Abdomen agudo por torsión de epiplón mayor simulando una apendicitis aguda / Acute abdomen due to torsion of greather omentun simulating acute appendicitis

La torsión del epiplón mayor es una patología poco frecuente con una clínica inespecífica, por lo que históricamente su diagnóstico es realizado en el quirófano ya que simula patologías como la apendicitis o colecistitis. Los métodos auxiliares de diagnóstico como las ecografías o las tomografías son de mucha utilidad para la sospecha de esta patología, aunque no cuenta con signos patognomónicos de la enfermedad, las imágenes asociadas a la clínica del paciente pueden llevar a un diagnóstico preciso. Presentamos el caso de un paciente joven de sexo masculino, que acudió al servicio de urgencias por cuadro de dolor abdominal tipo cólico de moderada intensidad en fosa iliaca derecha, acompañado de sensación febril, sin alteración de la analítica sanguínea, sin hallazgo de valor en la ecografía abdominal, que ante la persistencia del dolor y la fiebre se realizó una tomografía contrastada en la que se observó un empastamiento del epiplón sometiéndose a una laparoscopía exploradora con el hallazgo de una torsión del epiplón mayor.

Torsion of the greater omentum is a rare pathology with non-specific symptoms, so historically its diagnosis is made in the operating room since it simulates pathologies such as appendicitis or cholecystitis. Auxiliary diagnostic methods such as ultrasound or tomography are of very useful for the suspicion of this pathology, although it does not have pathognomonic signs of the disease, the images associated with the patient's symptoms can lead to a precise diagnosis. We present the case of a young male patient who came to the emergency department due to moderately intense colic-like abdominal pain in the right iliac fossa, accompanied by a feverish sensation, without alterations in blood tests, without any finding of value in the abdominal ultrasound, due to the persistence of pain and fever, a contrast-enhanced tomography was performed in which a filling of the omentum was observed, undergoing an exploratory laparoscopy with the discovery of a torsion of the greater omentum.

Sarcoma de Células Claras en pierna de mujer de 28 años / Clear cell sarcoma on 28 years old woman leg

Los tumores de partes blandas son tumores que se presentan en adultos, aproximadamente a los 60 años. De estos tumores los sarcomas son poco frecuentes y tienen preferencia en las extremidades y muchas veces invaden estructuras músculo aponeuróticas cercanas, y poca invasión vascular o nerviosa lo que las hace de fácil acceso con poca morbilidad para su biopsia. El diagnóstico de los tumores de partes blandas se basa en el estudio histológico de anatomía patológica y, a veces se debe asociar a estudios de citogenética para poder tener un diagnóstico específico. El tratamiento principal es quirúrgico y puede llegar estar asociado a terapia adyuvante.

Soft tissue tumors are tumors that occur in adult's age, at about 60 age. Of these tumors, sarcomas are rare and have preference in the extremities, and often invade nearby muscle-fascia structures, and little vascular or nerve invasion, making them easily accessible with little morbidity for biopsy. The diagnosis of soft tissue tumors is based on the histological study of pathological anatomy and, sometimes, it must be associated with cytogenetic studies in order to have specific diagnosis. The main treatment is surgical and may end up being associated with adjuvant therapy.

Experiencia inicial en el tratamiento laparoscópico de la hernia inguinal en la ii cátedra de clínica quirúrgica, hospital de clínicas. FCM-UMA / Initial experience in laparoscopic inguinal hernioplasty in ii service of surgery, hospital de clinicas. FCM-UMA

