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The article cites a research study that examines the role of MiR- Par3L axis in breast cancer progression. It examined normal tissues and Par3L expressions in breast cancer tissues and cells. Par3L was found to be frequently down-regulated in human breast cancer cells and tissues and Par3L low-expression was associated with aggressive clinicopathological features and poor clinical outcome of breast cancer patients.

Tumor‐specific microRNA (miRNA) imaging strategies are critical for investigating mechanisms associated with cancer progression; however, nonspecific signal leakage and false‐positive signaling limit their selectivity and efficiency. In this paper, an endogenously activated and self‐reinforced DNA lipid nanodevice (LND) for spatial‐specific and high‐contrast imaging of miRNAs in living cells and animals is presented. The LND is functionalized on cholesterol‐based lipid micelles (CLMs) containing smart response and self‐fueling DNA components that display redox‐activatable and autocatalytic miRNA probing activities, respectively. The LNDs are initially silenced and selectively activated using glutathione, an endogenous microenvironmental factor overexpressed in tumor cells, to prevent nonspecific signal leakage. Subsequently, an autocatalytic DNA circuit is used for tumor‐specific and high‐contrast miRNA imaging. It is demonstrated that robust CLM nanoparticles can be easily assembled from a cholesterol‐conjugated G‐rich DNA sequence by stirring in a buffered solution, enabling the LND to enter cells naturally. In addition, in vitro and in vivo data illustrate that the enhanced biostability of DNA components on the surface of LNDs can be realized for minimizing false‐positive signals, making the system ideal for miRNA imaging in living mice. This smart LND technique has great potential for precise biomedical imaging and clinical diagnosis. [ABSTRACT FROM AUTHOR]

Chimeric antigen receptor T‐cell (CAR‐T) therapy is becoming an effective technique for the treatment of patients with relapsed/refractory hematologic malignancies. After analyzing patients with tumor progression and sustained remission after CAR‐T cell therapy, many factors were found to be associated with the efficacy of CAR‐T therapy. This paper reviews the factors affecting the effect of CAR‐T such as tumor characteristics, tumor microenvironment and immune function of patients, CAR‐T cell structure, construction method and in vivo expansion values, lymphodepletion chemotherapy, and previous treatment, and provides a preliminary outlook on the corresponding therapeutic strategies. [ABSTRACT FROM AUTHOR]

Background: Bladder cancer (BCa) is a highly malignant tumor, and if left untreated, it can develop severe hematuria and tumor metastasis, thereby endangering the patient's life. The purpose of this paper was to detect the expression of ATAD3A in BCa and research the relationship between ATAD3A and pathological features of bladder cancer and the prognosis of patients. Methods: First, the expression of ATAD3A in BCa and normal bladder tissues was analyzed based on the UALCAN and Oncomine public databases. Second, 491 cases of surgically resected bladder cancer specimens and 110 cases of normal adjacent tissues were immunohistochemically stained. The expression of ATAD3A was quantified, and the value and prognosis of ATAD3A as a biomarker of BCa were evaluated. Results: The expression of ATAD3A in bladder cancer tissues was higher than that in normal bladder mucosa. High expression of ATAD3A was correlated with patient age, tumor size, number of tumors, distant metastasis, lymph node metastasis, lymphovascular invasion, and TNM stage (p < 0.05). Overexpression of ATAD3A is closely related to cancer patient survival. The mean survival time of bladder cancer patients with high ATAD3A expression was shorter than those with low ATAD3A levels. According to the relative comparing result, the high ATAD3A expression herald reduced overall survival in BCa patients. Conclusions: The abnormal overexpression of ATAD3A may be related to the initiation and progress of bladder cancer. The upregulation of ATAD3A can be used as an effective indicator to diagnose bladder cancer and predict tumor progression. Furthermore, the combination of information from public databases and the results of clinical sample analysis can help us better understand the mechanism of action of molecular oncogenes in bladder cancer. [ABSTRACT FROM AUTHOR]

Prostate cancer morbidity and mortality are increasing globally and in China, and the rate of metastasis is also rising, limiting the therapeutic effect and clinical prognosis of prostate cancer. CD151 is considered to be the first promoter of tumor metastasis in the tetraspanin superfamily. Previous research has linked CD151 to the progression of a number of malignancies, including prostate cancer. However, a recent study found that CD151 can inhibit the progression of prostate cancer. As a result, this paper examines existing research on CD151 and prostate cancer progression in order to clarify the relationship and provide a possible reference for future studies. [ABSTRACT FROM AUTHOR]

Glioblastoma is the most aggressive and infiltrative glioma, classified as Grade IV, with the poorest survival rate among patients. Accurate and rigorously tested mechanistic in silico modeling offers great value to understand and quantify the progression of primary brain tumors. This paper presents a continuum‐based finite element framework that is built on high performance computing, open‐source libraries to simulate glioblastoma progression. We adopt the established proliferation invasion hypoxia necrosis angiogenesis model in our framework to realize scalable simulations of cancer, and has demonstrated to produce accurate and efficient solutions in both two‐ and three‐dimensional brain models. The in silico solver can successfully implement arbitrary order discretization schemes and adaptive remeshing algorithms. A model sensitivity analysis is conducted to test the impact of vascular density, cancer cell invasiveness and aggressiveness, the phenotypic transition potential, including that of necrosis, and the effect of tumor‐induced angiogenesis in the evolution of glioblastoma. Additionally, individualized simulations of brain cancer progression are carried out using pertinent magnetic resonance imaging data, where the in silico model is used to investigate the complex dynamics of the disease. We conclude by arguing how the proposed framework can deliver patient‐specific simulations of cancer prognosis and how it could bridge clinical imaging with modeling. [ABSTRACT FROM AUTHOR]

Technological progress within the last 15–20 years has significantly increased our knowledge about the molecular basis of cancer development, tumor progression, and treatment response. As a consequence, a vast number of biomarkers have been proposed, but only a small fraction of them have found their way into clinical use. The aim of this paper is to describe the specific demands a clinically relevant biomarker should meet and how biomarkers can be tested stepwise. We name this procedure the "triple‐R principle": robustness, reproducibility, and relevance. The usefulness of this principle is illustrated with the marker TP53. Since it is mutated in a broad spectrum of cancer entities, TP53 can be considered a very promising marker. Thus, TP53 has been studied in detail but there is still no explicit consensus about its clinical value. By considering our own experience and reviewing the literature, we demonstrate that a major problem of current biomarker research is disregard of whether the biomarker is prognostic or predictive. As an example, it is demonstrated that TP53 is not a prognostic marker, but rather a purely predictive marker, and that disregard of this fact has made this otherwise strong biomarker appear as not being clinically useful so far. Many biomarkers have been proposed for cancer, but only a small fraction of them are clinically useful. This paper describes the specific demands a clinically relevant biomarker should meet and how biomarkers can be tested stepwise. This is illustrated with the marker TP53, which has been studied in detail but for which there is still no explicit consensus about its clinical value. [ABSTRACT FROM AUTHOR]

