Hematopoyesis Clonal de Potencial Indeterminado (HCPI): más allá de un modelo de campo de cancerización / Clonal hematopoiesis of indeterminate potential (CHIP): Beyond a model of field cancerization

Resumen La Hematopoyesis Clonal de Potencial Indeterminado (HCPI), más conocida como CHIP por sus siglas en inglés, se define como la expansión clonal de Células Madre Hematopoyéticas (CMHs) que albergan una o más mutaciones somáticas (en la mayoría de los casos una sola mutación) sin un cáncer hematológico subyacente ni evidencia morfológica definitiva de displasia, con una frecuencia alélica mayor al 2%. Los individuos con HCPI progresan a malignidad a una tasa de cerca del 0.5% a 1% por año, convirtiéndose así en un modelo de campo de cancerización. Sin embargo, sus implicaciones van más allá debido a que se ha encontrado asociación con enfermedades inflamatorias crónicas, como enfermedad cardiovascular ateroesclerótica, diabetes y enfermedades autoinmunes. Además, es considerado un factor predictivo en pacientes con cáncer hematolológico y no hematológico que reciben quimioterapia y radioterapia.

Abstract Clonal hematopoiesis of indeterminate potential (CHIP) is the expansion of hematopoietic stem cells harboring one or more somatic mutations. These patients do not have underlying hematologic neoplasia, myelodysplasia, or dysplasia, but can progress to a malignant state at a rate of 0.5 to 1% per year. CHIP could be used as a model of field cancerization, since it has been associated with chronic inflammatory diseases, arteriosclerosis, diabetes, and autoimmune conditions. CHIP is also considered a predictive factor in hematological and non-hematological cancer patients receiving chemotherapy and radiotherapy.

Expression of CHMP4A and TSPYL-2 in early esophageal cancer and their significance / 临床与实验病理学杂志

Purpose To investigate the role of CHMP4A and TSPYL-2 in early pathogenesis of esophageal cancer.Methods Through comparison of the four subtractive libraries,early esophageal squamous cell carcinoma genes CHMP4A and TSPYL-2 were chosen for further study.Through RT-PCR and immunohistochemistry methods,CHMP4A and TSPYL-2's expression was detected in esophageal squamous cell carcinoma tissue,cancerous tissue and normal esophageal mucosa.Results CHMP4A and TSPYL-2 expression between esophageal squamous cell carcinoma and normal esophageal epithelium tissue had significant differences (P ＜ 0.05),and the CHMP4A gene expression in esophageal mucosa,field cancerization areas,esophageal squamous cell carcinoma tissue increased,while TSPYL-2 gene expression in esophageal mucosa,field cancerization areas,esophageal squamous cell carcinoma tissue decreased,which were consistent with the protein expression of CHMP4A and TSPYL-2.Conclusion CHMP4A and TSPYL-2 genes are differentially expressed in esophageal squamous cell carcinoma,which can be used as alternative genetic markers for further research.

Epithelial tumor development and exploration on the relationship between matrix / 实用肿瘤学杂志

We have confirmed that many of the intraepithelial neoplasia confined to in situ may never be found in some patients ,such as breast ,prostate and lung lesions ,but few of these lesions progress to malignancy are unexplained .Studies demonstrate that many invasive neoplasia and its precancerous lesions with similar genes changes,which provide the necessary premise for the late tumor metastatic ,just like specific promoter mutations driving the cancer development ,but the current radical view is that the mutations of the genes are not the driver of cancer development ,rather the microenvironment of the cells inhibits or promotes the development of tumor .Gen-eral view is that the epithelial cells are changed before the cell matrix in the development of neoplasia ,but recent evidences show that the cell matrix is the first to change .This paper will focus on how matrix changes affect the epithelial tumor development ,and this will bring new breakthrough for controlling epithelial tumors .

Una puesta al día en el tratamiento de las queratosis actínicas / An update on the treatment of actinic keratosis

Las queratosis actínicas son una de las causas más frecuentes de consultas dermatológicas. Están consideradas como lesiones premalignas que pueden evolucionar a carcinoma espinocelular invasor. Constituyen un marcador de fotodaño y actualmente se consideran como modelo de cancerización de campo. Existen diversos tipos de tratamientos que se clasifican en terapias dirigidas a la remoción de la lesión (crioterapia y / o quirúrgicos) y terapias dirigidas al campo de cancerización que incluyen: inmunomoduladores tópicos (imiquimod y diclofenaco), agentes quimioterapéuticos (5-Fluorouracilo y retinoides), Ingenol mebutato, dermoabrasión, peelings químicos, láser, terapia fotodinámica y terapias combinadas entre otras. El principal objetivo de esta revisión es realizar una actualización de las terapias dirigidas al campo de cancerización de las queratosis actínicas con sus respectivas indicaciones, ventajas y desventajas.

Actinic keratosis are one of the most common causes of dermatological consultation. Considered as premalignant lesions that can progress to invasive squamous cell carcinoma. Constitute a marker of photodamage and actually considered as a model of field cancerization. There are several types of treatments classified as therapies targeting the removal of the lesion (cryotherapy and / or surgery) and targeted therapies of field cancerization that include topical immunomodulators (imiquimod and diclofenac), chemotherapeutic agents (5-fluorouracil, and retinoids), ingenol mebutate, dermabrasion, chemical peels, laser, photodynamic therapy and combination therapies among others. The main objective of this review is to update therapies of field cancerization for actinic keratosis with their respective indications, advantages and disadvantages.