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Background: Colon cancer generally begins as a neoplastic growth of tissue, called polyps, originating from the inner lining of the colon wall. Most colon polyps are considered harmless but over the time, they can evolve into colon cancer, which, when diagnosed in later stages, is often fatal. Hence, time is of the essence in the early detection of polyps and the prevention of colon cancer. Methods: To aid this endeavor, many computer-aided methods have been developed, which use a wide array of techniques to detect, localize and segment polyps from CT Colonography images. In this paper, a comprehensive state-of-the-art method is proposed and categorize this work broadly using the available classification techniques using Machine Learning and Deep Learning. Conclusions: The performance of each of the proposed approach is analyzed with existing methods and also how they can be used to tackle the timely and accurate detection of colon polyps.

Express MS identification of biological tissues has become a much more accessible research method due to the application of direct specimen ionization at atmospheric pressure. In contrast to traditional methods of analysis employing GC-MS methods for determining the molecular composition of the analyzed objects it eliminates the influence of mutual ion suppression. Despite significant progress in the field of direct MS of biological tissues, the question of mass spectrometric profile attribution to a certain type of tissue still remains open. The use of modern machine learning methods and protocols (e.g., "random forests") enables us to trace possible relationships between the components of the sample MS profile and the result of brain tumor tissue classification (astrocytoma or glioblastoma). It has been shown that the most pronounced differences in the mass spectrometric profiles of these tumors are due to their lipid composition. Detection of statistically significant differences in lipid profiles of astrocytoma and glioblastoma may be used to perform an express test during surgery and inform the neurosurgeon what type of malignant tissue he is working with. The ability to accurately determine the boundaries of the neoplastic growth significantly improves the quality of both surgical intervention and postoperative rehabilitation, as well as the duration and quality of life of patients.Ékspress-identifikatsiia biologicheskikh tkaneĭ stala sushchestvenno bolee dostupnym metodom issledovaniia blagodaria primeneniiu metodov mass-spektrometrii s priamoĭ atmosfernoĭ ionizatsieĭ. V otlichie ot traditsionnykh metodov analiza, ispol'zuiushchikh khromato-mass-spektrometricheskie metody opredeleniia molekuliarnykh komponent issleduemykh ob"ektov, ona iskliuchaet vozmozhnost' ucheta éffektov podavleniia razlichnymi ionami drug druga po rezul'tatam izmereniĭ. Nesmotria na sushchestvennyĭ progress v oblasti priamoĭ mass-spektrometrii biologicheskikh tkaneĭ, vopros atributsii mass-spektrometricheskogo profilia opredelennomu vidu tkani ostaetsia otkrytym. Primenenie sovremennykh metodov mashinnogo obucheniia (sluchaĭnykh lesov) pozvoliaet prosledit' vzaimosviaz' mezhdu komponentami mass-spektrometricheskogo profilia i rezul'tatom identifikatsii tkani opukholi mozga (astrotsitomy ili glioblastomy). V dannoĭ rabote pokazano, chto osnovnye otlichiia v mass-spektrometricheskikh profiliakh étikh opukholeĭ obuslovleny ikh lipidnym sostavom. Poluchenie statisticheski dostovernykh razlichiĭ lipidnykh profileĭ astrotsitomy i glioblastomy pozvoliaet bystro provodit' analiz vo vremia khirurgicheskoĭ operatsii i soobshchat' neĭrokhirurgu, s kakoĭ tkan'iu on rabotaet. Vozmozhnost' tochnogo opredeleniia granits novoobrazovaniia sushchestvenno uluchshaet kachestvo i operativnogo vmeshatel'stva, i postoperatsionnoĭ reabilitatsii, ravno kak i prodolzhitel'nost' i kachestvo zhizni patsientov.

This minireview presents the contribution of estrogens and other hormones to the etiopathogenesis of tumors, as well as to the phenomena of perinatal programming/imprinting for various types of cancer. In addition, the importance of endocrine disruptors is discussed in the ontopathogeny of some oncologic diseases. The important role of stress and glucocorticoids, as referred to neoplastic growth, is highlighted. It is proposed that greater attention should be paid to the maintenance of the balance between cellular proliferation, the survival capacity of cells, and apoptosis as the basis for the bioregulation of normal and pathologic growth.