The invasion of cancer is brought about by continuous interaction of malignant cells with their surrounding tissue microenvironment. Investigating the remodeling of local extracellular matrix (ECM) by invading cells can thus provide fundamental insights into the dynamics of cancer progression. In this paper, we use an active untethered nanomechanical tool, realized as magnetically driven nanomotors, to locally probe a 3D tissue culture environment. We observed that nanomotors preferentially adhere to the cancer‐proximal ECM and magnitude of the adhesive force increased with cell lines of higher metastatic ability. We experimentally confirmed that sialic acid linkage specific to cancer‐secreted ECM makes it differently charged, which causes this adhesion. In an assay consisting of both cancerous and non‐cancerous epithelia, that mimics the in vivo histopathological milieu of a malignant breast tumor, we find that nanomotors preferentially decorate the region around the cancer cells. [ABSTRACT FROM AUTHOR]

The invasion of cancer is brought about by continuous interaction of malignant cells with their surrounding tissue microenvironment. Investigating the remodeling of local extracellular matrix (ECM) by invading cells can thus provide fundamental insights into the dynamics of cancer progression. In this paper, we use an active untethered nanomechanical tool, realized as magnetically driven nanomotors, to locally probe a 3D tissue culture environment. We observed that nanomotors preferentially adhere to the cancer‐proximal ECM and magnitude of the adhesive force increased with cell lines of higher metastatic ability. We experimentally confirmed that sialic acid linkage specific to cancer‐secreted ECM makes it differently charged, which causes this adhesion. In an assay consisting of both cancerous and non‐cancerous epithelia, that mimics the in vivo histopathological milieu of a malignant breast tumor, we find that nanomotors preferentially decorate the region around the cancer cells. [ABSTRACT FROM AUTHOR]

Non‐small cell lung cancer (NSCLC) is the commonest malignancy with high death rate around the world. LncRNA metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) is greatly overexpressed in multifarious cancers, including NSCLC. However, the precise mechanism of MALAT1 in NSCLC tumorigenesis is blurry. This paper aims to investigate the theory of MALAT1 action in NSCLC progression. The levels of MALAT1, microRNA (miR)‐185‐5p, and mouse double minute 4 protein (MDM4) were measured by quantitative real‐time polymerase chain reaction (qRT‐PCR) or western blot. Cell proliferation and apoptosis were, respectively, determined by 3‐(4, 5‐dimethyl‐2‐thiazolyl)‐2, 5‐diphenyl‐2‐H‐tetrazolium bromide (MTT) assay, and flow cytometry. Cell migratory and invasive abilities were inspected by transwell assay. The binding relationship between miR‐185‐5p and MALAT1 or MDM4 was confirmed by dual‐luciferase reporter assay. The impacts of MALAT1 on tumor growth in vivo were measured by a xenograft experiment. We found MALAT1 and MDM4 were upregulated and MALAT1 positively regulated the MDM4 expression. MALAT1 and MDM4 deletion significantly hindered the proliferation, metastasis, and expedited the apoptosis of NSCLC cells. MDM4 overexpression partly overturned the influence of MALAT1 downregulation on cell development. Moreover, miR‐185‐5p, as a target of MALAT1, could directly target MDM4, and miR‐185‐5p upregulation exerted inhibitory effects on NSCLC cells. Besides, knockdown of MALAT1 inhibited tumor growth in vivo through miR‐185‐5p/MDM4 axis in NSCLC. Collectively, MALAT1 contributed to proliferation, migration, invasion, and impeded apoptosis by regulating the MDM4 expression mediated by miR‐185‐5p in NSCLC cells. [ABSTRACT FROM AUTHOR]

Background: Tumor with adjacent lobe invasion (T‐ALI) is an uncommon condition. Controversy still exists regarding the optimal resection of adjacent lobe invasion, and the prognostic value in relation to fissure integrity at the tumor invasion point. The aims of this paper were to evaluate the prognosis of T‐ALI with regard to fissure integrity, and type of resection. Methods: This was a retrospective multicenter study which included all consecutive patients with T‐ALI undergoing surgical treatment. Based on radiological, intraoperative and histological findings, T‐ALI patients were differentiated into two groups based on whether the fissure was complete (T‐ALI‐A group) or incomplete (T‐ALI‐D Group) at the level of tumor invasion point. Clinico‐pathological features and survival of two study groups were analyzed and compared. Results: Study population included 135 patients, of these 98 (72%) were included into T‐ALI‐A group, and 37 (38%) into T‐ALI‐D Group. T‐ALI‐D patients had better overall survival than T‐ALI‐A patients (63.9 ± 7.0 vs. 48.9 ± 3.9; respectively, P = 0.01) who presented with a higher incidence of lymph node involvement (35% vs. 4%; P = 0.004), and recurrence rate (43% vs. 16%; P = 0.01). At multivariable analysis, T‐ALI‐D (P = 0.01), pN0 stage (P = 0.0002), and pT≤5 cm (P = 0.0001) were favorable survival prognostic factors. Conclusions: T‐ALI‐D presented a better prognosis than T‐ALI‐A while extent of resection had no effect on survival. Thus, in patients with small T‐ALI‐D and without lymph node involvement, sublobar resection of adjacent lobe rather than lobectomy could be indicated. Key points: The extent of resection of adjacent lobe had no effect on survival while T‐ALI‐D, pN0 stage, and pT≤5 cm were significant prognostic factors.In patients with small T‐ALI‐D and without lymph node involvement, sublobar resection of adjacent lobe could be indicated as an alternative to lobectomy. [ABSTRACT FROM AUTHOR]

Editorial Comment to Significance of dorsal bladder neck involvement in predicting the progression of non-muscle-invasive bladder cancer NMIBC recurrence and progression rate can be reduced by means of a correct endoscopic resection (TURBT) and tailored surveillance or bladder instillations. In this relevant paper, the authors outline, for the first time, the impact of dorsal bladder neck involvement (BNI) on the progression rate of non-muscle-invasive bladder cancer (NMIBC).[1] To demonstrate this statement, the authors report their wide retrospective single-center casistic (651 NMIBC patients over 18 years), excluding cases with concomitant upper urinary tract cancer, carcinoma in-situ or de novo metastatic disease. [Extracted from the article]

Tumor cell invasion and metastasis are the definitive cause of mortality in breast cancer (BC). Hypoxia and pro‐inflammatory cytokines upregulate the CD73 gene in the tumor microenvironment. Subsequently, CD73 triggers molecular and cellular signaling pathways by both enzymatic and nonenzymatic pathways, which finally leads to breast tumor progression and development. In this paper, we summarize current advances in the understanding of CD73‐driven mechanisms that promote BC development and mortality. Furthermore, we evaluate the therapeutic potential of CD73 targeting in BC. [ABSTRACT FROM AUTHOR]

