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New autochthonous ccRCC model - Nature.com

Posted: June 13th, 2017, 4:34am EDT

New autochthonous ccRCC model
Nature.com
A report in Nature Medicine describes the creation of a new autochthonous mouse model of clear cell renal cell carcinoma (ccRCC) based on deletion of Vhl, Trp53, and Rb1. Genetic and molecular analyses of the mouse tumours and comparison with data from ...

Radiotherapy-induced miR-223 prevents relapse of breast cancer by targeting the EGF pathway - Nature.com

Posted: February 15th, 2016, 4:42am EST

Radiotherapy-induced miR-223 prevents relapse of breast cancer by targeting the EGF pathway
Nature.com
(c) qRT–PCR of miR-223 (expressed as fold increase over the NIR cells) in MCF-10A mammary epithelial cells (left graph) and in MDA-MB-231 breast cancer cells (right graph) irradiated in vitro with 2 Gy. Data were normalized using U6 expression levels ...

Accessory parotid gland tumors: A series of 4 cases.

Fetched: June 23rd, 2017, 1:00am EDT

Accessory parotid gland tumors: A series of 4 cases.

Ear Nose Throat J. 2016 Jul;95(7):E35-8

Authors: Kakuki T, Takano K, Kurose M, Kondo A, Okuni T, Ogasawara N, Himi T

Abstract
Accessory parotid gland tumors are clinically rare, and their management remains unclear. In this article, we describe our experience with 4 patients-2 males and 2 females, aged 13 to 66 years-who were diagnosed with an accessory parotid gland tumor. All patients presented with an asymptomatic midcheek swelling, and all underwent fine-needle aspiration biopsy, ultrasonography, computed tomography, and magnetic resonance imaging. A standard parotidectomy was performed on all patients. Postoperatively, 2 patients were found to have a malignant tumor, while the other 2 had a pleomorphic adenoma. No patient experienced any obvious facial nerve injuries postoperatively, and no recurrences were observed. We discuss the preoperative evaluation, treatment, and prognosis of these tumors, and we briefly describe the literature. The first choice of treatment for accessory parotid gland tumors is surgical resection. In our experience, a standard parotidectomy approach is safe and cosmetically appealing.

PMID: 27434483 [PubMed - indexed for MEDLINE]

Acinar cell plasticity and development of pancreatic ductal adenocarcinoma.

Fetched: June 21st, 2017, 1:00am EDT

Acinar cell plasticity and development of pancreatic ductal adenocarcinoma.

Nat Rev Gastroenterol Hepatol. 2017 May;14(5):296-304

Authors: Storz P

Abstract
Acinar cells in the adult pancreas show high plasticity and can undergo transdifferentiation to a progenitor-like cell type with ductal characteristics. This process, termed acinar-to-ductal metaplasia (ADM), is an important feature facilitating pancreas regeneration after injury. Data from animal models show that cells that undergo ADM in response to oncogenic signalling are precursors for pancreatic intraepithelial neoplasia lesions, which can further progress to pancreatic ductal adenocarcinoma (PDAC). As human pancreatic adenocarcinoma is often diagnosed at a stage of metastatic disease, understanding the processes that lead to its initiation is important for the discovery of markers for early detection, as well as options that enable an early intervention. Here, the critical determinants of acinar cell plasticity are discussed, in addition to the intracellular and extracellular signalling events that drive acinar cell metaplasia and their contribution to development of PDAC.

PMID: 28270694 [PubMed - indexed for MEDLINE]

FOXA2 is a sensitive and specific marker for small cell neuroendocrine carcinoma of the prostate.

Fetched: June 19th, 2017, 1:00am EDT

FOXA2 is a sensitive and specific marker for small cell neuroendocrine carcinoma of the prostate.

Mod Pathol. 2017 Jun 16;:

Authors: Park JW, Lee JK, Witte ON, Huang J

Abstract
The median survival of patients with small cell neuroendocrine carcinoma is significantly shorter than that of patients with classic acinar-type adenocarcinoma. Small cell neuroendocrine carcinoma is traditionally diagnosed based on histologic features because expression of current immunohistochemical markers is inconsistent. This is a challenging diagnosis even for expert pathologists and particularly so for pathologists who do not specialize in prostate cancer. New biomarkers to aid in the diagnosis of small cell neuroendocrine carcinoma are therefore urgently needed. We discovered that FOXA2, a pioneer transcription factor, is frequently and specifically expressed in small cell neuroendocrine carcinoma compared with prostate adenocarcinoma from published mRNA-sequencing data of a wide range of human prostate cancers. We verified the expression of FOXA2 in human prostate cancer cell lines and xenografts, patient biopsy specimens, tissue microarrays of prostate cancers with lymph node metastasis, primary small cell neuroendocrine carcinoma, and metastatic treatment-related small cell neuroendocrine carcinoma and cases from a rapid autopsy program. FOXA2 expression was present in NCI-H660 and PC3 neuroendocrine cell lines, but not in LNCAP and CWR22 adenocarcinoma cell lines. Of the human prostate cancer specimens, 20 of 235 specimens (8.5%) showed diagnostic histologic features of small cell neuroendocrine carcinoma as judged histologically. Fifteen of 20 small cell neuroendocrine carcinoma tissues (75%) showed strong expression of FOXA2 (staining intensity 2 or 3). FOXA2 expression was also detected in 9 of 215 prostate cancer tissues (4.2%) that were histologically defined as adenocarcinoma. Our findings demonstrate that FOXA2 is a sensitive and specific molecular marker that may be extremely valuable in the pathologic diagnosis of small cell neuroendocrine carcinoma.Modern Pathology advance online publication, 16 June 2017; doi:10.1038/modpathol.2017.44.

