding inflammation and urothelial cell carcinoma, with special emphasis on the role that the inflammatory response is likely to have on recurrence risk and progression in superficial bladder cancer patients.

Keywords: Interleukins, bladder cancers, urothelial cancer, flogosis, inflammation.

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Subacute Paraneoplastic Cerebellar Degeneration in an Advanced Small Cell Lung Cancer Patient: Case Report and Literature Review
Pages 81-85
Maria Fernanda Evangelista Simões, Clarissa Maria de Cerqueira Mathias, Oddone Freitas Melro Braghiroli and Eldsamira da Silva Mascarenhas Schettini Sobrinho

DOI: http://dx.doi.org/10.6000/1927-7229.2015.04.02.4
Published: 13 May 2015


Abstract: Introduction: Paraneoplastic Cerebellar Degeneration (PCD) is a rare paraneoplastic syndrome, anddifficult to diagnose. PCD is associated withcertain types ofcancersuch asovarian cancer, uterus orits annexes, breast cancer, Hodgkin's lymphoma andsmall cell lung cancer (SCLC), however, this syndrome is not associated with metastatic dissemination. Here we report a caseof apatient with advanced SCLC, which develop PCD.

Case Report: Female patient, 51-year-old, largesmoker, with advancedSCLCwith involvementofabdominal lymph nodes, presented muscle weakness, without spinal cordlevel, during second-line treatment with Cisplatin and Irinotecan, even with important clinical response to chemotherapy. The patient developed nystagmusand cerebellarataxia.Cerebrospinal fluid analysisand brain magnetic resonance imagingwithoutfindings. The patient was assessed byneurologist,withclinical diagnosisof subacute PCD. Patient startedpulse therapy with methylprednisolone, withsignificant remission of neurological symptoms.

Discussion and conclusion: PCD finding, although rare, usually precedes the detection of a tumor, and it is important to start early research and treatment of cancer because of better survival and patient´s quality of life. This case differs from usual descriptions found in the literature because the patient developed PCD during good clinical response in second-line treatment. PCD evolves withprogression of the neurological conditionin weeksto monthsand thenstabilizes.The low incidencedifficult to establishtreatmentstrategies based onevidence for PCD, usually takingupaggressiveimmunotherapy, using intravenous immunoglobulin, plasmapheresis, steroids at high doses and/or immunosuppressive drugs.

Keywords: Paraneoplastic Cerebellar Degeneration, Small Cell Lung Cancer, Paraneoplastic Syndrome, Cerebellar ataxia, Nystagmus.

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Journal of Analytical Oncology

Solitary Extramedullary Plasmocytoma of the Thyroid Gland: A Case Report
Pages 1-4
Martin Balog, Ulrich Lang and Günther Winde
DOI:
http://dx.doi.org/10.6000/1927-7229.2015.04.01.1
Published: 12 February 2015


Abstract: Solitary extramedullary plasmocytoma (SEP) of the thyroid gland is a very rare disease. The diagnosis of SEP can be made after ruling out multiple myeloma. Histological examinations, immunohistochemical analysis with an overexpression of CD 138, CD 38 and kappa light chain reaction confirmed this uncommon condition in our case. Medullary carcinoma, MALT-Lymphoma and Non-Hodgkin Lymphoma of the thyroid should be excluded in the diagnosis.

Surgical resection and radiotherapy, or a combination of both, are standard treatment methods. However, because of rareness of this disease, no general therapy can be recommended.

We report about a 75 year old male patient and its involvement of the right remainder thyroid lobe by SEP five years post a Dunhill-Procedure due to multinodular goiter.

Keywords: Solitary, plasmocytoma, extramedullary, thyroid, multiple myeloma.
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IQGAP2 Displays Tumor Suppression Functions
Pages 86-93
Yanyun Xie, Anil Kapoor, Hao Peng, Jean-Claude Cutz, Lijian Tao and Damu Tang
DOI:
http://dx.doi.org/10.6000/1927-7229.2015.04.02.5
Published: 13 May 2015


Abstract: The IQGAP family consists of evolutionarily conserved scaffold proteins, IQGAP1, IQGAP2, and IQGAP3. IQGAP1 is 62 and 59% identical at the level of amino acid sequence to IQGAP2 and IQGAP3, respectively. IQGAPs possess the same domain structure with the individual motifs being highly homologous among IQGAPs. The conservation is even higher between IQGAP1 and IQGAP2. While the WW domain is 30% identical, other four motifs are 70 to 93% identical between both IQGAPs. Despite the high level identity, IQGAP1 and IQGAP2 display opposite impact on tumorigenesis. IQGAP1 is the most thoroughly examined, and clearly promotes cancer formation via its scaffold functions in facilitating the Raf-Mek-Erk and Wnt signalling. On the other hand, IQGAP2 is much less investigated and suppresses tumorigenesis. We will review the evidence that supports IQGAP2 reducing tumorigenesis, discuss its tumour suppression in the context of our updated knowledge on IQGAP1, and outline some future directions. Our emphasis will be placed on prostate cancer.

Keywords: IQGAP2, tumor suppression, Akt, hepatocellular carcinoma, gastric cancer, prostate cancer.

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Journal of Analytical Oncology

Clinically Relevant Brain Tumor Model and Device Development for Experimental Therapeutics
Pages 5-12
Kamalakannan Palanichamy, Kirstin Acus, John R Jacob and Arnab Chakravarti
DOI:
http://dx.doi.org/10.6000/1927-7229.2015.04.01.2
Published: 12 February 2015


Abstract: This paper assesses the subcutaneous, orthotopic, and transgenic mouse models used to study glioblastomas (GBMs) as well as delineates our model to overcome the limitations of these currently used models. Subcutaneous model involves the injection of GBM cells into hind leg or back of a mouse, whereas in orthotopic model, the injection of GBM cells into the cranium of mice is required. Neither subcutaneous nor orthotopic models accurately display the infiltrative growth pattern of the tumor into the brain parenchyma characteristic of GBMs in humans. Transgenic models are achieved by pronuclear microinjection (into the male pronucleus, immediately after fertilization) or the injection of DNA into embryonic stem cells. Transgenic models are similar to human GBMs in every way, except they are not as genetically complex. To overcome the limitations in these models, we have developed a brain tumor model that exhibits all the histologic hallmarks of human GBM. We used a flank model initially to enrich a tumorigenic population of GBM cells from patient biopsies and a subsequent intracranial implantation to achieve the characteristics of tumors similar to those observed in human patients. The cells enriched by this method were then implanted and subjected to standard treatments such as chemotheraphy and radiation. Subsequently, we determined the treatment efficacy and rate of recurrence. Currently, we are using this approach to determine the treatment resistance pathways leading to recurrence and for developing a better combinatorial approach by short-circuiting the aberrant signaling pathways that are up-regulated in the treatment resistance tumors.

Keywords: Brain tumor, In-vivo model, Glioblastoma, Glioma stem cell and Radiation shield.
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