High‐throughput sequencing methods have facilitated the identification of novel selenoproteins, which exert a vital role in the development and progression of tumor diseases. Recently, Selenoprotein M (SELM) is upregulated in several types of cancer. However, the biological roles of SELM in renal cell carcinoma (RCC) remain unclear. In this paper, quantitative reverse transcription PCR (qRT‐PCR) and Western blot were used to measure relative levels of SELM in a cohort of RCC tissues with matched normal tissues as well as human RCC cell lines. SELM expression was found to be upregulated in RCC. High level of SELM was related to poor prognosis of RCC. Furthermore, silence of SELM could inhibit the in vitro proliferative, migratory, and invasive capacities of RCC. In addition, downregulated SELM could impede in vivo tumorigenesis of RCC. SELM could activate the PI3K/Akt/mTOR pathway and mediate expressions of matrix metallopeptidase 2 and 9 (MMP2, MMP9). In conclusion, our study reveals the oncogenic function of SELM in RCC, and SELM may be a therapeutic and prognostic target for RCC. [ABSTRACT FROM AUTHOR]

This paper describes a microfluidic device for observation of cancer cell invasion induced by chemotaxis. The developed device has two main channels, the channel filled with cell suspension and the channel filled with solution containing chemotactic factor. These channels are connected via tapered orifice structures to capture multiple cancer cells in it to form cell clusters. Observation of cell invasions affected by cell adhesions is possible with this device. The devices were fabricated by using three‐dimensional lithography and PDMS (polydimethylsiloxane) molding. Invasion cells leaving the cell clusters and moving to the channel containing chemotactic factors through the orifices were successfully observed on the device. [ABSTRACT FROM AUTHOR]

Although an association between cancer progression and matrix metalloproteinase (MMP) 2 and MPP9 expression has been known, the expression, nuclear localization, and physiologically controlled activation of these two MMPs have not been investigated in malignant mesothelioma cells. We examined the expression and intracellular localization of MMP2/9 in ZL55 malignant mesothelioma cells, as well as their regulation by ADP. Using real‐time PCR, we showed that activation of the P2Y1 receptor by ADP increased the expression of MMP2/9 mRNAs; MMP2/9 collected from conditioned media also showed an increase in activity; and ADP induced the nuclear localization of MMP2/9. The effects of ADP on transcription of the MMPs were due to activation of c‐Src, Akt, and NF‐κB, while ERK1/2 phosphorylation was needed for the increase in enzymatic activity and the regulation of nuclear import. We also showed that the nuclear localization of MMP2/9 induced by ADP causes the cleavage and inactivation of poly‐ADP‐ribose polymerase‐1. These findings may help to elucidate the mechanisms regulating MMP2/9 activation in ZL55 human epithelioid mesothelioma cells, and perhaps other cells. Therapeutic approaches that promote ADP accumulation in a tumor environment may constitute an effective means to induce anticancer activity. This paper examines the expression, intracellular localization, and function of matrix metalloproteinase (MMP) 2 and MMP9 in ZL55 human epithelioid mesothelioma cells, as well as their regulation by ADP. We found that ADP activates an intracellular transduction system based on NF‐κB, c‐Src, Akt, and ERK1/2 that causes nuclear localization of MMP2/9, resulting in degradation of the DNA repair enzyme poly‐ADP‐ribose polymerase‐1. [ABSTRACT FROM AUTHOR]

In this paper, we first derive a new chemotaxis‐haptotaxis model of cancer invasion of tissue with density‐dependent jump probability and quorum‐sensing mechanisms, which is with degeneracy in diffusion. In the presence of generic logistic damping, we then prove the global existence of weak solutions. The approach adopted is the compactness analysis with Moser‐type iteration and artificial viscosity‐vanishing technique. [ABSTRACT FROM AUTHOR]

Abstract: While desired for the cure of allergy, regulatory immune cell subsets and nonclassical Th2‐biased inflammatory mediators in the tumour microenvironment can contribute to immune suppression and escape of tumours from immunological detection and clearance. A key aim in the cancer field is therefore to design interventions that can break immunological tolerance and halt cancer progression, whereas on the contrary allergen immunotherapy exactly aims to induce tolerance. In this position paper, we review insights on immune tolerance derived from allergy and from cancer inflammation, focusing on what is known about the roles of key immune cells and mediators. We propose that research in the field of AllergoOncology that aims to delineate these immunological mechanisms with juxtaposed clinical consequences in allergy and cancer may point to novel avenues for therapeutic interventions that stand to benefit both disciplines. [ABSTRACT FROM AUTHOR]

Risk stratification tools and prognostic models in non-muscle-invasive bladder cancer: a critical assessment from the European Association of Urology non-muscle-invasive bladder cancer guidelines panel. In this interesting paper, Kobayashi I et al. i compare the residual tumor rate in a prospective series of 117 high-risk non-muscle invasive bladder cancer patients treated with photodynamic diagnosis-assisted transurethral resection of the bladder tumor (PDD-TURBT) with a retrospective cohort of 306 cases that underwent a second TURBT after a first "white-light" (WLC) procedure (BRIGHT study). Bladder cancer prospective cohort study on high-risk non-muscle invasive bladder cancer after photodynamic diagnosis-assisted transurethral resection of the bladder tumor (BRIGHT study). [Extracted from the article]

Active surveillance (AS) is an increasingly prevalent treatment choice for low grade prostate cancer. Eligibility criteria for AS are varied and it is unclear if family history of prostate cancer should be used as an exclusion criterion when considering men for AS. To determine whether family history plays a significant role in the progression of prostate cancer for men undergoing active surveillance, PubMed searches of 'family history and prostate cancer', 'family history and prostate cancer progression' and 'factors of prostate cancer progression' were used to identify research publications about the relationship between family history and prostate cancer progression. These searches generated 536 papers that were screened and reviewed. Six publications were ultimately included in this analysis. Review of the six publications suggests that family history does not increase the risk of prostate cancer progression, whilst a subgroup analysis in one study found that family history increases the risk of prostate cancer progression only in African-Americans. A family history of prostate cancer does not appear to increase a patient's risk of having more aggressive prostate cancer and is therefore unlikely to be an important factor in determining eligibility for AS. Further studies are needed to better understand the relationship between race, family history, and eligibility for AS. [ABSTRACT FROM AUTHOR]

