క్యాన్సర్ సైన్స్ & థెరపీ

Introduction: SPIES is a novel endoscopic imaging technique with different modalities. Chroma enhances the sharpness of the displayed image. Clara uses a local brightness adaptation in the image to achieve a clearer visibility of darker regions within the image. SPIES Spectra A and B are based on color tone shift algorithms to increase contrast.
Objectives: To describe the different SPIES modalities and to test them on bladder tissue images and tissue simulating phantoms with controlled optical properties. Materials and methods: A bladder tumor image in both Chroma and Clara is analyzed on contrast related intensity fluctuations compared to the White Light image. To evaluate Spectra A and B, a validated tissue representing optical phantom model was used.
Results: Intensity fluctuations show the effect of the Chroma and Clara mode compared to White light. The SPIES A and B modalities change the effective spectral response in the imaging system. This was shown and measured in the phantom model by an increased absorbance for the superficial layers (Spectra A) and the deeper layers (Spectra B).
Conclusion: All SPIES modalities show visual and quantitative differences, expressed as increased image intensity or pixel-to-pixel intensity difference (Chroma and Clara) or increased contrast (Spectra A and B).

Molecular chaperones, also known as heat-shock proteins or HSPs, are a functionally conserved class of proteins whose primary function is to keep cellular proteins in their native conformation, under both physiological and stress conditions. In most cases these chaperones do not participate in the final mature structures that their ‘clients’ form. Apart from folding, chaperones play vital roles in cellular localization, transport, secretion and assembly of proteins in multiprotein complexes

In the last two decades the treatment of breast cancer has undergone multiple modifications, evolving from aggressive surgical interventions focused on the regional control, to the multidisciplinary treatment that allows local and systemic control of the disease. An example of this was the beginning of breast conserving surgery in the eighties [1], based on adjuvant breast radiotherapy. Some studies have shown that this association of treatments is an alternative to the mastectomy [2-4] in early stage breast cancer, offering similar local recurrences rates and overall survival.

Introduction: CTCF is an evolutionally conserved 11-zinc finger protein factor involved in an array of processes whose deregulation could lead to cellular transformation. Through interactions with ERα binding regions and ERregulated genes, CTCF was shown to compartmentalize the cellular genome into domains. It also colocalized with ERα in MCF7 cells and had interactions with ERα during histone deacetylase recruitment and fork-head activity. A fast-running isoform was previously shown to be expressed in breast cancer tissue but not in normal breast tissue. It is not clear whether there is a regulatory relationship between CTCF and ERα in breast cancer.
Aim: To determine whether CTCF expression regulated ERα expression in the ER+ MCF7 breast cancer cell line.
Methods: MCF7 breast cancer cells were transfected with either CTCF expression vectors or siRNA against CTCF. Following CTCF over-expression and knock-down, changes in endogenous expression of ERα gene and protein expression were monitored by quantitative polymerase chain reaction (using MIQE guidelines) and western blot analysis respectively.
Results: CTCF plasmid overexpression and siRNA knockdown was associated with cell rounding but with 96.4% and 95.7% cell viability respectively. Increase in CTCF mRNA on over-expression was associated with a rise in CTCF protein expression. siRNA knockdown of CTCF mRNA was accompanied by a corresponding decrease in CTCF protein expression. CTCF over-expression and knockdown appeared to inhibit the ability to detect ERα protein expression by western blotting. Neither the over-expression nor knockdown of CTCF altered ERα mRNA expression as detected by QPCR.
Conclusion: Alterations in CTCF mRNA expression did not affect ERα gene expression in MCF7 cells suggesting that CTCF interactions with the estrogen receptor in breast cancer may not be mediated via direct regulation of ERα mRNA expression.

Purpose: Biochemical hyponatremia is a common electrolyte abnormality in patients with cancer. In this prospective single center trial we aim to study the frequency of hyponatremia in patients receiving chemotherapy with special emphasis on syndrome of inappropriate secretion of anti-diuretic hormone (SIADH).
Patients and Methods: This is a prospective study of consecutive patients receiving different types of outpatient chemotherapy between January 2013 and June 2014. Serum Sodium was measured as part of routine assessment for all patients receiving chemotherapy. Euvolemic patients with hyponatremia (Na <135 mmol/L) were also tested for Serum and urine osmolality and urinary Na excretion. Criteria of SIADH are: serum Osmolality <275 mOsmol/ kg, urine Osmolality >100 mOsmol/kg and urinary Sodium >30 mmol/L.
Results: 1254 patients received different chemotherapy regimens were screened and 1150 fulfilled the inclusion criteria. Median age was 55 year (19-75). Biochemical hyponatremia developed in 105 (9.1%) of all patients and in 42/298 (14%), 25/357 (7%) and 38/495 (7.7%) of patients who received cisplatin, carboplatin/oxaliplatin and non-platinum chemotherapy regimens respectively. 68/105 (65%) fulfilled biochemical criteria of SIADH of which 26/42 (62%), 13/25 (52%) and 29/38 (76%) of hyponatremic patients received cisplatin, carboplatin/oxaliplatin and non-platinum regimens respectively. Cisplatin based regimens were significantly associated with SIADH compared to non-cisplatin regimens (OR: 1.521, 95% CI: 1.105-2.093; p=0.022).
Conclusion: 9.1% of euvolemic patients receiving out-patient chemotherapy manifest a degree of biochemical hyponatremia with highest risk associated with cisplatin based regimens. Hyponatremia can be attributed to SIADH in two thirds of cases.

Background: Most breast carcinomas are morphologically complex, comprising both in situ and invasive components that can be unifocal, multifocal, or diffuse. Pre-operative radiological mapping often reveals this complexity, but even in the era of modern multimodality breast imaging lesions may remain undetected. Methods: We studied the sub gross morphology of tumors in a series of invasive carcinomas determined to be unifocal on pre-operative multimodal radiological imaging. We focused on histological outcome, margin status, and type of surgery. All of the surgical specimens were documented in large-format histological slides.
Results: A total of 44.5% (344/773) of the tumors had separate invasive and/or in situ foci in large-format histopathology slides, in addition to the radiologically detected tumor focus. The foci occupied an area ≥ 40 mm in 29.0% (224/773) of the cases, indicating extensive disease. Close/dirty margin upon histological examination was associated with extensive disease (32.1% vs 5.6%, RR 5.6924, p < 0.0001), multifocality of the invasive component (26.0% vs 3.3%, RR=7.9755, p=0.0001), and breast conservation (15.4% vs 6.3%, RR=2.4476, p=0.0036), but the differences were found only for extensive tumors. Mastectomy was chosen as the primary or complete intervention in 28.3% (219/773) of cases, mostly in multifocal and extensive tumors.
Conclusion: Our results indicate the presence of extensive disease in a considerable number of breast cancer cases judged pre-operatively as unifocal. Removing the radiologically detectable tumor focus with “no ink on the tumor” may not be sufficient in such cases.