PMID: 28621319 [PubMed - as supplied by publisher]

Newly Described Entities in Salivary Gland Pathology.

Fetched: June 16th, 2017, 1:00am EDT

Newly Described Entities in Salivary Gland Pathology.

Am J Surg Pathol. 2017 Jun 13;:

Authors: Skálová A, Gnepp DR, Lewis JS, Hunt JL, Bishop JA, Hellquist H, Rinaldo A, Vander Poorten V, Ferlito A

Abstract
Salivary glands may give rise to a wide spectrum of different tumors. This review concentrates on 4 salivary gland tumors that have been accepted in the recent literature as new neoplastic entities: mammary analog secretory carcinoma, cribriform adenocarcinoma of minor salivary glands (CASG), sclerosing polycystic adenosis/adenoma (SPA), and the mucinous/secretory variant of myoepithelioma. Mammary analog secretory carcinoma is a distinctive low-grade malignant salivary cancer that harbors a characteristic chromosomal translocation, t(12;15) (p13;q25), resulting in an ETV6-NTRK3 fusion. Cribriform adenocarcinoma (CASG) is a distinct tumor entity that differs from polymorphous low-grade adenocarcinoma by location (ie, most often arising on the tongue), by prominent nuclear clearing, differing alterations of the PRKD gene family, and clinical behavior with frequent metastases at the time of presentation of the primary tumor. Early nodal metastatic disease is seen in most cases of CASG; yet, they are still associated with indolent clinical behavior, making it a unique neoplasm among all low-grade salivary gland tumors. SPA is a rare sclerosing tumor of the salivary glands characterized by the combination of cystic ductal structures with variable cell lining including vacuolated, apocrine, mucinous, squamous, and foamy cells, by prominent large acinar cells with coarse eosinophilic cytoplasmic zymogen-like granules, and by closely packed ductal structures, surrounded by a peripheral myoepithelial layer and stromal fibrosis with focal inflammatory infiltrates. SPA frequently harbors intraductal epithelial dysplastic proliferations ranging from mild dysplasia to severe dysplasia/carcinoma in situ. Moreover, SPA has been proven to be a clonal process by HUMARA assay and is associated with considerable risk of recurrence. Therefore, on the basis of all these newly recognized findings, we believe that SPA is likely a neoplasm, and we suggest the name "sclerosing polycystic adenoma." The mucinous variant of myoepithelioma is a myoepithelial tumor with foci of prominent cytoplasmic clearing frequently containing intracellular mucin material and having signet-ring morphology.

PMID: 28614209 [PubMed - as supplied by publisher]

Genetic ablation of Smoothened in pancreatic fibroblasts increases acinar-ductal metaplasia.

Fetched: June 14th, 2017, 1:00am EDT

Genetic ablation of Smoothened in pancreatic fibroblasts increases acinar-ductal metaplasia.

Genes Dev. 2016 Sep 01;30(17):1943-55

Authors: Liu X, Pitarresi JR, Cuitiño MC, Kladney RD, Woelke SA, Sizemore GM, Nayak SG, Egriboz O, Schweickert PG, Yu L, Trela S, Schilling DJ, Halloran SK, Li M, Dutta S, Fernandez SA, Rosol TJ, Lesinski GB, Shakya R, Ludwig T, Konieczny SF, Leone G, Wu J, Ostrowski MC

Abstract
The contribution of the microenvironment to pancreatic acinar-to-ductal metaplasia (ADM), a preneoplastic transition in oncogenic Kras-driven pancreatic cancer progression, is currently unclear. Here we show that disruption of paracrine Hedgehog signaling via genetic ablation of Smoothened (Smo) in stromal fibroblasts in a Kras(G12D) mouse model increased ADM. Smo-deleted fibroblasts had higher expression of transforming growth factor-α (Tgfa) mRNA and secreted higher levels of TGFα, leading to activation of EGFR signaling in acinar cells and increased ADM. The mechanism involved activation of AKT and noncanonical activation of the GLI family transcription factor GLI2. GLI2 was phosphorylated at Ser230 in an AKT-dependent fashion and directly regulated Tgfa expression in fibroblasts lacking Smo Additionally, Smo-deleted fibroblasts stimulated the growth of Kras(G12D)/Tp53(R172H) pancreatic tumor cells in vivo and in vitro. These results define a non-cell-autonomous mechanism modulating Kras(G12D)-driven ADM that is balanced by cross-talk between Hedgehog/SMO and AKT/GLI2 pathways in stromal fibroblasts.