In this paper, we prove that if the initial data is small enough, we obtain an explicit L ∞( Q T)-estimate for a two-dimensional mathematical model of cancer invasion, proving an explicit bound with respect to time T for the estimate of solutions. Copyright © 2017 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Accumulating papers have demonstrated that micro RNAs play an important role in the progression of lung cancer, mainly as oncogenic and tumor suppressive. Therefore, micro RNAs may influence the survival of lung cancer patients. In this meta-analysis, we evaluated the role of micro RNAs in affecting the overall survival in nonsmall cell lung cancer ( NSCLC) patients, which may provide valuable information for the treatment of nonsmall cell lung cancer. We used keywords to retrieve literatures from online databases PUBMED, EMBASE and Web of Science and included 12 studies into our investigation according to pre-set criteria. Then, we analyzed the data with stata13.1 to evaluate the micro RNAs role on the prognosis of NSCLC patients. NSCLC patients with higher micro RNAs expression levels tend to show lower overall survival. HR (hazard ratio): 2.49, 95% CI (confidence interval): 1.84-3.37. Besides, both oncogenic and tumor suppressive micro RNAs have an evident influence on prognosis with HR values of 2.60 (95% CI: 2.12-3.19) and 0.41 (95% CI: 0.05-0.34), respectively. micro RNAs, especially from tissue, have an influence on overall survival of NSCLC patients, which indicates that micro RNAs could serve as potential prognostic markers for NSCLC and may provide a treatment strategy for advanced NSCLC patients. [ABSTRACT FROM AUTHOR]

Although human papillomavirus (HPV) vaccines offer enormous promise for the ultimate control and possible elimination of cervical cancer, barriers to uptake and coverage of the vaccine both in high- and low/middle-income settings mean that advances in secondary prevention continue to be essential to prevent unnecessary deaths and suffering from cervical cancer for decades to come. While cytology (the Pap smear) has reduced cervical cancer incidence and prevalence in jurisdictions where it has been systematically implemented in population-based programs-mainly in high-income settings-limitations inherent to this method, and to program delivery, leave many women still vulnerable to cervical cancer. Recent evidence has confirmed that screening based on HPV testing prevents more invasive cervical cancer and precancerous lesions, and offers innovative options such as self-collection of specimens to improve screening uptake broadly. In this paper, we review key advances, future opportunities, and ongoing challenges for secondary prevention of cervical cancer using HPV-based testing. [ABSTRACT FROM AUTHOR]

The first paper in this section is a meta-analysis of randomized trials into the effect of two intravesical agents used to reduce tumour recurrence in high-risk superficial bladder cancer. This is the highest level of evidence-based medicine and the results presented here suggest that intravesical BCG is superior to mitomycin C. There was no difference in the effect of the two agents on disease progression or survival. In a study from Amsterdam and Rome, the authors describe a phase I trial into the toxicity and safety of intravesical gemcitabine, and found that it was well tolerated with no systemic toxicity. In a paper from Taiwan the link between viral infections and tumour foundation is evaluated, in this case specifically infections with the Epstein-Barr virus and its correlation with urothelial cancer. The authors found that there was indeed a strong association between infection with this virus and a considerable proportion of primary urothelial TCCs. To assess, in a systematic review and meta-analysis, the relative effectiveness of intravesical mitomycin C and bacillus Calmette-Guérin (BCG) for tumour recurrence, disease progression and overall survival in patients with medium- to high-risk Ta and T1 bladder cancer. The major medical databases were searched comprehensively up to June 2003, and relevant journals hand-searched for randomized controlled trials, in any language, that compared intravesical mitomycin C with BCG in medium- to high-risk patients with Ta or T1 bladder cancer. Twenty-five articles were identified but only seven were considered eligible for the analysis. This represented 1901 evaluable patients in all, 820 randomized to mitomycin C and 1081 to BCG. Six trials had sufficient data for meta-analysis and included 1527 patients, 693 in the mitomycin and 834 in the BCG arm. There was no significant difference between mitomycin C and BCG for tumour recurrence in the six trials, with a weighted mean log hazard ratio, LHR, (variance) of −0.022 (0.005). However, there was significant heterogeneity between trials ( P = 0.001). A subgroup analysis of three trials that included only high-risk Ta and T1 patients indicated no heterogeneity ( P = 0.25) and a LHR for recurrence of −0.371 (0.012). With mitomycin C used as the control in the meta-analysis, a negative ratio is in favour of BCG and, in this case, was highly significant ( P < 0.001). The seventh trial (in abstract form only) used BCG in low doses for two arms of the trial (27 mg and 13.5 mg) compared with a standard dose of mitomycin C (30 mg), and reported a significantly lower recurrence rate with BCG (27 mg) than for mitomycin C ( P = 0.001). Only two trials included sufficient data to analyse disease progression and survival, representing 681 patients (338 randomized to BCG and 343 to mitomycin C). There was no significant difference between mitomycin C and BCG for disease progression, with a LHR of 0.044 (0.04) ( P = 0.16), or survival, at −0.112 (0.03) ( P= 0.50). Adverse events were slightly more frequent with BCG. Local toxicity (dysuria, cystitis, frequency and haematuria) were associated with both mitomycin C (30%) and BCG (44%). Systemic toxicity, e.g. chills, fever and malaise, occurred with both agents (12% and 19%, respectively) although skin rash was more common with mitomycin C. Tumour recurrence was significantly lower with intravesical BCG than with mitomycin C only in those patients at high risk of tumour recurrence. However, there was no difference in disease progression or survival, and the decision to use either agent might be based on adverse events and cost. [ABSTRACT FROM AUTHOR]

Aim Treatment with pertuzumab-trastuzumab-taxane combinations has become the international standard of care for patients with HER2-positive metastatic breast cancer. In this paper we discuss the practicalities of treating patients with this combination with a particular focus on treatment in the Australian setting. Method An expert panel was convened to discuss practical aspects for use of pertuzumab in the Australian clinical setting. The findings of this panel are reported in this article. Results The combination of pertuzumab-trastuzumab-docetaxel has established efficacy in patients with HER2-positive metastatic breast cancer, prolonging progression-free and overall survival compared to trastuzumab-taxane combinations. In Australia, combinations of pertuzumab and trastuzumab with docetaxel or paclitaxel are reimbursed. Management of treatment related side-effects such as diarrhea, febrile neutropenia and neuropathy typically include dose reduction or switching taxane. Specific patients with poorer tolerance of chemotherapy such as the elderly or those from Asian backgrounds may require particular management strategies. Conclusions The advent of targeted therapies for women with metastatic HER2-positive breast cancer has markedly improved survival. Combinations of pertuzumab-trastuzumab and a taxane are the standard of care in patients with good performance status. Given prolongation of survival and the importance of quality of life endpoints, the treatment paradigm for patients with metastatic HER2-positive breast cancer is changing rapidly. Careful management of toxicities is required, and dose reduction or switching taxane may be necessary. Further research is required on the efficacy of pertuzumab combinations in patients with brain metastases, and on those who relapse quickly following adjuvant therapy. [ABSTRACT FROM AUTHOR]

