Laser Disrupts AKT Hydrogen Network in Cancer.

The cancer metastatic process is supported by the strong AKT hydrogen bond network. This network is formed by positive feedback loops generated in the cancer hypoxic microenvironment through the genomic AKT signaling locus. Laser paired photons disrupt the hydrogen network of the AKT active site by laser catalyzed fusion inducing the disappearance of the malignant phenotype.

Lysosome AKT Targeting in Metastatic Cancer.

Metastatic cancer is caused by hyperactivated lysosomes. Such activation causes a fungus, Aspergillus fumigatus, to permanently activate the AKT gene network that controls the lysosome through positive feedback loops. Targeting such a network by the redox balance change, and with an antifungal medication eliminates the metastatic phenotype, the complexity and robustness of the cancer.

Lysosome activates AKT inducing cancer and metastasis.

Hyperactivated lysosome causes cancer and induces metastasis or cancer relapse. Such activation occurs during excessive, intense, and protracted oxidative burst in the lysosome. The burst induces the formation of the constitutively active (permanently active) AKT locus generating cancer complexity and robustness.

Muon disrupts AKT hydrogen bond network in cancer.

A cancer microenvironment generates strong hydrogen bond network system by the positive feedback loops supporting cancer complexity and robustness. Such network functions through the AKT locus generating high entropic energy supporting cancer metastatic robustness. Charged lepton particle muon follows the rule of Bragg effect during a collision with hydrogen network in cancer cells.

AKT as Locus of Hydrogen Bond Network in Cancer.

Generation and maintenance of a cancer complexity and robustness are impossible without hydrogen element. It is essential element for the cancer signaling through the AKT locus. Hyperactivated AKT locus by a positive feedback loops from the cancer hypoxic microenvironment generates a hydrogen bond network.

AKT as Locus of Cancer Unknown Primary Site.

Cancer of unknown primary site is a metastasis developed by the positive feedback loops of primary cancer forming extreme cancer robustness. Such robustness occurs only in metastatic cancer or in relapsed lymphoma, myeloma, plasmocytoma, or leukemia. However, when it develops in primary cancer, hypoxic microenvironment generates positive feedback loops which hyperactivate AKT locus, forming extreme robustness that forcing cancer cells to migrate to the distant site, but primary cancer loosing that property or remains silent.

AKT as Locus of Cancer Positive Loops Conversion and Chemotherapy.

A cancer positive-feedback loops conversion is the phenomenon and principal mechanism for AKT locus chemotherapy. Such chemotherapy is the approach to target cancer robustness and complexity through the AKT signaling locus. The hypoxic cancer microenvironment generates a powerful signaling interactome with positive-feedback loops that generates cancer robustness through the AKT locus.

Switching to BCL-6 Negativity in Relapsed Diffuse Large B Cell Lymphoma Correlated with More Aggressive Disease Course.

Diffuse large B-cell lymphoma (DLBCL) is the most frequent, complex and heterogeneous lymphoma of adulthood. Heterogeneity is expressed at clinical, genetic, and molecular levels. It is known that BCL-6 expression is a favorable prognostic factor in DLBCL.

AKT as locus of cancer phenotype.

Cancer robustness is generated by the positive feedback loops. The positive loops hyperactivate AKT locus forming a cancer phenotype in leukemia, lymphoma, myeloma, plasmocytoma, sarcoma and carcinoma. The positive loops inducing AKT hyperphosphorylation increase activity of the AKT locus and the nodal associated and interconnected signaling genes.

Right thyroid hemiagenesis with adenoma and hyperplasia of parathyroid glands -case report.

Background: Thyroid hemiagenesis is a rare anomaly, more commonly seen on the left side (ratio 4:1) and in females (ratio 3:1). The first to describe this anomaly was Handfield Jones in 1852.

Case Presentation: We present a 66 year old female patient with right thyroid hemiagenesis, parathyroid adenoma on the side of hemiagenesis and parathyroid hyperplasia on the contralateral side.

Regional distribution and molecular interaction of caveolins in bladder smooth muscle.

Unlabelled: What's known on the subject? and What does the study add? Caveolae are specialised regions of bladder smooth muscle (BSM) cell membranes where specific signalling pathways are regulated. Caveolin proteins are involved in caveolar biogenesis and function as signal transduction regulators. Expression of caveolin-1, -2, and -3 has been previously identified in the bladder; however, the distribution and relative expression of these proteins have not been defined.

AKT as locus of cancer multidrug resistance and fragility.

Complexity and robustness of cancer hypoxic microenvironment are supported by the robust signaling networks of autocrine and paracrine elements creating powerful interactome for multidrug resistance. These elements generate a positive feedback loops responsible for the extreme robustness and multidrug resistance in solid cancer, leukemia, myeloma, and lymphoma. Phosphorylated AKT is a cancer multidrug resistance locus.

AKT as locus of cancer positive feedback loops and extreme robustness.

A positive feedback loops induce extreme robustness in metastatic cancer, relapsed leukemia, myeloma or lymphoma. The loops are generated by the signaling interactome networks of autocrine and paracrine elements from cancer hypoxic microenvironment. The elements of the networks are signaling proteins synthesized in hypoxic microenvironment such as the vascular endothelial growth factor, HIF-1α, hepatocyte growth factor, and molecules nitric oxide and H(2)O(2).

AKT as locus of cancer angiogenic robustness and fragility.

