ارتباط بیان مهارکننده عامل القایی هیپوکسی- 1 آلفا با میزان تهاجم عروقی در سرطان روده بزرگ

زمینه: کمبود فشار اکسیژن (هیپوکسی) یک پدیده شایع در تومورهاي انسانی است که با افزایش القاي فرآیند رگزایی (آنژیوژنزیس) موجب رشد ، به نا م HIF1α از طریق اتصال به یک سري زیر واحدهاي پروتئین (HIF1AN) بقا و تهاجم تومور میشود. مهارکننده عامل القایی هیپوکسی HIF1α) موجب مهار عامل القایی هیپوکسی (CBP/P300) کپ بایندیگ پروتئین پی 300 ) میشود. HIF1AN) هدف: مطالعه به منظور تعیین ارتباط بیان مهارکننده عامل القایی هیپوکسی ) با میزان تهاجم عروقی در تومور روده انجام شد. مواد و روشها: این مطالعه تحلیلی در سالهاي 1391 تا 1393 بر روي 101 بیمار مبتلا به سرطان روده انجام شد که از لحاظ وضعیت تهاجم رنگ و از نظر HIF1AN عروقی به دو گروه دارا و فاقد تهاجم عروقی تقسیم شدند. بلوكهاي پارافینه تومور به روش ایمنوهیستوشیمی با نشانگر HIF1AN شدت رنگپذیري و تعداد سلولها ارزیابی شدند. ارتباط میزان بیان نشانگر با شاخص هاي آسی ب شناسی و با آزمون هاي آماري همبستگی و مجذور کاي تحلیل شد. با افزایش تهاجم HIF1AN در دو گروه مورد مطالعه متفاوت بود. بین کاهش میزان بیان پروتئین HIF1AN یافتهها: واکنش ایمنوشیمیایی HIF1AN عروقی و رگزایی تومور سرطان روده ارتباط معنیداري دیده شد. بین بیان با عمق تومور و تمایز آن ارتباطی وجود نداشت. HIF1AN نتیجهگیري: با توجه به یافتهها به نظر میرسد پروتئین در سرطان روده نقش مهارگر تومور دارد و کاهش بیان این پروتئین در هسته سلولهاي توموري روده موجب افزایش بیان عوامل رگزایی و تهاجم عروقی میشود. کلیدواژهها: تهاجم عروقی، رگزایی، مهارکننده عامل القایی هیپوکسی، سرطان روده بزر

Estrogen receptor beta expression in prostate adenocarcinoma

<p>Abstract</p> <p>Background</p> <p>Prostate cancer is the most commonly diagnosed cancer in men and the second leading cause of cancer death in men. Estrogen induction of cell proliferation is a crucial step in carcinogenesis of gynecologic target tissues, and there are many studies recently done, showing that prostate cancer growth is also influenced by estrogen. The characterization of estrogen receptor beta (ER-b) brought new insight into the mechanisms underlying estrogen signalling. In the present study, we investigated the expression of estrogen receptor-b (ER-b) in human prostate cancer tissues.</p> <p>Methods</p> <p>We selected 52 paraffin-embedded blocks of prostate needle biopsies in a cross-sectional study to determine frequency and rate of ER-b expression in different grades of prostate adenocarcinoma according to Gleason grading system. Immunohistochemical staining of tissue sections by monoclonal anti ER-b antibody was performed using an Envision method visualising system.</p> <p>Results</p> <p>ER-b expression was seen in tumoral cells of prostatic carcinoma in all 29 cases with low and intermediate tumors (100%) and 19 of 23 cases with high grade tumor (83%). Mean rate of ER-b expression in low & intermediate grade cancers was 68.41% (SD = 25.63) whereas high grade cancers showed 49.48% rate of expression (SD = 28.79).</p> <p>Conclusions</p> <p>ER-b expression is reduced in high grade prostate cancers compared to low & intermediate grade ones (<it>P </it>value 0.027).</p

Investigation of FIH-1 and SOCS3 expression in KRAS mutant and wild-type patients with colorectal cancer

Abstract Colorectal cancer (CRC) is a multistep process based on the accumulation of somatic mutations in genes such as APC and KRAS. Data on the presence of mutations in KRAS gene in CRC and its relationship with clinicopathological parameters and expression of genes involved in tumor progression are scarce. We unbiasedly examined the KRAS status in samples from 99 patients and its correlation with clinicopathological parameters such as age, sex, tumor location, lymph node metastasis, tumor stage, tumor grade, and vascular invasion. Consistent with reports of other researchers, 38.4 % of our samples harbored KRAS mutation in their genomes with preferential mutation in codon 12 (89.4 %). Nevertheless, unlike previous reports, we were not able to correlate KRAS status with clinicopathological parameters (P > 0.05) except for vascular invasion. Patients with KRAS mutation have more vascular invasion compared with patient having wild-type KRAS. Next, we investigated the expression of two tumor suppressor genes, factor-inhibiting hypoxia-inducible factor 1 (FIH-1) and suppressor of cytokine signaling (SOCS3), in both KRAS mutant and wild-type groups and looked for any correlation between their expression and clinicopathological parameters. Although the expression of both genes was not regular, none of the clinicopathological parameters were associated with the expressions of FIH-1 and SOCS3 at mRNA level (P>0.05). However, decline in FIH-1 expression at protein level in KRAS mutant group was correlated with stage IV and grade 2 of tumor (P≤ 0.05). Our results demonstrated that there is no or low correlation between KRAS status, FIH-1, and SOCS3 expression with epidemiologic and clinicpathological characteristics in CRC

Trigeminal Neuralgia as the First Clinical Manifestation of Anti-Hu Paraneoplastic Syndrome Induced by a Borderline Ovarian Mucinous Tumor

Paraneoplastic neurologic syndrome (PNS) is an uncommon manifestation of cancer that is not caused by the tumor or metastasis. Trigeminal neuralgia (TN) is an initial symptom of this disease, but it has rarely been reported in the literature. Here, we report the case of a 76-year-old woman who presented with classic TN, followed by limbic encephalitis due to an underlying ovarian intestinal-type mucinous borderline tumor, with the presence of anti-Hu antibodies. She recovered quickly after removal of the tumor and was essentially free of symptoms 2 weeks after surgery. Because PNS precedes the tumor in approximately 60% of cases, its rapid detection and treatment are crucial. Therefore, we propose that PNS be considered during the management of TN when brain imaging is normal, as it is followed by other central and/or peripheral neurological manifestations as well as the presence of systemic symptoms such as anemia, fatigability, loss of appetite, or weight loss