RESUMEN
BACKGROUND AND STUDY AIM: In principle, additional surgery is performed after endoscopic submucosal dissection for early gastric cancer if the vertical margin is positive, regardless of lesion damage. The recurrence rate of vertical margin-positive lesions due to lesion damage after endoscopic submucosal dissection is unknown, and unnecessary surgeries may be performed. In this study, we investigated whether there was a difference in the recurrence rate between vertical margin-positive lesions due to lesion damage and vertical margin-negative lesions. PATIENTS AND METHODS: We included 1,294 intramucosal gastric cancer lesions that were resected by endoscopic submucosal dissection between January 2008 and December 2016, without additional surgery. The lesions were divided into the Damage and No damage groups based on vertical margin status. The Damage group had only one non-curative indication: a positive vertical margin due to lesion damage. The No damage group had no non curative indications. We compared the recurrence rate between the Damage and No damage groups. RESULTS: The recurrence rates of the Damage and No damage groups were 0% (0/23; 95% confidence interval: 0-14.8%) and 0% (0/1,271; 95% confidence interval: 0-0.003%), respectively, with no statistically significant difference. CONCLUSIONS: In intramucosal gastric cancer, the recurrence rate of vertical margin-positive lesions due to lesion damage was 0%, which did not differ from that of vertical margin-negative lesions with curative resection. Follow-up, instead of additional surgery, may be an option for patients with non-curative resection when the only non-curative indication is a positive vertical margin due to lesion damage.
Asunto(s)
Resección Endoscópica de la Mucosa , Neoplasias Gástricas , Mucosa Gástrica , Humanos , Recurrencia Local de Neoplasia , Estudios Retrospectivos , Resultado del TratamientoRESUMEN
Observation of the microvasculature using narrow band imaging (NBI) with magnifying endoscopy is useful for diagnosing superficial squamous cell carcinoma. Increased vascular density is indicative of cancer, but not many studies have reported differences between cancerous and noncancerous areas based on an objective comparison. We observed specimens of endoscopic submucosal dissection (ESD) using NBI magnification, and determined the vascular density of cancerous and noncancerous areas. A total of 25 lesions of esophageal squamous cell carcinoma that were dissected en bloc by ESD between July 2013 and December 2013 were subjected to NBI magnification. We constructed a device that holds an endoscope and precisely controls the movement along the vertical axis in order to observe submerged specimens by NBI magnification. NBI image files of both cancerous (pathologically determined invasion depth, m1/2) and surrounding noncancerous areas were created and subjected to vascular density assessment by two endoscopists who were blinded to clinical information. The invasion depth was m1/2 in 20, m3/sm1 in four and sm2 in one esophageal cancer lesion. Mean vascular density was significantly increased in cancerous areas (37.6 ± 16.3 vessels/mm2) compared with noncancerous areas (17.6 ± 10.0 vessels/mm2) (P < 0.05). The correlation coefficients between vascular density determined by two endoscopists were 0.86 and 0.81 in cancerous and noncancerous areas, respectively. Receiver operating curve (ROC) analysis revealed that the area under the curve (AUC) of vascular density was 0.895 (95% CI, 0.804-0.986). For this ROC curve, sensitivity was 78.3% and specificity was 87.0% when the cutoff value of vascular density was 26 vessels/mm2. NBI magnification confirmed significant increases in vascular density in cancerous areas compared with noncancerous areas in esophageal squamous cell carcinoma. The rates of agreement between vascular density values determined by two independent operators were high.
Asunto(s)
Carcinoma de Células Escamosas/irrigación sanguínea , Neoplasias Esofágicas/irrigación sanguínea , Esofagoscopía/métodos , Esófago/irrigación sanguínea , Microvasos/patología , Imagen de Banda Estrecha/métodos , Anciano , Carcinoma de Células Escamosas/diagnóstico por imagen , Carcinoma de Células Escamosas/patología , Neoplasias Esofágicas/diagnóstico por imagen , Neoplasias Esofágicas/patología , Carcinoma de Células Escamosas de Esófago , Esófago/patología , Femenino , Humanos , Aumento de la Imagen/métodos , Masculino , Microvasos/diagnóstico por imagen , Persona de Mediana Edad , Curva ROC , Sensibilidad y EspecificidadRESUMEN
The classification of neoplasms of adenohypophysial cells is misleading because of the simplistic distinction between adenoma and carcinoma, based solely on metastatic spread and the poor reproducibility and predictive value of the definition of atypical adenomas based on the detection of mitoses or expression of Ki-67 or p53. In addition, the current classification of neoplasms of the anterior pituitary does not accurately reflect the clinical spectrum of behavior. Invasion and regrowth of proliferative lesions and persistence of hormone hypersecretion cause significant morbidity and mortality. We propose a new terminology, pituitary neuroendocrine tumor (PitNET), which is consistent with that used for other neuroendocrine neoplasms and which recognizes the highly variable impact of these tumors on patients.