PMID: 27633013 [PubMed - indexed for MEDLINE]

Pancreatic acinar cell carcinoma presenting with panniculitis, successfully treated with FOLFIRINOX: A case report.

Fetched: June 9th, 2017, 1:00am EDT

Pancreatic acinar cell carcinoma presenting with panniculitis, successfully treated with FOLFIRINOX: A case report.

Mol Clin Oncol. 2017 Jun;6(6):866-870

Authors: Yoshihiro T, Nio K, Tsuchihashi K, Ariyama H, Kohashi K, Tsuruta N, Hanamura F, Inadomi K, Ito M, Sagara K, Okumura Y, Nakano M, Arita S, Kusaba H, Oda Y, Akashi K, Baba E

Abstract
Pancreatic acinar cell carcinoma (PACC) is a rare tumor of the exocrine pancreas, representing only 1% of all pancreatic malignancies. A 50-year-old man presented with edema of the thumb joints bilaterally, followed by an appearance of masses in the bilateral lower extremities and fever (38°C). The masses were diagnosed as panniculitis by skin biopsy, and multiple intraperitoneal masses were incidentally detected on pelvic magnetic resonance imaging performed to investigate the leg abnormalities. The patient was referred to the Kyushu University Hospital for further investigation, and fluorodeoxyglucose-positron emission tomography/computed tomography (CT) revealed high-uptake tumors in the pancreatic tail, in the periphery of the liver, and in the pelvis. Laboratory examinations revealed high serum concentrations of pancreatic exocrine enzymes, such as lipase, trypsin, elastase 1 and pancreatic phospholipase A2. Histological examination of a bioptic specimen obtained from a hepatic lesion revealed proliferation of atypical cells arranged in a tubular or glandular pattern. Immunohistochemical staining revealed that the atypical cells were positive for cytokeratin (CK)7, CK19 and lipase, but negative for CK20 and thyroid transcription factor-1, leading to a final diagnosis of acinar cell carcinoma of the pancreatic tail (T4bN0M1, stage IV according to the 7th edition of the TNM Classification of Malignant Tumors). Combined chemotherapy with oxaliplatin, irinotecan and fluorouracil (FOLFIRINOX) was administered and fever was soon alleviated. The serum levels of lipase also declined and panniculitis completely resolved. As of the start of the 8th course of chemotherapy, the levels of the pancreatic exocrine enzymes were within normal ranges and CT revealed partial response. Therefore, the severe lipase hypersecretion syndrome was well controlled by the FOLFIRINOX regimen and shrinkage of the mass was also achieved. Thus, the FOLFIRINOX regimen may represent an effective treatment option for advanced PACC.

PMID: 28588779 [PubMed - in process]

Permalink for 'Surfactant Protein A and Napsin A in the Immunohistochemical Characterization of Canine Pulmonary Carcinomas: Comparison With Thyroid Transcription Factor-1.'

Surfactant Protein A and Napsin A in the Immunohistochemical Characterization of Canine Pulmonary Carcinomas: Comparison With Thyroid Transcription Factor-1.

Fetched: June 7th, 2017, 1:00am EDT

Surfactant Protein A and Napsin A in the Immunohistochemical Characterization of Canine Pulmonary Carcinomas: Comparison With Thyroid Transcription Factor-1.

Vet Pathol. 2017 Jan 01;:300985817712559

Authors: Beck J, Miller MA, Frank C, DuSold D, Ramos-Vara JA

Abstract
Thyroid transcription factor-1 (TTF-1) is a specific and sensitive marker for canine pulmonary tumors but is also expressed in thyroid carcinomas, which commonly metastasize to lung. Napsin A and surfactant protein A (SP-A) are used in the histologic diagnosis of non-small-cell lung cancer in humans but have not been thoroughly evaluated in neoplasms of dogs. The objective of this study was to compare the efficacy of immunohistochemistry for SP-A, napsin A, and TTF-1 in the diagnosis of canine pulmonary carcinomas. TTF-1, napsin A, and SP-A antibodies were applied to 67 formalin-fixed, paraffin-embedded canine pulmonary tumors. Although each marker had good sensitivity, only 3% (2/67) of lung tumors were negative for SP-A compared with 7% (5/67) and 9% (6/67) for napsin A and TTF-1, respectively. Each antigen was detected in a greater percentage of cells of tumors with acinar or papillary patterns compared with those with squamous differentiation. SP-A immunoreactivity was absent in all 113 nonpulmonary tumors tested. Of 108 normal tissues, SP-A was detected only in lung and in 1 of 6 adrenal, 1 of 3 endometrial, and 1 of 4 hepatic sections. Based on these findings, SP-A and napsin A are useful markers of canine lung epithelial neoplasia. Of these, SP-A is the most sensitive and specific (a possible pitfall is the need to distinguish entrapped normal pulmonary epithelial cells or alveolar macrophages from neoplastic cells) and can be used in combination with TTF-1 or napsin A to improve detection and differentiation of pulmonary carcinomas from metastatic tumors in the canine lung.