Introducción: Las hernias inguinales representan el 75 % de todas las hernias de la pared abdominal, y con un riesgo de por vida de 27 % en hombres y 3 % en las mujeres. La reparación de estas hernias es uno de los procedimientos quirúrgicos más utilizados en el mundo. En la década de los 90, la progresiva evolución de la cirugía hacia técnicas mínimamente invasivas culmina con la aparición de la cirugía laparoscópica. Objetivo: describir nuestra experiencia en el tratamiento de las hernias inguinales por videolaparoscopia. Pacientes y métodos: Estudio observacional, descriptivo, retrospectivo, de corte transversal. Se presentan 25 casos de pacientes sometidos a el tratamiento de la hernia inguinal por el abordaje video laparoscópico (TEP-TAPP), en el periodo 2010-2015 Resultados: En este estudio tuvimos en el 100% de los casos pacientes de sexo masculino. El tiempo de evolución de la enfermedad en promedio fueron de 20 meses. Los diagnósticos pre operatorios fueron hernia inguinal izquierda no complicada en 8 pacientes, hernia inguinal derecha no complicada en 12 pacientes y hernia inguinal bilateral no complicada en 5 pacientes. Las técnicas empleadas fueron TEP (Totalmente extra peritoneal) en 5 pacientes y TAPP (Trans-Abdominal Pre-Peritoneal) en 20 pacientes. En todos los casos, el medio de fijación fue con tacker helicoidal de titanio. En promedio la estancia hospitalaria fue de 1,8 días. El tiempo quirúrgico, en promedio fue de 83 minutos. En cuanto a las complicaciones, hemos tenido 3 pacientes con complicaciones post quirúrgicas seroma, inguinodinia e infección del sitio quirúrgico. Conclusión: Actualmente, el tratamiento quirúrgico de la hernia inguinal tiene muy buenos resultados por vía laparoscopia, comparadas con las técnicas abiertas, faltando aun seguimiento de los pacientes en el tiempo para tener resultados concluyentes acerca de la eficacia de la técnica.

Introduction: Inguinal hernia are the 75% of the abdominal wall hernia, with a risk during all life of 27% in male gender and 3% in female. The treatment of this disease is one of the most common procedures in the world. At 90´s, the evolution of the minimal invasive approach ends with the laparoscopic surgery appearance. Objective: to describe our initial experience in the laparoscopic approach of inguinal hernia. Patients and method: An observational, retrospective study of 25 patients who underwent TAPP or TEP approach for hernia disease. Results: All of 25 patients were male gender. The average of disease evolution until surgery was 20 moths.Pre-ops diagnosis were: left inguinal hernia in 8 cases, right inguinal hernia in 12 cases and bilateral hernia in 5 cases. We performed TEP approach in 5 patients and 20 TAPP approach in 20 patients. The fixation was with titanium tackers in all cases. Average of discharge from hospital was 1,8 days. The surgical time average was 83 minutes. 3 patients had some morbidity, included: seroma, inguinodynia and surgical site infection Conclusion: Actually, the laparoscopic approach for the inguinal hernia treatment have very good results comparing to open approach, but we need more patients follow up to establish the efficacy of the technique.

Manejo percutáneo de colecciones abdominales en el hospital distrital de Villa Elisa / Percutaneous treatment of abdominal collections in the district hospital of Villa Elisa

Los abscesos abdominales se definen como colecciones localizadas que presentan pus, gérmenes en el frotis o crecen en el cultivo. Estas adquieren importancia cuando se hacen sintomáticas. En el manejo actual, el drenaje percutáneo es el tratamiento de elección por múltiples ventajas, reservándose el drenaje quirúrgico para ciertos casos. Esto se debe al avance de la tecnología de los métodos auxiliares de diagnóstico por imágenes, especialmente la ecografía.Objetivo: demostrar la factibilidad del manejo percutáneo de colecciones intra-abdominales en un hospital periférico de baja complejidad y con disponibilidad de ecógrafo.Diseño: retrospectivo, longitudinal, observacional, cuantitativo, no aleatorio, con componente analítico.Pacientes y método: pacientes con diagnóstico de colección intra-abdominal de distintas etiologías, internados en el Servicio de Cirugía del Hospital Distrital de Villa Elisa, desde junio de 2014, hasta setiembre de 2015.Resultados: 5 pacientes estudiados, 60% del sexo femenino, el cuadro de presentación fue conformado por dolor abdominal, distensión, plastrón palpable y fiebre. Laboratorialmente, leucocitosis con neutrofilia. En todos se realizó el drenaje de la colección bajo pantalla ecográfica con catéteres multipropósito de 10Fr, con la técnica del trocar. Se obtuvo el éxito en el tratamiento en el 80% de los casos. Conclusión: el manejo de colecciones abdominales es factible en hospitales periféricos de baja complejidad.