Most cell signaling and surveillance circuits are physically maintained through a dense network of protein-protein interactions (PPIs). Genetic mutations, epigenetic changes as well as alterations in cellular microenvironment can markedly rewire the patterns of PPIs, which leads to neoplastic growth of cancer cells. There are accumulating evidences that drugs that target-specific PPI pairs may provide an opportunity to treat cancers with a higher specificity and efficacy than those inhibiting enzymatic activity of oncogenic proteins. Therefore, identification of driving PPIs in a given cancer not only improves our understanding for individual cancers, but it also provides therapeutic opportunities to cure the specific cancer. In this review, we introduce some examples of aberrant PPI complexes identified in several major types of cancers, and recent technical developments that permit assessment of PPI strength in clinical specimens. Finally, we discuss the potential use of such PPI profiling for the purpose of precision medicine.

While it is often assumed that oncogenic processes in metazoans can influence species interactions, empirical evidence is lacking. Here, we use the cnidarian Hydra oligactis to experimentally explore the consequences of tumor associated phenotypic alterations for its predation ability, relationship with commensal ciliates and vulnerability to predators. Unexpectedly, hydra's predation ability was higher in tumorous polyps compared to non-tumorous ones. Commensal ciliates colonized preferentially tumorous hydras than non-tumorous ones, and had a higher replication rate on the former. Finally, in a choice experiment, tumorous hydras were preferentially eaten by a fish predator. This study, for the first time, provides evidence that neoplastic growth has the potential, through effect(s) on host phenotype, to alter biotic interactions within ecosystems and should thus be taken into account by ecologists.

Resveratrol (RV) is a polyphenol nonflavonoid compound present in strongly pigmented vegetables and fresh fruits as well as dried nuts such as peanuts. High concentrations of this natural compound were found in the modern Western world in the peel of the red grape (Vitis vinifera) but usage of this natural drug in popular medicine was documented much earlier. RV exhibits diverse biological activities such as antitumor, antioxidant, antiviral, and phytoestrogenic, but at high concentrations RV may show cytotoxic effects. Other natural substances behave in a similar way, such as curcumin and a semipurified fraction of the whole neem oil. The bioproperties of these natural products are also discussed. Administration of RV to cultured cells alters the permeability and fluidity of the cell membrane. The literature ascribes to RV an antiproliferative action which renders it a good candidate for the control of neoplastic growth. The authors also examine the possibility of using nanoparticles as potential vehicles for drug (RV) delivery. This specific topic is rapidly expanding and results referring to the action of carbon nanotubes and graphene sheets are also illustrated. A brief overview of other bioactive substances and potential candidates for nano-delivery is also discussed.

SUMMARYAggressive neoplastic growth can be initiated by a limited number of genetic alterations, such as the well-established cooperation between loss of cell architecture and hyperactive signaling pathways. However, our understanding of how these different alterations interact and influence each other remains very incomplete. Using Drosophila paradigms of imaginal wing disc epithelial growth, we have monitored the changes in Notch pathway activity according to the polarity status of cells (scrib mutant). We show that the scrib mutation impacts the direct transcriptional output of the Notch pathway, without altering the global distribution of Su(H), the Notch dedicated transcription factor. The Notch-dependent neoplasms require however, the action of a group of transcription factors, similar to those previously identified for Ras/scrib neoplasm (namely AP-1, Stat92E, Ftz-F1, and bZIP factors), further suggesting the importance of this transcription factor network during neoplastic growth. Finally our work highlights some Notch/scrib specificities, in particular the role of the PAR domain containing bZIP transcription factor and Notch direct target Pdp1 for neoplastic growth.