PMID: 28578631 [PubMed - as supplied by publisher]

No Functional Role for microRNA-342 in a Mouse Model of Pancreatic Acinar Carcinoma.

Fetched: June 4th, 2017, 1:00am EDT

No Functional Role for microRNA-342 in a Mouse Model of Pancreatic Acinar Carcinoma.

Front Oncol. 2017;7:101

Authors: Dooley J, Lagou V, Pasciuto E, Linterman MA, Prosser HM, Himmelreich U, Liston A

Abstract
The intronic microRNA (miR)-342 has been proposed as a potent tumor-suppressor gene. miR-342 is found to be downregulated or epigenetically silenced in multiple different tumor sites, and this loss of expression permits the upregulation of several key oncogenic pathways. In several different cell lines, lower miR-342 expression results in enhanced proliferation and metastasis potential, both in vitro and in xenogenic transplant conditions. Here, we sought to determine the function of miR-342 in an in vivo spontaneous cancer model, using the Ela1-TAg transgenic model of pancreatic acinar carcinoma. Through longitudinal magnetic resonance imaging monitoring of Ela1-TAg transgenic mice, either wild-type or knockout for miR-342, we found no role for miR-342 in the development, growth rate, or pathogenicity of pancreatic acinar carcinoma. These results indicate the importance of assessing miR function in the complex physiology of in vivo model systems and indicate that further functional testing of miR-342 is required before concluding it is a bona fide tumor-suppressor-miR.

PMID: 28573106 [PubMed - in process]

Targeting of the P2X7 receptor in pancreatic cancer and stellate cells.

Fetched: May 14th, 2017, 1:00am EDT

Targeting of the P2X7 receptor in pancreatic cancer and stellate cells.

Int J Cancer. 2016 Dec 01;139(11):2540-52

Authors: Giannuzzo A, Saccomano M, Napp J, Ellegaard M, Alves F, Novak I

Abstract
The ATP-gated receptor P2X7 (P2X7R) is involved in regulation of cell survival and has been of interest in cancer field. Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer and new markers and therapeutic targets are needed. PDAC is characterized by a complex tumour microenvironment, which includes cancer and pancreatic stellate cells (PSCs), and potentially high nucleotide/side turnover. Our aim was to determine P2X7R expression and function in human pancreatic cancer cells in vitro as well as to perform in vivo efficacy study applying P2X7R inhibitor in an orthotopic xenograft mouse model of PDAC. In the in vitro studies we show that human PDAC cells with luciferase gene (PancTu-1 Luc cells) express high levels of P2X7R protein. Allosteric P2X7R antagonist AZ10606120 inhibited cell proliferation in basal conditions, indicating that P2X7R was tonically active. Extracellular ATP and BzATP, to which the P2X7R is more sensitive, further affected cell survival and confirmed complex functionality of P2X7R. PancTu-1 Luc migration and invasion was reduced by AZ10606120, and it was stimulated by PSCs, but not by PSCs from P2X7(-/-) animals. PancTu-1 Luc cells were orthotopically transplanted into nude mice and tumour growth was followed noninvasively by bioluminescence imaging. AZ10606120-treated mice showed reduced bioluminescence compared to saline-treated mice. Immunohistochemical analysis confirmed P2X7R expression in cancer and PSC cells, and in metaplastic/neoplastic acinar and duct structures. PSCs number/activity and collagen deposition was reduced in AZ10606120-treated tumours.

PMID: 27513892 [PubMed - indexed for MEDLINE]

Frequent IDH2 R172 Mutations in Undifferentiated and Poorly-Differentiated Sinonasal Carcinomas.

Fetched: May 13th, 2017, 1:00am EDT

Frequent IDH2 R172 Mutations in Undifferentiated and Poorly-Differentiated Sinonasal Carcinomas.