Abdominal abscess are defined as localized collections of pus, germs visualizated in a frotis or grow in culture. These become important when they become symptomatic. Actually, percutaneous drainage is the gold standard, reserving the surgery approach for a few special cases. This is due to the advanced of technology, particularly the ultrasound. Objective: to demonstrate the feasibility of percutaneous management of intraabdominal collections in a peripheral low complexity hospital, with ultrasound availability. Design: retrospective, longitudinal, observational, quantitative, no randomized, with analytical component. Patients and methods: patients with diagnosis of intraabdominal collections, admitted in surgery service of the Hospital Distrital of Villa Elisa, from June of 2014 to September of 2015. Results: 5 patients studied, 60% female, with clinical of abdominal pain, distension, palpation of abdominal mass or fever. Laboratorial findings neutrophilic leukocytosis. In all cases, percutaneous drainage was made it under ultrasound view, using 10 Fr multipurpose catheter, using trocar technique. Success was possible in 80% of the cases. Conclusion: the management of abdominal collections is possible in peripheral low complexity hospitals.

Cirujanos generales y vólvulo de ciego / General surgeons and cecal volvulus

Introducción: Se define el vólvulo de ciego como la torsión del segmento cecal sobre su propio eje o sobre el mesentérico. Es una causa poco frecuente de obstrucción intestinal. Material y método: Estudio retrospectivo, observacional, descriptivo de los expedientes clínicos del archivo de la II CCQ, de enero de 2009 hasta mayo de 2014. Resultados: Encontramos 6 pacientes, 3 masculinos y 3 femeninos. La sintomatología fue de obstrucción intestinal. Constatamos la gangrena colónica en el 66% de los pacientes. Realizamos resección en el 83% de los casos. Un caso fue tratado con éxito con una cecostomía. La mortalidad fue del 33%. Conclusiones: No debemos olvidar el vólvulo de ciego como causa de oclusión intestinal. La conducta terapéutica más realizada fue la resección del segmento colónico con gangrena, con confección de la colostomía necesaria.

Background: Cecal volvulus is defined as cecal segment torsion on its axis or the mesentery. Is an unusual cause of intestinal obstruction. Material and method: A retrospective, observational, descriptive of the clinical records of the II Service of Surgery, between January 2009 to May 2014. Results: We found 6 patients, 3 of male gender and 3 women. Symptomatology was intestinal obstruction. We find colonic gangrene in 66% of patients. We made a resection in 83% of the cases. One case was successfully treated with a cecostomy. Mortality was 33% Conclusions: We must not forget the cecal volvulus as a cause of intestinal obstruction. The most performed therapeutic behavior was colonic segment resection with gangrene, with the making of required colostomy.

Tubacin suppresses proliferation and induces apoptosis of acute lymphoblastic leukemia cells.

Over the past decade, histone deacetylase inhibitors have increasingly been used to treat various malignancies. Tubacin (tubulin acetylation inducer) is a small molecule that inhibits histone deacetylase 6 (HDAC6) and induces acetylation of α-tubulin. We observed a higher antiproliferative effect of tubacin in acute lymphoblastic leukemia (ALL) cells than in normal hematopoietic cells. Treatment with tubacin led to the induction of apoptotic pathways in both pre-B and T cell ALL cells at a 50% inhibitory concentration (IC(50)) of low micromolar concentrations. Acetylation of α-tubulin increases within the first 30 min following treatment of ALL cells with tubacin. We also observed an accumulation of polyubiquitinated proteins and poly(ADP-ribose) polymerase (PARP) cleavage. Furthermore, the signaling pathways activated by tubacin appear to be distinct from those observed in multiple myeloma. In this article, we demonstrate that tubacin enhances the effects of chemotherapy to treat primary ALL cells in vitro and in vivo. These results suggest that targeting HDAC6 alone or in combination with chemotherapy could provide a novel approach to treat ALL.

Choline kinase alpha depletion selectively kills tumoral cells.

Choline Kinase (ChoK) comprises a family of cytosolic enzymes involved in the synthesis of phosphatidylcholine (PC), the most abundant phospholipid in eukaryotic cell membranes. One of the ChoK isoforms, Choline Kinase alpha (ChoKalpha), is found over expressed in human tumours. Chemical inhibitors able to interfere with ChoK activity have proven to be effective antitumoral drugs in vitro and in vivo. To validate the use of selective ChoKalpha inhibitors in cancer therapy, we have developed a genetic strategy to interfere specifically with ChoKalpha activity based on the generation of a shRNA against the alpha isoform of ChoK. Here we demonstrate that specific inhibition of ChoKalpha by shRNA has antitumor activity. The specific depletion of ChoKalpha induces apoptosis in several tumor-derived cell lines from breast, bladder, lung and cervix carcinoma tumors, while the viability of normal primary cells is not affected. Furthermore, this selective antiproliferative effect is achieved both under in vitro and in vivo conditions, as demonstrated by an inducible ChoKalpha suppression system in human tumour xenografts. These results demonstrate that ChoKalpha inhibition is a useful antitumoral strategy per se, and provides definitive and non-ambiguous evidence that ChoKalpha can be used as an efficient and selective drug target for cancer therapy.