Esophageal adenocarcinoma is the fastest rising cancer in the United States. It develops from long-standing gastroesophageal reflux disease which affects >20% of the general population. It carries a very poor prognosis with 5-year survival <20%. The disease is known to sequentially progress from reflux esophagitis to a metaplastic precursor, Barrett's esophagus and then onto dysplasia and esophageal adenocarcinoma. However, only few patients with reflux develop Barrett's esophagus and only a minority of these turn malignant. The reason for this heterogeneity in clinical progression is unknown. To improve patient management, molecular changes which facilitate disease progression must be identified. Animal models can provide a comprehensive functional and anatomic platform for such a study. Rats and mice have been the most widely studied but disease homology with humans has been questioned. No animal model naturally simulates the inflammation to adenocarcinoma progression as in humans, with all models requiring surgical bypass or destruction of existing antireflux mechanisms. Valuable properties of individual models could be utilized to holistically evaluate disease progression. In this review paper, we critically examined the current animal models of Barrett's esophagus, their differences and homologies with human disease and how they have shaped our current understanding of Barrett's carcinogenesis. [ABSTRACT FROM AUTHOR]

Many oncology studies incorporate a blinded independent central review (BICR) to make an assessment of the integrity of the primary endpoint, progression free survival. Recently, it has been suggested that, in order to assess the potential for bias amongst investigators, a BICR amongst only a sample of patients could be performed; if evidence of bias is detected, according to a predefined threshold, the BICR is then assessed in all patients, otherwise, it is concluded that the sample was sufficient to rule out meaningful levels of bias. In this paper, we present an approach that adapts a method originally created for defining futility bounds in group sequential designs. The hazard ratio ratio, the ratio of the hazard ratio (HR) for the treatment effect estimated from the BICR to the corresponding HR for the investigator assessments, is used as the metric to define bias. The approach is simple to implement and ensures a high probability that a substantial true bias will be detected. In the absence of bias, there is a high probability of accepting the accuracy of local evaluations based on the sample, in which case an expensive BICR of all patients is avoided. The properties of the approach are demonstrated by retrospective application to a completed Phase III trial in colorectal cancer. The same approach could easily be adapted for other disease settings, and for test statistics other than the hazard ratio. Copyright © 2015 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Genetic alterations can drive oncogenic events and cancer development. However, this is only half of the story. It is now evident that tumor progression only occurs if powerful stress signaling pathways and microenvironmental signals are overcome. Two recent Nature Cell Biology papers study how niche signals of primary and target organ barriers have to be overridden for oncogenes to allow for colorectal cancer (CRC) initiation and metastasis (Urosevic et al, ; Whissell et al, ). Two recent papers in NCB elucidate stromal signals and intrinsic cellular stress pathways as critical barriers for tumor progression and metastasis, respectively. [ABSTRACT FROM AUTHOR]

One of the hallmarks of cancer is aberrant DNA methylation, which is associated with abnormal gene expression. Both hypermethylation and silencing of tumour suppressor genes as well as hypomethylation and activation of prometastatic genes are characteristic of cancer cells. As DNA methylation is reversible, DNA methylation inhibitors were tested as anticancer drugs with the idea that such agents would demethylate and reactivate tumour suppressor genes. Two cytosine analogues, 5-azacytidine ( Vidaza) and 5-aza-2′-deoxycytidine, were approved by the Food and Drug Administration as antitumour agents in 2004 and 2006 respectively. However, these agents might cause activation of a panel of prometastatic genes in addition to activating tumour suppressor genes, which might lead to increased metastasis. This poses the challenge of how to target tumour suppressor genes and block cancer growth with DNA-demethylating drugs while avoiding the activation of prometastatic genes and precluding the morbidity of cancer metastasis. This paper reviews current progress in using DNA methylation inhibitors in cancer therapy and the potential promise and challenges ahead. Linked Articles This article is part of a themed section on Epigenetics and Therapy. To view the other articles in this section visit [ABSTRACT FROM AUTHOR]

Purpose: Tracking the progression of low grade tumors (LGTs) is a challenging task, due to their slow growth rate and associated complex internal tumor components, such as heterogeneous enhancement, hemorrhage, and cysts. In this paper, the authors show a semiautomatic method to reliably track the volume of LGTs and the evolution of their internal components in longitudinal MRI scans. Methods: The authors' method utilizes a spatiotemporal evolution modeling of the tumor and its internal components. Tumor components gray level parameters are estimated from the follow-up scan itself, obviating temporal normalization of gray levels. The tumor delineation procedure effectively incorporates internal classification of the baseline scan in the time-series as prior data to segment and classify a series of follow-up scans. The authors applied their method to 40 MRI scans of ten patients, acquired at two different institutions. Two types of LGTs were included: Optic pathway gliomas and thalamic astrocytomas. For each scan, a "gold standard" was obtained manually by experienced radiologists. Themethod is evaluated versus the gold standard with threemeasures: gross total volume error, total surface distance, and reliability of tracking tumor components evolution. Results: Compared to the gold standard the authors' method exhibits a mean Dice similarity volumetric measure of 86.58% and a mean surface distance error of 0.25 mm. In terms of its reliability in tracking the evolution of the internal components, the method exhibits strong positive correlation with the gold standard. Conclusions: The authors' method provides accurate and repeatable delineation of the tumor and its internal components, which is essential for therapy assessment of LGTs. Reliable tracking of internal tumor components over time is novel and potentially will be useful to streamline and improve followup of brain tumors, with indolent growth and behavior. [ABSTRACT FROM AUTHOR]

Raman spectroscopy is an optical technique capable of identifying chemical constituents of a sample by their unique set of molecular vibrations. Research on the applicability of Raman spectroscopy in the differentiation of cancerous versus normal tissues has been ongoing for many years, and has yielded successful results in the context of prostate, breast, brain, skin, and head and neck cancers as well as pediatric tumors. Recently, much effort has been invested on developing noninvasive "Raman" probes to provide real-time diagnosis of potentially cancerous tumors. In this regard, it is feasible that the Raman technique might one day be used to provide rapid, minimally invasive real-time diagnosis of tumors in patients. Raman spectroscopy is relatively new to the field of radiation therapy. Recent work involving cell lines has shown that the Raman technique is able to identify proteins and other markers affected by radiation therapy. Although this work is preliminary, one could ask whether or not the Raman technique might be used to identifymolecular markers that predict radiation response. This paper provides a brief review of Raman spectroscopic investigations in cancer detection, benefits and limitations of this method, advances in instrument development, and also preliminary studies related to the application of this technology in radiation therapy response assessment. [ABSTRACT FROM AUTHOR]

Background Recent trials on rectal cancer have demonstrated significant improvements in local recurrence without improvements in overall survival. The aim of this paper was to define the influence of local recurrence on survival in a prospective series of patients who underwent R0 or R1 resections for rectal cancer. Methods Patients presenting with rectal cancer from 1996 to 2012 were prospectively audited. The study included patients who underwent an R0 or R1 resection. Local recurrence was defined as cancer regrowth detected in the pelvis regardless of whether or not new metastases were found elsewhere. Kaplan- Meier curves, smoothed hazard functions and Cox models using both time since diagnosis and age as the time scale were used to define the influence of local recurrence on overall survival. Results The study involved 483 patients, of mean age 66 years (standard deviation = 13) and a median follow-up of 5.2 years. The results at 5 years were overall survival 71% (95% confidence interval ( CI) 66-75), local recurrence 7% (95% CI 5-10) and distant recurrence 18% (95% CI 14-22). Patients diagnosed with local recurrence died faster than patients diagnosed with either distant recurrence or no recurrence, and this was particularly obvious for younger patients (local hazard ratio (HR) 54, 95% CI 12-253 and distant HR19, 95% CI 4-80). Local recurrence that developed early following surgery also had worse survival outcomes. Conclusions Within this cohort of rectal cancer patients, the early development of local recurrence was the single most important indicator of a reduced survival, and carried a worse prognosis than the development of distant metastases alone. [ABSTRACT FROM AUTHOR]