© 2017, Springer Science+Business Media, LLC. Emerging evidence implicates myristoylated alanine-rich C-kinase substrate (MARCKS), a major substrate of protein kinase C (PKC), in a critical role for cancer development and progression. MARCKS is tethered to the plasma membrane but can shuttle between the cytosol and plasma membrane via the myristoyl-electrostatic switch. Phosphorylation of MARCKS by PKC leads to its translocation from the plasma membrane to the cytosol where it functions in actin cytoskeletal remodeling, Ca2+ signaling through binding to calmodulin, and regulation of exocytic vesicle release in secretory cells such as neurons and airway goblet cells. Although the contribution of MARCKS to various cellular processes has been extensively studied, its roles in neoplastic disease have been conflicting. This review highlights the molecular and functional differences of MARCKS that exist between normal and tumor cells. We also discuss the recent advances in the potential roles of MARCKS in tumorigenesis, metastasis, and resistance to anti-cancer therapies, with a focus on addressing the inconsistent results regarding the function of MARCKS as a promoter or inhibitor of oncogenesis.

Portal vein thrombosis in patients with liver cirrhosis may be due neoplastic growth invading portal vein or due to non-neoplastic causes. The indications for treating PVT in cirrhotic individuals are diffi cult to be established but at least are of great benefi t in acute PVT. Investigating the cause of portal vein thrombosis in cirrhotic patient prepared for splenectomy including virology and immune markers, AFP, triphasic CT. Factor V Leiden mutation and prothrombin gene 20210. The case showed non-neoplastic portal vein thrombosis due to portal pyemia with underlying prothrombin gene 20210 polymorphism. The early initiation of anticoagulation after the diagnosis of acute PVT may be the only predictive factor for complete PV recanalization with preservation of liver function.

Deep benign fibrous histiocytoma (DBFH) is a rare mesenchymal tumor compared with cutaneous fibrous histiocytoma. As the diagnosis of DBFH may be clinically difficult, the presence of DBFH is usually confirmed after its excision. In this case study, we report a case of a 31-year-old man who lived with a painless mass in his right thigh for 15 years. After its examination by preoperative ultrasound and magnetic resonance imaging, the tumor was completely excised. Further histologic evaluation revealed neoplastic growth composed of proliferating spindle cells forming short fascicles and a storiform pattern. The patient was diagnosed with DBFH on the basis of its intraoperative, radiologic, and histopathologic features. Keywords: Benign fibrous histiocytoma, Soft tissue tumor, DBFH subcutaneous, Thigh

Radiotherapy is still a treatment of choice for many malignancies, often in combination with other strategies. However, its efficacy is limited by the dose that can be safely administered without eliciting serious side-effects, as well as the fact that recurrence is common, particularly in large tumours. Combining radiotherapy with drugs that could sensitise cells to radiation and/or reduce the factors that promote the recovery of the surviving cancer cells is a promising approach. Ionising radiation has been shown to induce senescence and the accumulation of senescent cells creates a microenvironment that facilitates neoplastic growth. This provides a rationale to test the addition of anti-senescent drugs, some of which are already available in the clinic, to radiotherapy protocols. Here, we discuss the relevance of radiotherapy-induced senescent cell accumulation and the potential interventions to minimise its negative effects.

Upper urinary tract urothelial carcinoma (UTUC) can be defined as any neoplastic growth that affects the lining of the urinary tract from the renal calyces to the distal ureter. UTUC has similar behaviors to urothelial cell carcinoma in bladder (UBC), but prognosis and tumor characteristics are different. However, UTUC is known as a relatively rare disease and has poor prognosis than UBC.