The aggresome pathway as a target for therapy in hematologic malignancies.

Misfolded or unfolded proteins are often refolded with the help of chaperones or degraded by the 26S proteasome. An alternative fate of these proteins is the aggresome pathway. The microtubule-organizing center (MTOC) transports unfolded proteins to lysosomes and are degraded through autophagy. Histone deacetylase 6 (HDAC6) deacetylates alpha-tubulin, which is thought to be a component of the MTOC. Recently, two small molecule inhibitors of the aggresome pathway and HDAC6 have been described. One inhibitor, tubacin, prevents deacetylation of alpha-tubulin and produces accumulation of polyubiquitinated proteins and apoptosis. Tubacin acts synergistically with the proteasome inhibitor, bortezomib, to induce cytotoxicity in one type of hematologic malignancy, multiple myeloma. The other, LBH589, is a pan HDAC inhibitor and hydroxamic acid derivative that induces apoptosis of multiple myeloma cells resistant to conventional therapies. In this review, we summarize recent reports on targeting the aggresome pathway and HDAC6 in hematologic malignancies.

Role of the aggresome pathway in cancer: targeting histone deacetylase 6-dependent protein degradation.

Misfolded or aggregated proteins have two fates: they are either refolded with the help of chaperones or degraded by the proteasome. Cells also have an alternative pathway that involves intracellular "storage bins" for misfolded intracellular proteins known as aggresomes. Aggresomes recruit motor proteins that transport misfolded or aggregated proteins to chaperones and proteasomes for subsequent destruction. There is emerging evidence that inhibiting the aggresome pathway leads to accumulation of misfolded proteins and apoptosis in tumor cells through autophagy. We discuss the role of aggresomes in cancer and the potential to target this pathway for therapy.

Symmetrical bis-quinolinium compounds: new human choline kinase inhibitors with antiproliferative activity against the HT-29 cell line.

Studies have been aimed at the establishment of structure-activity relationships that define choline kinase inhibitory and antiproliferative activities of 40 bisquinolinium compounds. These derivatives have electron-releasing groups at position 4 of the quinolinium ring. It is found that the enzymatic inhibition is closely related to the size of the linker, the 3,3'-biphenyl moiety being the most suitable. On the other hand, the antiproliferative activity against the HT-29 cancer cell line is less influenced by the linker type and by substituent R(4). The corresponding QSAR equation was obtained for the whole set of compounds for the antiproliferative activity, the electronic parameter sigma(R) of R(4), the molar refractivity of R(8), and the lipophilic parameters clog P and pi(linker). The most potent antiproliferative agent so far described is 40 for which an IC(50) = 0.45 microM was predicted by the QSAR equation, while its experimental value is IC(50) = 0.20 microM.

Inhibition of choline kinase renders a highly selective cytotoxic effect in tumour cells through a mitochondrial independent mechanism.

Tumour cells are frequently altered in their phospholipid metabolism. Choline kinase (ChoK, E.C. 2.7.1.32) activity, the first enzyme involved in the synthesis of phosphatidylcholine, is increased in a large number of human tumours and tumour-derived cell lines. We have previously reported that MN58b, a specific inhibitor of ChoK, has anti-tumoral activity. Here we show the high specificity of MN58b as a cytotoxic drug towards tumour cells, and explore further the basis of its mechanism of action in order to provide a rational understanding for its antitumoral activity. A dramatic difference in the response to the treatment of primary, normal and non-tumorigenic human cells when compared to tumour-derived cell lines was observed. In normal cells, blockage of de novo PCho synthesis by MN58b results in a reversible cell cycle arrest at G0/G1 phase. In contrast, ChoK inhibition in tumour cells promotes the induction of apoptosis. This effect depends on the cell cycle phase, being G1 the critical phase. Regarding the mechanism of apoptosis engagement, a loss of mitochondrial potential was observed 10-20 min after cytochrome c release, but caspase 3 activation preceded the loss of mitochondrial potential, indicating that activation of caspase 3 is independent of cytochrome c release. Our results are consistent with a non-intrinsic process as the mechanism underlying the induction of apoptosis by ChoK inhibition in tumoral cells.