DOI: 10.1111/his.14273 © 2020 John Wiley & Sons Ltd Sir: The major premise of Delahunt et al. in response to our paper by Varma et al. 1 is that all intraductal carcinomas of the prostate (IDCPs) are retrograde extensions of high-grade prostate adenocarcinoma into prostatic ducts. 5 In these cases, when the IDCP was either not adjacent to invasive carcinoma or when 80% of the tumour was IDCP and there was only adjacent microinvasive carcinoma, the authors concluded that the extensive IDCP did not represent retrograde extension from the adjacent limited carcinoma. [Extracted from the article]

This paper presents commentaries on the microscopic morphology of esophageal squamous epithelium; the frequency of duplication of the muscularis mucosae (MM) in Barrett's esophagus (BE); the significance of multilayered epithelium; whether cells in the lamina propria reflect those in the epithelium; how stem cells are identified in the squamous esophagus; dilated intercellular spaces; the metastasizing potential of early carcinoma-dependent, molecular or immunohistochemical tests that improve diagnosis; the role of immunohistochemistry IHC in grading of neoplasia in Barrett's esophagus and defining the risk of progression to adenocarcinoma; the roles of CDX1 and CDX2 in squamous and cardiac mucosa; and the role of desmosomal cadherins and lectins in squamous and cardiac mucosa. [ABSTRACT FROM AUTHOR]

This review paper discusses the main molecular alterations of endometrial carcinoma, the most common cancer of the female genital tract. Two clinicopathological variants are recognized: the oestrogen-related (type I, endometrioid carcinoma) and the non-oestrogen-related (type II, non-endometrioid carcinoma). Whereas type I shows microsatellite instability and mutations in PTEN, PIK3 CA, K- RAS and CTNNB1 (beta-catenin), type II exhibits TP53 mutations and chromosomal instability. Recent investigations regarding the role of non-coding RNA have provided important information regarding tumour progression. Understanding pathogenesis at the molecular level is essential for identifying biomarkers of potential use in targeted therapies. [ABSTRACT FROM AUTHOR]

What's known on the subject? and What does the study add? Today, angiogenesis is known to play a key role in cancer growth and development. Emerging cancer treatments are based on the suppression of angiogenesis, and modern imaging techniques investigate changes in the microvasculature that are caused by angiogenesis. As for other forms of cancers, angiogenesis is well recognised as a fundamental process in the development of prostate cancer. The novelty of this extensive report on angiogenesis in cancer, with particular attention on prostate cancer and the imaging techniques able to detect it, is the new prospective to the subject. In contrast with the other available reviews, this report goes from 'theory' to 'practice', establishing a clear link between angiogenesis development and imaged angiogenesis features. Once the key role of angiogenesis in the development of cancer and in particular prostate cancer has been fully described, attention is turned to the current imaging methods with the potential to assess the angiogenesis process and, as a consequence, to detect and localise prostate cancer. As confirmed by all available statistics, cancer represents a major clinical and societal problem in the developed world. The form of cancer with the highest incidence in men is prostate cancer. For prostate cancer, as well as for most forms of cancer, detection of the disease at an early stage is critical to reduce mortality and morbidity., Today, it is well known that pathological angiogenesis represents a crucial step in cancer development and progression. Comparable with most forms of cancer, angiogenesis also plays a fundamental role for prostate cancer growth., As a consequence, angiogenesis is an ideal target not only for novel anti-angiogenic therapies, but also for modern imaging techniques that aim at cancer localisation by detection of angiogenic microvascular changes., These techniques are mainly based on magnetic resonance, ultrasound, and nuclear imaging., This paper provides a comprehensive review of the available studies on angiogenesis in prostate cancer and its use by modern and emerging imaging techniques for prostate cancer localisation. [ABSTRACT FROM AUTHOR]

The article presents abstracts on papers related to colorectal disease including "Audit of colorectal cancer follow up- what is the rationale of present day practice?," by G. Bromley and colleagues, "Have all the changes in colorectal cancer care reduced stage of disease?," by A. Godden and colleagues, and "Urgent referrals for colorectal cancer: can patients go 'straight-to-test'?," by A. Torrance, A. Patel, and J. Singh.

Please cite this paper as: Chan YC, Banerjee J, Choi SY, Sen CK. miR-210: The master hypoxamir. Microcirculation 19: 215-223, 2012. Abstract MicroRNAs are small non-coding RNAs implicated mainly in post-transcriptional gene silencing by interacting with the untranslated region of the transcript. miR-210 represents major hypoxia-inducible miRs, also known as hypoxamirs, which is ubiquitously expressed in a wide range of cells, serving versatile functions. This review article summarizes the current progress on biogenesis of miR-210 and its physiological roles including arrest of cell proliferation, repression of mitochondrial respiration, arrest of DNA repair, vascular biology, and angiogenesis. Given the fact that miR-210 is aberrantly expressed in a number of diseases such as tumor progression, myocardial infarction and cutaneous ischemic wounds, miR-210 could serve as an excellent candidate for prognostic purposes and therapeutic intervention. With the advancement of computational prediction, high-throughput target validation methodology, sequencing, proteomic analysis, and microarray, it is anticipated that more down-stream targets of miR-210 and its associated biological consequences under hypoxia will be unveiled establishing miR-210 as a major hub in the biology of hypoxia-response. [ABSTRACT FROM AUTHOR]

Pleural malignancies, including primary malignant pleural mesothelioma and secondary pleural metastasis of various tumours resulting in malignant pleural effusion, are frequent and lethal diseases that deserve devoted translational research efforts for improvements to be introduced to the clinic. This paper highlights select clinical advances that have been accomplished recently and that are based on preclinical research on pleural malignancies. Examples are the establishment of folate antimetabolites in mesothelioma treatment, the use of PET in mesothelioma management and the discovery of mesothelin as a marker of mesothelioma. In addition to established translational advances, this text focuses on recent research findings that are anticipated to impact clinical pleural oncology in the near future. Such progress has been substantial, including the development of a genetic mouse model of mesothelioma and of transplantable models of pleural malignancies in immunocompetent hosts, the deployment of stereological and imaging methods for integral assessment of pleural tumour burden, as well as the discovery of the therapeutic potential of aminobiphosphonates, histone deacetylase inhibitors and ribonucleases against malignant pleural disease. Finally, key obstacles to overcome towards a more rapid advancement of translational research in pleural malignancies are outlined. These include the dissection of cell-autonomous and paracrine pathways of pleural tumour progression, the study of mesothelioma and malignant pleural effusion separately from other tumours at both the clinical and preclinical levels, and the expansion of tissue banks and consortia of clinical research of pleural malignancies. [ABSTRACT FROM AUTHOR]