J Pathol. 2017 May 11;:

Authors: Dogan S, Chute DJ, Xu B, Ptashkin RN, Chandramohan R, Casanova-Murphy J, Nafa K, Bishop JA, Chiosea SI, Stelow EB, Ganly I, Pfister DG, Katabi N, Ghossein RA, Berger MF

Abstract
Sinonasal undifferentiated carcinoma (SNUC) is a high-grade malignancy with limited treatment options and poor outcome. A morphologic spectrum of 47 sinonasal tumors including 17 (36.2%) SNUCs were analyzed at genomic level. Thirty carcinomas (Cohort 1) were subjected to a hybridization exon-capture next-generation sequencing assay (MSK-IMPACT(TM) ) to interrogate somatic variants in 279 or 410 cancer-related genes. Seventeen sinonasal tumors (Cohort 2) were examined only for presence of IDH1/2 exon 4 mutations by Sanger sequencing. IDH2 R172 single nucleotide variants were overall detected in 14 (82.4%) SNUCs, in 2 (20%) poorly-differentiated carcinomas with glandular/acinar differentiation, and in one of 2 high-grade neuroendocrine carcinomas, large cell type (HGNEC). No IDH2 mutation was detected in any of 5 olfactory neuroblastomas or in any of 5 SMARCB1-deficient carcinomas. Among 12 IDH2-mutated cases in Cohort 1, 5 (41.7%) harbored co-existing TP53 mutations, 4 (33.3%) CDKN2A/2B loss-of-function alterations, 4 (33.3%) MYC amplification, and 3 (25%) had concurrent SETD2 mutations. AKT1 E17K and KIT D816V hotspot variants were each detected in one IDH2-mutated SNUC. The vast majority of SNUCs and variable proportions of other poorly differentiated sinonasal carcinomas may be amenable to IDH2-targeted therapy.

PMID: 28493366 [PubMed - as supplied by publisher]

HOXB13 a useful marker in pleomorphic giant cell adenocarcinoma of the prostate: a case report and review of the literature.

Fetched: May 11th, 2017, 1:00am EDT

HOXB13 a useful marker in pleomorphic giant cell adenocarcinoma of the prostate: a case report and review of the literature.

Virchows Arch. 2017 May 08;:

Authors: Larnaudie L, Compérat E, Conort P, Varinot J

Abstract
We report the case of an 81-year-old patient with a pleomorphic giant cell adenocarcinoma of the prostate. After diagnosis, he rapidly developed bone metastasis and died within 1 year. This variant of acinar adenocarcinoma is extremely rare and prognosis is poor. This entity has been included into the 2016 WHO classification. The principal differential diagnosis is urothelial carcinoma. To assess the prostatic origin, routine immunohistochemistry can be problematic. Loss of epitopes in this poorly differentiated entity can occur, such as loss of expression of PSA and p504s. We recently described a very sensitive and specific marker of prostate cancer, HOXB13, which once again has proven to be highly specific and sensitive. This is the first description of a pleomorphic giant cell prostate cancer expressing HOXB13.

PMID: 28484843 [PubMed - as supplied by publisher]

miR-29a-deficiency does not modify the course of murine pancreatic acinar carcinoma.

Fetched: May 5th, 2017, 1:00am EDT

miR-29a-deficiency does not modify the course of murine pancreatic acinar carcinoma.

Oncotarget. 2017 Apr 18;8(16):26911-26917

Authors: Dooley J, Lagou V, Garcia-Perez JE, Himmelreich U, Liston A

Abstract
The development of cancers involves the complex dysregulation of multiple cellular processes. With key functions in simultaneous regulation of multiple pathways, microRNA (miR) are thought to have important roles in the oncogenic formation process. miR-29a is among the most abundantly expressed miR in the pancreas. Together with altered expression in pancreatic cancer cell lines and biopsies, and known oncogenic functions in leukemia, this expression data has identified miR-29a as a key candidate for miR involvement in pancreatic cancer biology. Here we used miR-29a-deficient mice and the TAg model of pancreatic acinar carcinoma to functionally test the role of miR-29a in vivo. We found no impact of miR-29a loss on the development or growth of pancreatic tumours, nor on the survival of tumour-bearing mice. These results suggest that, despite differential expression, miR-29a is oncogenically neutral in the pancreatic acinar carcinoma context. If these results are extended to other models of pancreatic cancer, they would reduce the attractiveness of miR-29a as a potential therapeutic target in pancreatic cancer.

PMID: 28460473 [PubMed - in process]

Permalink for 'Xp11 Translocation Renal Cell Carcinomas (RCCs) With RBM10-TFE3 Gene Fusion Demonstrating Melanotic Features and Overlapping Morphology With t(6;11) RCC: Interest and Diagnostic Pitfall in Detecting a Paracentric Inversion of TFE3.'

Xp11 Translocation Renal Cell Carcinomas (RCCs) With RBM10-TFE3 Gene Fusion Demonstrating Melanotic Features and Overlapping Morphology With t(6;11) RCC: Interest and Diagnostic Pitfall in Detecting a Paracentric Inversion of TFE3.