Influence of the linker in bispyridium compounds on the inhibition of human choline kinase.

Studies have been aimed to establish the structure-activity relationship that define choline kinase (ChoK) inhibitory potency and antiproliferative activity of a set of 25 bispyridinium compounds with electron-releasing groups at position 4. Here we report that, according to their inhibitory activities against human ChoK, the enzymatic inhibitory potency is closely related to the size of the linker, the 3,3'-biphenyl moiety being the most suitable. The N-methylanilino and its derivatives, 4-chloro-N-methylanilino and 3,5-dichloro-N-methylanilino, render higher ChoK inhibitory and antiproliferative activities against the HT-29 human colon cancer cell line.

Choline kinase inhibition induces the increase in ceramides resulting in a highly specific and selective cytotoxic antitumoral strategy as a potential mechanism of action.

Choline kinase (ChoK, E.C. 2.7.1.32) is involved in the synthesis of phosphatidylcholine (PC), and has been found to be increased in human tumors and tumor-derived cell lines. Furthermore, ChoK inhibitors have been reported to show a potent and selective antitumoral activity both in vitro and in vivo. Here, we provide the basis for a rational understanding of the antitumoral activity of ChoK inhibitors. In normal cells, blockage of de novo phosphorylcholine (PCho) synthesis by inhibition of ChoK promotes the dephosphorylation of pRb, resulting in a reversible cell cycle arrest at G0/G1 phase. In contrast, ChoK inhibition in tumor cells renders cells unable to arrest in G0/G1 as manifested by a lack of pRb dephosphorylation. Furthermore, tumor cells specifically suffer a drastic wobble in the metabolism of main membrane lipids PC and sphingomyelin (SM). This lipid disruption results in the enlargement of the intracellular levels of ceramides. As a consequence, normal cells remain unaffected, but tumor cells are promoted to apoptosis. Thus, we provide in this study the rationale for the potential clinical use of ChoK inhibitors.

Choline kinase activation is a critical requirement for the proliferation of primary human mammary epithelial cells and breast tumor progression.

Breast cancer is still one of the most important tumors among women in industrialized countries. Improvement in both understanding the molecular events associated with the disease and the development of new additional treatments is still an important goal to be achieved. Choline kinase (ChoK) is increased in human mammary tumors with high incidence, and this activation is associated with clinical variable indicators of greater malignancy. Here, we have investigated the role of ChoK in the development of breast cancer and found that ChoK is both necessary and sufficient for growth factor-induced proliferation in primary human mammary epithelial cells and an absolute requirement for the specific mitogenic response to heregulin in breast tumor-derived cells. These results demonstrate that ChoK plays an essential role in both normal human mammary epithelial cell proliferation and breast tumor progression. Furthermore, inhibition of ChoK shows a strong in vivo antitumor activity against human breast cancer xenografts. Thus, ChoK constitutes a novel bona fide molecular target for the treatment of breast cancer patients.

A novel 4,4'-bispyridyl-5,5'-perfluoroalkyl-2,2'-bisoxazol with antitumoral activity via cell cycle arrest and induction of apoptosis.

The compound 6a is a novel bisoxazol derivative with high cytotoxic properties in vitro against different human tumor-derived cell lines and with similar efficiency against epithelial, haematopoietic and mesenchymal tumor cells. Although the molecular mechanism is not yet fully defined, cell cycle analysis revealed that 6a induces efficiently G0/G1 phase arrest in colon adenocarcinoma HT-29 cells in a dose- and time-dependent manner. Induction of cell death is observed, a possible explanation for the antiproliferative profile of the molecule. The compound was well tolerated at doses that allowed to examine its antitumor activity against human xenografts of the HT-29 cell line implanted s.c. in nude mice. Treatment of mice with 4 mg/kg of the compound resulted in a 60% inhibition of tumor growth. These observations support the use of 6a for the generation of more potent derivatives that could be used as new anticancer agents.

From Ras signalling to ChoK inhibitors: a further advance in anticancer drug design.