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Adenoma/clasificación , Tumores Neuroendocrinos/clasificación , Neoplasias Hipofisarias/clasificación , HumanosRESUMEN
OBJECTIVE: The objective was to assess involvement of loss of the PRKAR1A gene encoding a type 1α regulatory subunit of cAMP-dependent protein kinase A located on 17q24 in a Carney complex (CNC)-related pituitary adenoma. DESIGN: We investigated aberrations of the PRKAR1A gene in a CNC patient with a GH-producing pituitary adenoma, whose family has three other members with probable CNC. METHODS: A gene mutation was identified by a standard DNA sequencing method based on PCR. DNA copy number was measured to evaluate allelic loss on 17q24 by quantitative PCR. The breakpoints of deletion were determined by cloning a rearranged region in the deleted allele. RESULTS: A PRKAR1A mutation of c.751_758del8 (p.S251LfsX16) was found in genomic DNA obtained from a pituitary adenoma, but not leukocytes from the patient. Reduced DNA copy number at loci including the PRKAR1A gene on 17q24 was detected in both the tumor and leukocytes, suggesting a deletion at the loci at the germline level. The deletion size was determined to be â¼ 0.5 Mb and this large deletion was also found in two other family members. CONCLUSION: This is the first case showing a CNC-related pituitary adenoma with the combination of somatic mutation and a large inherited deletion of the PRKAR1A gene. Biallelic inactivation of PRKAR1A appears to be necessary for the development of CNC-related pituitary adenoma.
Asunto(s)
Adenoma/genética , Complejo de Carney/genética , Subunidad RIalfa de la Proteína Quinasa Dependiente de AMP Cíclico/genética , Eliminación de Gen , Mutación de Línea Germinal/genética , Neoplasias Hipofisarias/genética , Adenoma/diagnóstico , Anciano , Complejo de Carney/diagnóstico , Femenino , Humanos , Persona de Mediana Edad , Linaje , Neoplasias Hipofisarias/diagnóstico , Adulto JovenRESUMEN
Pituitary adenoma with neuronal choristoma (PANCH) is a rare condition that includes ganglion cells and GH-producing tumor that is characterized by sparsely granulated somatotroph cell type. However, the pathophysiology of this condition remains to be elucidated. We report a case of 46-year-old woman with acromegaly caused by PANCH. The patient had a large and invasive macroadenoma that was resistant to preoperative therapy with somatostatin analogue (SSA) and dopamine agonist. Histological examination showed typical diffuse, chromophobe-type adenoma containing ganglion cells, and sparsely granulated somatotroph cell type, which were consistent with PANCH. Genetic analysis showed heterozygous germline missense mutation in the AIP gene that results in Y261X amino acid substitution. The clinical characteristics of acromegaly associated with AIP mutations are reportedly macroadenomas with tumor extension and invasion, lower decreases in GH and IGF-I and less tumor shrinkage with SSA treatment, and sparsely granulated somatotroph cell type, which are comparable with those observed in PANCH. Taken together, the mutation in AIP gene may explain the clinical characteristics and pathogenesis of PANCH.
Asunto(s)
Acromegalia/genética , Adenoma/genética , Encefalopatías/genética , Coristoma/genética , Adenoma Hipofisario Secretor de Hormona del Crecimiento/genética , Péptidos y Proteínas de Señalización Intracelular/genética , Somatotrofos , Acromegalia/complicaciones , Acromegalia/etiología , Adenoma/complicaciones , Encefalopatías/complicaciones , Encefalopatías/patología , Coristoma/complicaciones , Coristoma/patología , Análisis Mutacional de ADN , Femenino , Adenoma Hipofisario Secretor de Hormona del Crecimiento/complicaciones , Humanos , Péptidos y Proteínas de Señalización Intracelular/fisiología , Persona de Mediana Edad , Mutación Missense/fisiología , Neuronas/patologíaRESUMEN
A total of 69 gastric carcinomas of very old people (aged > or = 85) were collected and pathologically analyzed in comparison with those of young to middle-aged (30-39) and elderly (65-69) people, with special attention to their phase. In the very old, almost all (34/35) carcinomas in the early phase belonged to well-differentiated categories. In the advanced phase, half of them (17/34) were classified into poorly differentiated categories when determined from the predominant pattern, but a well-differentiated pattern almost always coexisted in the superficial site. Thus, the gastric carcinomas in the very old may principally develop as well-differentiated carcinomas which then progress to poorly differentiated carcinomas with time, in contrast to those of the young to middle-aged, most of which emerged from the very early phase as poorly differentiated lesions. The gross features of the carcinomas were also in line with these histological observations. The carcinomas of the elderly showed distinct similarity to those of the very old. The results suggest that poorly differentiated carcinomas of the young to middle-aged and the old may be better classified and analyzed separately in view of the generally recognized etiological (e.g., specifically close causal relationship with environmental factors of the intestinal-type carcinoma of the old) and biological (e.g., practically no tendency for hematogenous metastasis of the diffuse-type carcinoma of the young to middle-aged) differences, although in the General Rules for Gastric Cancer Study of Japan, both are placed in the same category, por (por2).
Asunto(s)
Anciano de 80 o más Años , Neoplasias Gástricas/patología , Adenocarcinoma/patología , Adenocarcinoma/cirugía , Adulto , Factores de Edad , Anciano , Carcinoma de Células en Anillo de Sello/patología , Carcinoma de Células en Anillo de Sello/cirugía , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estadificación de Neoplasias , Neoplasias Gástricas/clasificación , Neoplasias Gástricas/cirugíaRESUMEN
Recently cases of ganglioneurocytoma and cerebral neurocytoma, very rare variants of central neurocytoma, have been reported. The former is characterized by differentiation toward ganglion cells and the latter by extraventricular origin in the cerebrum, but their existence as distinct clinicopathological entities, is controversial. We report an unusual case of neurocytoma, which arose extraventricularly from the frontal lobe, formed a large cystic lesion and showed ganglioid differentiation, in a 11-year-old girl. Following subtotal tumor resection, she showed a satisfactory clinical course and no evidence of recurrence. This is a very rare case of central neurocytoma-like tumor outside the ventricular system and also of ganglioneurocytoma. This case may provide some insight into the tumorigenesis and widen the clinicopathological concept of neurocytoma.