Fetched: April 26th, 2017, 1:00am EDT

Xp11 Translocation Renal Cell Carcinomas (RCCs) With RBM10-TFE3 Gene Fusion Demonstrating Melanotic Features and Overlapping Morphology With t(6;11) RCC: Interest and Diagnostic Pitfall in Detecting a Paracentric Inversion of TFE3.

Am J Surg Pathol. 2017 May;41(5):663-676

Authors: Xia QY, Wang XT, Zhan XM, Tan X, Chen H, Liu Y, Shi SS, Wang X, Wei X, Ye SB, Li R, Ma HH, Lu ZF, Zhou XJ, Rao Q

Abstract
Xp11 translocation renal cell carcinomas (RCC) are characterized by several different translocations involving the TFE3 gene. Tumors with different specific gene fusions may have different clinicopathologic manifestations. Only 3 RBM10-TFE3 RCCs have been reported to date. Here, we added 4 cases of this rare type of tumors with clinicopathologic, immunohistochemical, molecular, and ultrastructural analyses. Most tumors had similar patterns with mixed architectures as follows: acinar, tubular and papillary patterns of epithelioid cells combined with sheets of small cells with "pseudorosette-like" architectures, mimicking the typical morphology of t(6;11) RCC. Cytoplasmic vacuolization, nuclear groove, and psammoma bodies were observed in most cases. Immunohistochemically, all 4 cases demonstrated moderate to strong immunoreactivity for TFE3, Cathepsin K, CD10, Ksp-cadherin, E-cadherin, P504S, RCC marker, PAX8 and vimentin, whereas negativity for TFEB, HMB45, and CK7. CKpan and Melan-A were at least focally expressed. The antibody to Ki-67 showed labeling of 3% to 8% (mean, 5%) of tumor cell nuclei. ;Of interest, several immunostainings demonstrated expression discrepancy in different histology patterns. RBM10-TFE3 fusion transcripts were identified in all cases by reverse transcription-polymerase chain reaction. By fluorescence in situ hybridization, all 4 cases showed unusual split signals with a distance <1 signal diameter (co-localized or subtle split signals) and usually had false-negative results. We also observed ultrastructures, including melanin pigment, nuclear groove, numerous glycogens, mitochondrion with areas of high electron density material, basement membrane material, and cell junctions with poor development. All 4 patients were alive with no evidence of recurrent disease. Our report adds to the known data regarding RBM10-TFE3 RCC.

PMID: 28288037 [PubMed - indexed for MEDLINE]

Permalink for 'Prognostic values of clinicopathological characteristics and survival outcomes in prostate infiltrating ductal carcinoma: a population-based study.'

Prognostic values of clinicopathological characteristics and survival outcomes in prostate infiltrating ductal carcinoma: a population-based study.

Fetched: April 22nd, 2017, 1:00am EDT

Prognostic values of clinicopathological characteristics and survival outcomes in prostate infiltrating ductal carcinoma: a population-based study.

Oncotarget. 2017 Mar 10;:

Authors: Wu YP, Chen SH, Wang ST, Li XD, Cai H, Lin YZ, Xue XY, Wei Y, Zheng QS, Xu N

Abstract
Infiltrating ductal carcinoma (IDC) is a rare histologic subtype of prostate cancer. We investigated the clinicopathological features and prognosis of IDC compared with acinar cell carcinoma (ACC). We identified 3814 men diagnosed with prostate cancer between 2004 to and 2013 in the Surveillance, Epidemiology, and End Results database, including 511 IDC and 3303 ACC cases. Prostate cancer-specific survival (PCSS) was compared using univariate and multivariate Cox proportional hazards models. Generally, IDC occurred in older men (≥ 65 years old) and presented with larger sizes, and higher grades, American Joint Committee on Cancer (AJCC) stages, AJCC T stages, lymph node positive rates and metastasis rates. Men with IDC were less likely to undergo radical prostatectomy, but more likely to be treated with adjuvant radiation than men with ACC. Five-year PCSS rates were significantly worse in IDC. In the multivariate analysis, patients with ACC had a better PCSS than patients with IDC. In conclusion, IDC has unique clinicopathological characteristics and has worse prognosis than ACC. Multivariable Cox regression analysis showed that age over 85 years, higher grade and T stage, and metastasis at diagnosis were independent prognostic factors of worse survival outcomes, whereas radical prostatectomy was an independent prognostic factor of better survival outcomes.

PMID: 28423709 [PubMed - as supplied by publisher]

Prognostic Factors Associated With Decreased Survival in Patients With Acinic Cell Carcinoma of the Parotid Gland.

Fetched: April 22nd, 2017, 1:00am EDT

Prognostic Factors Associated With Decreased Survival in Patients With Acinic Cell Carcinoma of the Parotid Gland.