Angiogenesis get full robustness in metastatic cancer, relapsed leukemia or lymphoma when complex positive feedback loop signaling systems become integrative. A cancer hypoxic microenvironment generates positive loops inducing formation of the vascular functional shunts. AKT is an upstream angiogenic locus of integrative robustness and fragility activated by the positive loops.

Increased angiogenesis-associated poor outcome in acute lymphoblastic leukemia: a single center study.

Angiogenesis in solid tumors is important for tumor growth, invasion, and metastasis. However, angiogenesis plays also an important role in hematological malignancies. We have analyzed the expression of vascular endothelial growth factor (VEGF) in the leukemic blast cells and microvessel density (MVD) in the bone marrow biopsy samples of the patients with acute lymphoblastic leukemia (ALL).

Loss of bladder smooth muscle caveolae in the aging bladder.

Aims: Caveolae are specialized regions of the cell membrane that modulate signal transduction and alterations in these structures affect bladder smooth muscle (BSM) contraction. Since bladder dysfunctions are common in the elderly, we evaluated the effect of aging on the morphology of caveolae and caveolin protein expression in BSM.

Methods: Caveolar morphology (number, size, and depth) in BSM was determined from electron microscopy images of young (10 weeks), adult (6-month old), and old (12-month old) rat urinary bladders.

Outcome prediction of advanced mantle cell lymphoma by international prognostic index versus different mantle cell lymphoma indexes: one institution study.

The aim of this study was to evaluate the prognostic significance of international prognostic index (IPI), mantle cell lymphoma IPI (MIPI), simplified MIPI (sMIPI), and MIPI biological (MIPIb), as well as their correlation with immunophenotype, clinical characteristics, and overall survival (OS), in a selected group of 54 patients with advanced-stage mantle cell lymphoma (MCL), treated uniformly with CHOP. Seventeen patients had IV clinical stage (CS), while other 37 had leukemic phase at presentation. Diffuse type of marrow infiltration was verified in 68.

Molecular reactions and ultrastructural damage in the chronically ischemic bladder.

Purpose: Clinical and basic research data suggest that pelvic ischemia may contribute to bladder overactivity. We characterized the molecular and ultrastructural reactions of the chronically ischemic bladder.

Materials And Method: A model of pelvic ischemia was developed by creating iliohypogastric/pudendal arterial atherosclerosis in rabbits.

Oxidative modification of mitochondrial integrity and nerve fiber density in the ischemic overactive bladder.

Purpose: To our knowledge the mechanism of neurodegeneration in the overactive bladder remains unknown. We examined mitochondrial integrity and searched for markers of oxidative neural injury in the ischemic overactive bladder.

Materials And Methods: A rabbit model of overactive bladder was developed by inducing moderate pelvic ischemia.

Oxidative stress and neurodegeneration in penile ischaemia.

Objective: To seek markers of oxidative stress and examine neural structural integrity in chronic penile ischaemia using a rabbit model of arteriogenic erectile dysfunction (ED), as the role of ischaemia in penile neuropathy and the oxidative mechanism of neurodegeneration in ED remains unknown.

Materials And Methods: A rabbit model of atherosclerosis-induced ED was developed by partial balloon de-endothelialization of the iliac arteries. After 10 weeks, intracavernosal blood flow and erectile function in the arteriogenic ED group were compared with age-matched controls.

AKT as locus of fragility in robust cancer system.

Metastatic cancer is a complex positive feedback loop system. Such as system has a tendency to acquire extreme robustness. Signaling pathways controlling that robustness can fail completely if an essential element from the signaling is removed.

Effects of ischemia on tachykinin-containing nerves and neurokinin receptors in the rabbit bladder.

Objectives: Our previous studies showed marked changes in efferent nerve structure and reactivity in the ischemic bladder. The goal of this study was to examine the effects of bladder ischemia on tachykinin (TK) containing sensory nerves and neurokinin receptors (NKR) in a rabbit model.

Methods: We recorded bladder blood flow and spontaneous contractions in treated animals at week 8 after the induction of iliac arteries atherosclerosis and in age-matched controls.

Locus of fragility in robust breast cancer system.

Functional heterogeneous redundancy of breast cancer makes this tumor to be robust. Signaling mechanisms which control cancer responses are crucial for controlling robustness. Identification of locus of fragility in cancer represents basic mechanism to target robustness.

Inactivated tumor suppressor Rb by nitric oxide promotes mitosis in human breast cancer cells.

Inactivation of tumor suppressor protein retinoblastoma (Rb) is important mechanism for the G1/S transition during cell cycle progression. Human breast cancer cells T47D release great amount of nitric oxide (NO), but its relation to tumor suppressor Rb is unknown. In this study, it is shown that NO induces phosphorylation and inactivation of Rb tumor suppressor protein, increasing G2/M phase and cell proliferation of breast cancer cells T47D.

TOR kinase and Ran are downstream from PI3K/Akt in H2O2-induced mitosis.

Hydrogen peroxide (H2O2) activates signaling cascades essential for cell proliferation via phosphatidylinositol-3-kinase (PI3K) and Akt. Here we show that induction of mitogenic signaling by H2O2 activates sequentially PI3K, Akt, mammalian target of rapamycin (mTOR), and Ran protein. Akt activation is followed by signaling through the mTOR kinase and upregulation of Ran in primary type II pneumocytes, a cell type implicated in the development of lung adenocarcinoma.