Please cite this paper as: Increased regulatory T-cell frequencies in patients with advanced melanoma correlate with a generally impaired T-cell responsiveness and are restored after dendritic cell-based vaccination. Experimental Dermatology 2010; 19: e213-e221. Abstract: Naturally occurring CD4+ CD25+ regulatory T-cell (Treg) activity is assumed to facilitate tumor development and progression. To elucidate the possible role of Tregs in the course of melanoma progression, we analysed the frequency of Tregs in the peripheral blood of patients at melanoma stages I-IV and in patients at melanoma stage IV that underwent dendritic cell (DC)-based immunotherapy. Using CD25, Foxp3, CD127 and HLA-DR as Treg associated markers, we observed increased Treg frequencies in patients at the late melanoma stage (stage IV) when compared to healthy donors. Accumulation of Tregs in patients with progressed melanoma correlated with a general reduction of T-cell responsiveness to the recall antigens tetanus toxoid and tuberculin-GT. However, DC-based immunotherapy not only restored antigen-specific immunity, but also decreased the frequency of Tregs in peripheral blood of patients with melanoma. These findings indicate that tumor progression in patients with melanoma result in general immunosuppression that is associated with Treg expansion in the periphery and can be overcome by DC-based vaccination. [ABSTRACT FROM AUTHOR]

This paper summarises how scaffold proteins affects and regulate the JNK signalling pathway. We believe that some of these scaffold proteins, by virtue of their anchoring and catalytic properties contribute to a high degree of specificity of intra cellular signalling pathways that regulate the progression through the cell cycle. [ABSTRACT FROM AUTHOR]

Objective: A combination of quantitative data and illustrative narratives may allow cancer survivorship researchers to disseminate their research findings more broadly. We identified recent, methodologically rigorous quantitative studies on return to work after cancer, summarized the themes from these studies, and illustrated those themes with narratives of individual cancer survivors. Methods: We reviewed English-language studies of return to work for adult cancer survivors through June 2008, and identified 13 general themes from papers that met methodological criteria (population-based sampling, prospective and longitudinal assessment, detailed assessment of work, evaluation of economic impact, assessment of moderators of work return, and large sample size). We drew survivorship narratives from a prior qualitative research study to illustrate these themes. Results: Nine quantitative studies met four or more of our six methodological criteria. These studies suggested that most cancer survivors could return to work without residual disabilities. Cancer site, clinical prognosis, treatment modalities, socioeconomic status, and attributes of the job itself influenced the likelihood of work return. Three narratives—a typical survivor who returned to work after treatment, an individual unable to return to work, and an inspiring survivor who returned to work despite substantial barriers—illustrated many of the themes from the quantitative literature while providing additional contextual details. Conclusion: Illustrative narratives can complement the findings of cancer survivorship research if researchers are rigorous and transparent in the selection, analysis, and retelling of those stories. Copyright © 2009 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Aims: To describe survival from oral metastases, particularly gingival metastases, and to identify clinical prognostic variables. Materials and Methods: A series of 39 patients were studied, analysing age, gender, primary tumour site, oral metastases site and histological type. Results: Mean age: 62.3±9.2 years, with similar prevalence by gender. The most frequent sites for primary tumours were the kidney (20.5%), lung (20.5%) and breast (20.5%). Gingival metastases represented 63.6% of all oral soft tissue metastases (7/11). The average time between primary tumour diagnosis and appearance of the gingival metastases was 9.7±13.4 months. The median survival time since gingival metastases appearance was 5.2 months [95% confidence interval (CI)=0–13.6]; no statistically significant difference with other oral locations was found by the Kaplan–Meier curves (log rank: 0.29; p>0.05). Oral metastases involving the gingiva were more frequently found in the maxilla (85.7% versus 14.3%), whereas intra-osseous metastatic tumours were more frequent in the mandible (77.8% versus 22.2%; p<0.05; odds ratio=21; 95% CI=2.0–210.1). None of the variables considered had a prognostic value as indicated by the Kaplan–Meier test. Practical implications: The data in this paper show that 25% (and in other studies up to 37%) of oral metastases came from unknown primary tumours; thus a biopsy with histopathologic analysis is mandatory for every patient with a gingival mass. Conclusions: This study reinforces the significance of gingival metastases as a poor prognosis indicator. Dental practitioners should suspect that gingival masses mimicking benign or inflammatory lesions may represent a sign of underlying malignant tumours. [ABSTRACT FROM AUTHOR]

The objectives were to evaluate the beneficial effect of intra-operative echographic plaque site localization and to assess the rate of complications of postplaque insertion. This paper is a descriptive study of 48 patients with choroidal melanoma who underwent iodine-125 (I125) or ruthenium-106 (Ru106) plaque radiotherapy with intra-operative echographic confirmation of plaque placement with the aid of a nonradioactive plaque (dummy) at McGill University Health Centre from 1997 to 2003. Patients' mean age was 63.7 years; 52% (25/48) male, 48% (23/48) female. Twenty-seven percent (13/48) of the tumors were confined to the right eye and 73% (35/48) to the left eye. Forty-eight percent (23/48) of the tumors were located posterior to the equator, 14.6% (7/48) were anterior to the equator, 18.7% (9/48) in posterior pole, and 18.7% (9/48) at equator. Sixty-nine percent (33/48) received I125 and 31% (15/48) had Ru106 treatment. Ninety percent of the dummy plaques were initially positioned suboptimally and required repositioning under echographic guidance. At mean follow-up of 18.8 months, there was no tumor-related death or metastasis, but one patient required enucleation. The dummy plaque technique under echographic visualization resulted in reduction of radioactive exposure time during surgery of up to 50%. Intra-operative echographic utilization has the ability to localize precisely the tumor–plaque relationship, thereby optimizing the radiation delivered to the choroidal melanoma, while minimizing the surgeon's exposure time. [ABSTRACT FROM AUTHOR]