Cancer is a genetic disease, most prominent in developed countries, with still a high mortality rate. Cancer cells are continuously proliferating, and this uncontrolled growth is mediated by the activation of different signal transduction pathways that ultimately lead to the carcinogenic process. Consequently, a large effort has been devoted to design specific molecules that interfere with these signaling cascades involved in tumorigenesis. In the last decades, research has resulted in improvements in both detection and treatment of cancer. However, it is still necessary to develop novel antitumoral therapies that would allow an appropriate treatment for each cancer patient. These novel, tumor- and patient-specific therapies will have a dramatic impact in improving the overall survival rates. Ras is one of the most important oncogenes so far identified in human carcinogenesis. Understanding the regulation of Ras-dependent signalling under normal and oncogenic environments may provide clues for the design of efficient specific antitumor strategies. In this review we will illustrate how the family of Ras GTPases may be a valid model for the development of new cancer therapies.

Inhibition of choline kinase as a specific cytotoxic strategy in oncogene-transformed cells.

Cancer treatment is in the need of selective drugs that can interfere specifically with signalling pathways affected during the carcinogenic process. Identification of new potential molecular targets is the key event in the design of new anticancer strategies. Once identified, attempts for the generation of specific molecules to regulate their function can be achieved. The relevance of deregulation of choline kinase (ChoK, E.C. 2.7.1.32) in oncogene-driven cell transformation has been previously demonstrated. Here we provide strong evidence that MN58b, a selective inhibitor of ChoK, is rather specific to this enzyme, with no effect on a variety of oncogene-activated signalling pathways involved in the regulation of cell proliferation. MN58b does not affect MAPKs, PI3K, and other enzymes involved in the regulation of phospholipid metabolism such as phospholipases C, D, and A2, CTP:phosphocholine cytidylyltransferase, or diacylglycerol choline-phosphotransferase. Consistent with this specificity, ectopic expression of ChoK resulted in resistance to its inhibitor. Finally, nontransformed cells were able to resume cell proliferation after removal of the drug, while transformed cells were irreversibly affected. These results indicate that inhibition of ChoK is a rather specific strategy for the cytotoxic treatment of transformed cells.

Phospholipase D and choline kinase: their role in cancer development and their potential as drug targets.

Malignant cells result from the accumulation of genetic alterations that impinge into the components of signal transduction pathways controlling cell growth, differentiation and apoptosis. One of the critical pathways is related to the regulation of the phospholipid homeostasis. The identification of the molecular components involved in normal cell growth regulation altered upon transformation is required for the development of chemotherapeutic interventions against transformed cells. Discovery of new chemotherapeutic agents is one of the most promising ways to improve our success against cancer, and rational drug design is a key factor to achieve this goal. Evidence supporting choline kinase and phospholipase D as such novel targets is provided.

Choline kinase inhibitory effect and antiproliferative activity of new 1,1',1"-(benzene-1,3,5-triylmethylene)tris[4-[(disubstituted)amino]pyridinium] tribromides.

Four derivatives of 1,1'-(benzene-1,3-diylmethylene)bis[4-[(disubstituted)amino]-pyridinium] dibromides (2-5) and six derivatives of 1,1',1"-(benzene-1,3,5-triylmethylene)-tris[4-[(disubstituted)amino]pyridinium] tribromides (6-11) were synthesised and examined for their inhibition of human choline kinase (ChoK) and antiproliferative activities. The latter are more potent as ChoK inhibitors than the former, but the antiproliferative activities against the HT-29 cell line show the opposite tendency. The higher affinity of the trispyridinium compared with the bispyridinium ones may be due to direct binding of the third pyridinium group to ChoK or may arise from a reduction of the unfavourable entropy of binding via an increase of the 'local concentration' of pyridinium groups.

Overexpression of choline kinase is a frequent feature in human tumor-derived cell lines and in lung, prostate, and colorectal human cancers.

Carcinogenesis is a long process that results in the accumulation of genetic alterations primarily in genes involved in the regulation of signalling pathways relevant for the regulation of cell growth and the cell cycle. Alteration of additional genes regulating cell adhesion and migration, angiogenesis, apoptosis, and drug resistance confers to the cancer cells a more malignant phenotype. Genes that participate in the regulation of some critical metabolic pathways are also altered during this process. Choline kinase (ChoK) has been reported to belong to the latter family of cancer-related genes. Recently, we have reported that increased activity of ChoK is observed in human breast carcinomas. Here, we provide further evidence that ChoK dysregulation is a frequent event found in a variety of human tumors such as lung, colorectal, and prostate tumors. Furthermore, a large panel of human tumor-derived cell lines also show increased ChoK activity when compared to appropriate non-tumorigenic or primary cells. These findings strongly support the role of ChoK alterations in the carcinogenic process in human tumors, suggesting that ChoK could be used as a tumor marker.