J Oral Maxillofac Surg. 2017 Feb;75(2):416-422

Authors: Liu Y, Su M, Yang Y, Zhao B, Qin L, Han Z

Abstract
PURPOSE: Acinic cell carcinoma (ACC) of the parotid gland is relatively rare. This study aimed to estimate 5-year survival and to identify prognostic factors associated with survival of ACC of the parotid gland.
MATERIALS AND METHODS: Thirty-seven patients with ACC of the parotid gland were included in this retrospective cohort study. They were treated in Beijing Stomatological Hospital from January 2000 to December 2011. Predictor variables, including age, gender, tumor stage, nodal stage, perineural invasion, and margin status, were analyzed. The Cox regression model was used to determine prognostic factors for overall survival (OS) and disease-free survival (DFS).
RESULTS: Of the 37 patients, 20 were men (54.1%). Mean age was 42 years (range, 13 to 73 yr). Six patients (16.2%) had T3 or T4 tumors and 5 (13.5%) had positive neck nodes. The 5-year OS and DFS were 86.5 and 78.3%, respectively. Positive margin status was associated with worse OS. Patients older than 60 years with a fixed mass, high-grade tumor and nodal stage, perineural invasion, and angiolymphatic invasion had adverse OS and DFS (P < .05).
CONCLUSIONS: The present study identified several important prognostic factors associated with OS and DFS in patients with ACC. These prognostic variables include symptoms at presentation, clinical tumor stage and pathologic nodal status, and histopathology-related factors. All these factors were important in patient therapy and could prolong survival rate.

PMID: 27474461 [PubMed - indexed for MEDLINE]

Therapeutic potential of targeting acinar cell reprogramming in pancreatic cancer.

Fetched: April 21st, 2017, 1:00am EDT

Therapeutic potential of targeting acinar cell reprogramming in pancreatic cancer.

World J Gastroenterol. 2016 Aug 21;22(31):7046-57

Authors: Wong CH, Li YJ, Chen YC

Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a common pancreatic cancer and the fourth leading cause of cancer death in the United States. Treating this life-threatening disease remains challenging due to the lack of effective prognosis, diagnosis and therapy. Apart from pancreatic duct cells, acinar cells may also be the origin of PDAC. During pancreatitis or combined with activating KRas(G12D) mutation, acinar cells lose their cellular identity and undergo a transdifferentiation process called acinar-to-ductal-metaplasia (ADM), forming duct cells which may then transform into pancreatic intraepithelial neoplasia (PanIN) and eventually PDAC. During ADM, the activation of mitogen-activated protein kinases, Wnt, Notch and phosphatidylinositide 3-kinases/Akt signaling inhibits the transcription of acinar-specific genes, including Mist and amylase, but promotes the expression of ductal genes, such as cytokeratin-19. Inhibition of this transdifferentiation process hinders the development of PanIN and PDAC. In addition, the transdifferentiated cells regain acinar identity, indicating ADM may be a reversible process. This provides a new therapeutic direction in treating PDAC through cancer reprogramming. Many studies have already demonstrated the success of switching PanIN/PDAC back to normal cells through the use of PD325901, the expression of E47, and the knockdown of Dickkopf-3. In this review, we discuss the signaling pathways involved in ADM and the therapeutic potential of targeting reprogramming in order to treat PDAC.

PMID: 27610015 [PubMed - indexed for MEDLINE]

Ductal Spread Versus High-Grade Prostatic Intraepithelial Neoplasia: A Diagnostic Pitfall.

Fetched: April 19th, 2017, 10:15am EDT

Ductal Spread Versus High-Grade Prostatic Intraepithelial Neoplasia: A Diagnostic Pitfall.

Int J Surg Pathol. 2016 Dec;24(8):718-719

Authors: Acosta AM, Sharif A, Groth JV, Kajdacsy-Balla A

Abstract
Ductal spread (DS) of acinar adenocarcinoma of the prostate can lead to an incomplete replacement of the benign epithelium by cancer cells, resulting in a lesion that can be indistinguishable from high-grade prostatic intraepithelial neoplasia (HGPIN). Kovi and colleagues demonstrated 30 years ago that there is a significant association between the presence of DS and local extent of invasive adenocarcinoma, making the distinction between DS and HGPIN clinically relevant. However, despite the existence of certain morphologic features that are suggestive of DS, a definitive differentiation between the aforementioned lesions cannot always be attained.

PMID: 27605089 [PubMed - indexed for MEDLINE]

Salivary acinic cell carcinoma: reappraisal and update.

Fetched: April 9th, 2017, 1:00am EDT

Salivary acinic cell carcinoma: reappraisal and update.