Mandibular accessory condyle is rare. Literature search found most of the accessory condyles to arise from the mandibular coronoid process due to hyperactivity of attached temporalis muscle. Although neoplastic growth at mandibular coronoid mimicking an accessory condyle also been cited. Absence of report in recent publications regarding accessory mandibular condyle arising from the main mandibular condyle makes this anomali extremely rare. The present case report is about a true accessory mandibular condyle which caused the patient facial and occlusal disharmony. A 3D computerized tomographic imaging ascertained the exact location of the accessory condyle, its origin and resting position of the accessory and the main condylar head. The facial and occlusal disharmony settled completely within a short postoperative time following surgical intervention and mild elastic traction.Delta Med Col J. Jan 2016 4(1): 45-50

Pseudomyxoma peritonei (PMP) is a rare disease with neoplastic growth of mucin-secreting cells in the peritoneal cavity, resulting in mucinous ascites. The septum of intra-abdominal fluid collection is a key imaging finding characteristic to PMP. In magnetic resonance imaging (MRI), multi-b value diffusion-weighted imaging (DWI) is a method used to obtain an accurate apparent diffusion coefficient. The clinical utilities of DWI using lower b values as diagnostic imaging are rarely highlighted. This report describes a case of PMP in which DWI using b values of 100 and 500 s/mm(2) exclusively visualized many thick septa with low signal intensity in peritoneal effusion. The septa could not be recognized in DWIs with b values of zero or 1000 s/mm(2), as with ultrasonography, computed tomography, and conventional MRI. A discrepancy between DWI using lower b values and other MRI sequences or imaging modalities indicates a specific capability of DWI using low b values: the ability to visualize septa of intra-abdominal fluid collection much thicker than in real cases. Results for this case suggest that DWI using low b values might present clinical potential for the preoperative diagnosis of PMP.

Mitochondria are dynamic organelles that exchange a multiplicity of signals with other cell compartments, in order to finely adjust key biological routines to the fluctuating metabolic needs of the cell. During neoplastic transformation, cells must provide an adequate supply of the anabolic building blocks required to meet a relentless proliferation pressure. This can occur in conditions of inconstant blood perfusion leading to variations in oxygen and nutrient levels. Mitochondria afford the bioenergetic plasticity that allows tumor cells to adapt and thrive in this ever changing and often unfavorable environment. Here we analyse how mitochondria orchestrate the profound metabolic rewiring required for neoplastic growth.