Soft-tissue sarcomas can be divided into translocation-associated (TA) and non-TA sarcomas, the latter of which is often characterized by pleomorphic cytomorphology and aneuploidy. The aberrant expression of MAD2, an essential component of the mitotic spindle checkpoint, has been recently shown to promote aneuploidy. The aim of the present paper was to assess MAD2 status on immunohistochemistry in 50 TA sarcomas with known fusion genes and 50 non-TA pleomorphic sarcomas. MAD2 was overexpressed in 26 TA (52%) and 33 non-TA sarcomas (66%). Notably, the MAD2 overexpression was frequently detected in TA sarcomas with atypical or high-grade morphology, such as round cell liposarcoma and fibrosarcomatous dermatofibrosarcoma protuberans. The MAD2 overexpression was significantly frequent in non-TA sarcomas compared with TA tumors without such atypical or high grade morphology ( P = 0.012). In addition, sarcomas with MAD2 overexpression were significantly rich in abnormal mitotic figures, including multipolar mitoses and anaphase bridges, compared to MAD2-negative tumors ( P = 0.003), although the overall mitotic activity was equivalent between the sarcomas with or without the MAD2 overexpression. These data suggest that the aberrant MAD2 expression is potentially associated with pleomorphic morphology and abnormal mitosis in soft-tissue sarcomas, as well as with high-grade tumor progression in its TA subset. [ABSTRACT FROM AUTHOR]

In younger women at high risk for developing breast cancer the value of mammography is limited by a higher prevalence of breast tissue density, low rate of DCIS in gene carriers, faster growing tumours and concerns over radiation exposure. We report on our experience of MR screening in high risk patients over a three year period. Women at high risk of developing breast cancer were offered an MRI scan and an Ultrasound in addition to their annual mammogram for two years. The following MR-protocol was used: pre-contrast T2 STIR sequence and pre contrast 3D FLASH sequence, post contrast axial dynamic 3D FLASH sequence. Seventy two women consented to participate in this study. One hundred thirty nine breast MRI examinations were performed. Two pre-cancerous lesions and an axillary lymph node metastasis were found, but the majority of the lesions were benign. Difficulties in screening young women at high risk are discussed in this paper. In our study three lesions of significance were detected. Two lesions were precancerous thus curable. The recall rates show the difficult nature of screening younger breasts. MRI generated more findings judged as uncertain, so short term-term follow up studies or MR-guided biopsy techniques are required. [ABSTRACT FROM AUTHOR]

The article offers an overview of platform and poster presentations from the 55th Annual Scientific Meeting of the American Society of Cytopathology. A paper investigated the factors influencing the variability in atypical squamous cells to squamous intraepithelial lesions (ASC/SIL) ratios among pathologists. Another presentation investigated the expression of fatty acid synthase (FAS) in ovarian serous carcinoma and its relationship to cancer stage and progression.

Background: Correctly visualising the extent of the disease in cervical cancer is difficult with today's conventional imaging modalities. This paper presents the interim analysis of an on-going prospective study to evaluate the potential role of FDG-PET with software fusion with CT images in 3 different clinical settings of cervical cancer. Methods: In Group 1, 10 patients with early stage cervical cancer underwent FDG-PET 6 months after surgery. Group 2 consisted of 17 patients with locally advanced cervical cancer who underwent FDG-PET as part of the staging procedure. In Group 3, 12 patients with verified relapse and 3 patients with a strong suspicion thereof underwent FDG-PET before starting any therapy. The FDG-PET results were compared with the results of the standard conventional work-up. All patients had a follow-up time of at least 6 months. Results: All FDG-PET scans in Group 1 were true negative. In Group 2, FDG-PET detected previously unknown locations of metastases in 4 patients, and a synchronous pulmonary carcinoma in 1 patient, resulting in a change in treatment plan for 4 patients. One false negative FDG-PET result was recorded. In Group 3, FDG-PET results led to a change in treatment plan for 3 patients. Conclusions: We conclude that FDG-PET provides crucial information in the pre-treatment staging procedure in patients with locally advanced or relapsed cervical cancer. However, in the follow-up of early cervix cancer, FDG-PET 6 months post-operatively offered no clinical benefit in this small group of patients. [ABSTRACT FROM AUTHOR]

Authors from the USA sought to establish the relationship between tumour volume, pathological stage and outcomes after radical prostatectomy. In a large series of patients they found that tumour volume was correlated directly with pathological stage, and that it was independently correlated with PSA recurrence. The authors suggested that tumour volume had a potential use for prognostication in patients undergoing radical prostatectomy. Two papers, one from the USA and one from Germany, advise a re-staging TUR in patients with superficial bladder cancer who are at high risk of early tumour progression. In a large series of patients they found that residual tumour after initial resection was commoner than might be expected, and that the second resection indicated the way to earlier radical treatment and a better prognosis. OBJECTIVE To establish the relationship between tumour volume (TV), pathological stage and outcome after radical prostatectomy (RP), as TV is theoretically an important variable in prostate cancer pathology, but to date it has not been routinely reported and its independent prognostic significance is not well defined. PATIENTS AND METHODS The study included 431 consecutive patients undergoing RP for clinically localized cancer, from January 2000 to January 2002, who had a pathological examination of totally submitted whole-mount processed RP specimens. In addition to Gleason grade, tumour stage and margin assessment by standard techniques, TV was determined by digital planimetry. The total TV or index TV, for cases with obvious discrete separate tumours, were correlated with pathological stage and prostate-specific antigen (PSA) recurrence. RESULTS The mean (range) follow-up was 25.4 (6–51) months, and the mean TV for all patients was 3.28 (0.4–38.8) mL. There was a direct correlation between TV and pathological stage ( P < 0.001). The TV for organ-confined and extraprostatic disease was 2.09 and 6.02 mL, respectively ( P < 0.001). In a multivariate analysis, TV was an independent predictor of PSA recurrence ( P = 0.04). The mean TV for patients with PSA recurrence vs no recurrence was 6.8 and 2.6 mL, respectively ( P < 0.001). CONCLUSION TV correlates directly with pathological stage in RP specimens; furthermore, it is independently correlated with PSA recurrence. TV has potential use for prognostication in patients undergoing RP, and may be combined with other well established clinical variables to aid in predicting outcomes. [ABSTRACT FROM AUTHOR]

Aims : Immunohistochemistry is frequently employed to aid the distinction between mesothelioma and pulmonary adenocarcinoma metastatic to the pleura, but there is uncertainty as to which antibodies are most useful. We analysed published data in order to establish sensitivity and specificity of antibodies used to distinguish between these tumours with a view to defining the most appropriate immunohistochemical panel to use when faced with this diagnostic problem. Methods and results : A systematic analysis of the results of 88 published papers comparing immunohistochemical staining of a panel of antibodies in mesothelioma with epithelioid areas, and pulmonary adenocarcinoma metastatic to the pleura. Results for a total of 15 antibodies were analysed and expressed in terms of sensitivity and specificity. The most sensitive antibodies for identifying pulmonary adenocarcinoma were MOC-31 and BG8 (both 93%), whilst the most specific were monoclonal CEA (97%) and TTF-1 (100%). The most sensitive antibodies to identify epithelioid mesothelioma were CK5/6 (83%) and HBME-1 (85%). The most specific antibodies were CK5/6 (85%) and WT1 (96%). Conclusions : No single antibody is able to differentiate reliably between these two tumours. The use of a small panel of antibodies with a high combined sensitivity and specificity is recommended. [ABSTRACT FROM AUTHOR]