Background Perivascular epithelioid cell tumors (PEComa) are exceedingly rare mesenchymal neoplasms arising in a variety of anatomic sites. mTOR inhibitors are active in these neoplasms. However, no other effective treatments are available in those patients progressing to them. The PI3K–Akt–mTOR signaling pathway modulates neoplastic growth through signaling activation of ER and the EGF receptor family of receptor tyrosine kinases. ER drives PI3K/AKT activation in response to mTORC1 inhibition. This provides a rationale for combining anti-estrogens and mTORC1 inhibitors. Methods We retrospectively identified patients with advanced PEComa treated with mTOR inhibitors since January 2002 at Fondazione IRCCS Istituto Nazionale dei Tumori, Milan – Italy. In a subgroup of them, exemestane was added at the time of progression. Results Twenty-eight patients with advanced PEComa treated with mTOR inhibitors were identified. Twenty–six were evaluable for response. Twelve out 26 (46%) had a PR and seven (27%) a SD, with a median PFS of 7 months. At the time of progression to sirolimus, 5 patients received a combination of sirolimus and exemestane and one of sirolimus, exemestane and GnRH. Three patients out 6 had a PR, 2 out 6 had a SD, and 1 out 6 had a PD, with a median PFS of 6 months. In this subgroup of patients treated with the combination, previous PFS to mTOR inhibitors was 6.6 months. Conclusions In this small retrospective series, the combination of mTOR inhibitors and exemestane obtained a reversion of resistance to mTOR inhibitors in one half of patients. Legal entity responsible for the study The authors. Funding Has not received any funding. Disclosure R. Sanfilippo: Honoraria (self), Research grant / Funding (institution), Travel / Accommodation / Expenses: Lilly; Honoraria (self), Research grant / Funding (institution), Travel / Accommodation / Expenses: PharmaMar; Research grant / Funding (institution): Advanchen Laboratories; Research grant / Funding (institution): Amgen Dompe; Research grant / Funding (institution): AROG Pharmaceuticals; Research grant / Funding (institution): Bayer; Research grant / Funding (institution): Blueprint Medicines; Research grant / Funding (institution): Daiichi Sankyo; Research grant / Funding (institution): Deciphera; Research grant / Funding (institution): Eisai; Research grant / Funding (institution): Epizyme Inc; Research grant / Funding (institution): Galxo; Research grant / Funding (institution): Karyopharm; Research grant / Funding (institution): Novartis; Research grant / Funding (institution): Pfizer. C. Fabbroni: Research grant / Funding (institution): Advanchen Laboratories; Research grant / Funding (institution): Amgen Dompe’; Research grant / Funding (institution): AROG Pharmaceuticals; Research grant / Funding (institution): bayer; Research grant / Funding (institution): Blueprint Medicines; Research grant / Funding (institution): Daiichi Sankyo; Research grant / Funding (institution): Deciphera; Research grant / Funding (institution): Eisai; Research grant / Funding (institution): Lilly; Research grant / Funding (institution): Epizyme Inc; Research grant / Funding (institution): Glaxo; Research grant / Funding (institution): Karyopharm Pharmaceuticals; Research grant / Funding (institution): Novartis; Research grant / Funding (institution): Pfizer; Research grant / Funding (institution): PharmaMar. E. Fumagalli: Research grant / Funding (institution): Advenchen Laboratories; Research grant / Funding (institution): Amgen dompe’; Research grant / Funding (institution): AROG Pharmaceuticals; Research grant / Funding (institution): Bayer; Research grant / Funding (institution): Blueprint Medicines; Research grant / Funding (institution): Daiichi Sankyo; Research grant / Funding (institution): Deciphera; Research grant / Funding (institution): Eisai; Research grant / Funding (institution): Lilly; Research grant / Funding (institution): Epizyme; Research grant / Funding (institution): Novartis; Research grant / Funding (institution): PharmaMar; Research grant / Funding (institution): Glaxo; Research grant / Funding (institution): karyopharm Pharmaceuticals; Research grant / Funding (institution): Pfizer. R. Bertulli: Research grant / Funding (institution): Karyopharm Pharmaceuticals; Research grant / Funding (institution): Pfizer; Research grant / Funding (institution): Novartis; Research grant / Funding (institution): Eisai; Research grant / Funding (institution): Lilly; Research grant / Funding (institution): Advenchen Laboratories; Research grant / Funding (institution): Amgen dompe’; Research grant / Funding (institution): AROG Pharmaceuticals; Research grant / Funding (institution): Bayer; Research grant / Funding (institution): Blueprint Medicines; Research grant / Funding (institution): Daiichi Sankyo ; Research grant / Funding (institution): Deciphera; Research grant / Funding (institution): Epizyme; Research grant / Funding (institution): Glaxo; Research grant / Funding (institution): PharmaMar. S. Stacchiotti: Research grant / Funding (institution): Karyopharm Pharmaceuticals; Research grant / Funding (institution): Eisai; Research grant / Funding (institution): PharmaMar; Research grant / Funding (institution): Glaxo; Research grant / Funding (institution): Novartis; Research grant / Funding (institution): Lilly; Research grant / Funding (institution): Deciphera; Research grant / Funding (institution): Advenche Laboratories; Research grant / Funding (institution): Amgen; Research grant / Funding (institution): AROG Pharmaceuticals; Research grant / Funding (institution): Bayer; Research grant / Funding (institution): Blueprint Medicines; Research grant / Funding (institution): Daiichi Sankyo; Research grant / Funding (institution): Epizyme; Research grant / Funding (institution): Pfizer. P.G. Casali: Honoraria (self), Advisory / Consultancy, Research grant / Funding (institution): Bayer; Honoraria (self), Advisory / Consultancy, Research grant / Funding (institution): Deciphera; Honoraria (self), Advisory / Consultancy, Research grant / Funding (institution): Eisai; Honoraria (self), Advisory / Consultancy, Research grant / Funding (institution): Lilly; Honoraria (self), Advisory / Consultancy, Research grant / Funding (institution): Pfizer; Honoraria (self), Advisory / Consultancy, Research grant / Funding (institution): Nektar Therapeutics; Research grant / Funding (institution): Advenchen Laboratories; Research grant / Funding (institution): Novartis; Research grant / Funding (institution): Blueprint Midicines; Research grant / Funding (institution): AROG Pharmaceuticals; Research grant / Funding (institution): Amgen dompe’; Research grant / Funding (institution): Daiichi Sankyo; Research grant / Funding (institution): Epizyme; Research grant / Funding (institution): Glaxo; Research grant / Funding (institution): KaryopharmPharmaceuticals; Research grant / Funding (institution): PharmaMar. All other authors have declared no conflicts of interest.

In normal and tumourous calluses of sunflower and tobacco the level of extractable auxins was determined by Avena coleoptile straight growth test. Auxin activity was detected practically in two zones: I - at position with Rf 0.2-0.4 and II - at position with Rf 0.6-0.9. The tumour tissues of sunflower and tobacco plants, representing different types of neoplastic growth exhibit a 3 times higher auxin activity as compared with that of the corresponding normal tissues. Tobacco tissues, on the other hand, had a higher auxin level than the corresponding sunflower tissues and they exhibited different proportions in the activity of zones I and II, which points to a dominance of genetic regulation of hormone metabolism in these plants.

Graft-versus-host disease-associated angiomatosis (GVHD-AA) is an uncommon manifestation of chronic GVHD consisting of friable vascular proliferations. Using fluorescence in situ hybridization, we demonstrate the presence of donor-derived endothelial cells within areas of GVHD-AA. This is the first documented occurrence of a benign neoplastic growth in relationship to a form of chronic GVHD.

The temporomandibular joint (TMJ) is decisive for normal jaw function such as chewing, swallowing, speaking, oral health, and nutrition. Temporomandibular disorders (TMDs) refer to a group of disorders affecting the TMJ, masticatory muscles, and the associated structures. TMDs are considered as a multifactorial disorder. These conditions have been unable to reveal a common etiology or biological basis in terms of apparent signs and symptoms, and hence considered a heterogeneous group of health problems associated with chronic pain. These disorders share the symptoms of pain, limited mouth opening, and joint noises. The causes of TMDs range from traumatic injury to immune-mediated systemic disease to neoplastic growth to incompletely understood neurobiological mechanisms. This article presents an overview of the various etiological factors, signs, and symptoms related to TMDs.

Cervical cancer is the most common gynecological malignancy in the developing countries like India. In addition to human papillomavirus (HPV) infection, host genetic factors play an important role in viral persistence and neoplastic growth. IL-10, a multifunctional cytokine, plays an active role to promote tumor growth in the presence of HPV. The present study aims to find out the impact of IL-10 promoter polymorphisms at -1082A/G (rs1800896), -819C/T (rs1800872), and -592C/A (rs1800871) sites along with IL-10 production and HPV infection in the progression of cervical cancer. We have genotyped a total of 506 subjects, 256 cases (208 cervical cancer + 48 precancer), and 250 healthy controls by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method followed by sequencing. IL-10 serum concentration was measured by enzyme-linked immunosorbent assay. The frequency of IL-10 -592 variant genotype (AA) was found significantly reduced in cases as compare to controls while -1082 variant genotype (GG) was found ~4-fold higher risk of cervical cancer (p =

The overwhelming majority of the pituitary tumours are benign adenomas that remain a serious challenge to endocrinologists and neurosurgeons by virtue of great variety of their early manifestations, the impossibility to predict the neoplastic growth, and the influence exerted on the patients' quality of life. Most pituitary adenomas are sporadic tumours and only few of them develop in the framework of hereditary syndromes. The present review is focused on the variants of hereditary syndromes with special reference to various pituitary neoplasms. The molecular and genetic studies revealed several genetic defects that are believed to contribute to the formation of pituitary adenomas. Moreover, a few genes were identified responsible for the development of hereditary forms of pituitary tumours. Identification of such genes and pathogenetic mechanisms underlying the development of pituitary microadenomas is of paramount importance for the improvement of their diagnostics and treatment that in its turn may promote the understanding of pathogenesis of sporadic adenomas and improve their prognosis.