Eur Arch Otorhinolaryngol. 2016 Nov;273(11):3511-3531

Authors: Vander Poorten V, Triantafyllou A, Thompson LD, Bishop J, Hauben E, Hunt J, Skalova A, Stenman G, Takes RP, Gnepp DR, Hellquist H, Wenig B, Bell D, Rinaldo A, Ferlito A

Abstract
Epidemiologic and clinicopathologic features, therapeutic strategies, and prognosis for acinic cell carcinoma of the major and minor salivary glands are critically reviewed. We explore histopathologic, histochemical, electron microscopic and immunohistochemical aspects and discuss histologic grading, histogenesis, animal models, and genetic events. In the context of possible diagnostic difficulties, the relationship to mammary analog secretory carcinoma is probed and a classification is suggested. Areas of controversy or uncertainty, which may benefit from further investigations, are also highlighted.

PMID: 26685679 [PubMed - indexed for MEDLINE]

MULTIHORMONAL ISLET CELL CARCINOMAS IN THREE KOMODO DRAGONS (VARANUS KOMODOENSIS).

Fetched: April 2nd, 2017, 1:00am EDT

MULTIHORMONAL ISLET CELL CARCINOMAS IN THREE KOMODO DRAGONS (VARANUS KOMODOENSIS).

J Zoo Wildl Med. 2017 Mar;48(1):241-244

Authors: Eustace R, Garner MM, Cook K, Miller C, Kiupel M

Abstract
Multihormonal pancreatic islet cell carcinomas were found in one female and two male captive geriatric Komodo dragons (Varanus komodoensis). Gross changes in the pancreas were visible in two of the cases. Clinical signs noted in the Komodo dragons were lethargy, weakness, and anorexia. Histologically, the tumors were comprised of nests and cords of well-differentiated neoplastic islet cells with scant amounts of eosinophilic cytoplasm and round, euchromatic nuclei, with rare mitoses. Infiltration by the islet cell tumor into the surrounding acinar tissue was observed in all cases, but no metastatic foci were seen. Multihormone expression was observed in all tumors, which labeled strongly positive for glucagon and somatostatin and focally positive for polypeptide. Pancreatic islet cell neoplasms should be considered in the differential diagnosis for geriatric Komodo dragons presenting with weakness, lethargy, and poor appetite.

PMID: 28363070 [PubMed - in process]

Histologic Features of Stromogenic Carcinoma of the Prostate (Carcinomas with Reactive Stroma Grade 3).

Fetched: March 22nd, 2017, 1:00am EDT

Histologic Features of Stromogenic Carcinoma of the Prostate (Carcinomas with Reactive Stroma Grade 3).

Hum Pathol. 2017 Mar 14;:

Authors: De Vivar AD, Sayeeduddin M, Rowley D, Cubilla A, Miles B, Kadmon D, Ayala G

Abstract
Prostatic carcinoma, like many other carcinomas, generates a stromal reaction. This phenomenon is well established in the scientific literature. The normal parenchymal smooth muscle phenotype switches to a myofibroblastic phenotype in response to the presence of cancer cells, with an expansion of the extracellular matrix compartment. The amount of reactive stroma is a predictor of biochemical recurrence in both radical prostatectomies and biopsies. It is a predictor of prostate cancer specific death in prostatectomies. The aim of this study is to improve our histologic understanding of reactive stroma in prostate cancer and to determine the histologic features of the malignant epithelium found in stromogenic carcinomas or carcinomas with reactive stromal grade 3. Tissue microarrays of 800 patients and H&E stained sections of 120 radical prostatectomies, previously determined to contain high proportion of areas with stromogenic carcinoma, were evaluated and findings systematically recorded. We identified 3 histologic patterns of reactive stroma: extracellular matrix rich, cellular variant and edematous/myxoid variant. The most common pattern of carcinoma in stromogenic areas is of the acinar type with angulated glands and periglandular halos. The nuclei are enlarged, opened, with prominent nucleoli. Luminal borders are undulated and amorphous pink secretion is often seen. Perineural invasion is frequently identified. Because of the clinical relevance, identification and quantification of areas with high reactive stromal grade by pathologists and reproducibility of our findings by others become essential. We believe that with the previously proposed grading system and the present morphologic description, both can be achieved.

PMID: 28315427 [PubMed - as supplied by publisher]

Salivary gland-like breast carcinomas: An infrequent disease.

Fetched: March 19th, 2017, 1:00am EDT

Salivary gland-like breast carcinomas: An infrequent disease.

Pathol Res Pract. 2016 Nov;212(11):1034-1038

Authors: Sherwell-Cabello S, Maffuz-Aziz A, Ríos-Luna NP, Bautista-Piña V, Rodríguez-Cuevas S

Abstract
OBJECTIVE: To show the incidence, as well as the clinical and histopathological characteristics, of patients diagnosed with mammary salivary gland-like carcinomas at our institution.
MATERIALS AND METHODS: A retrospective study was conducted in all women diagnosed with breast cancer at our institution from January 2005 to February 2016. Patients with diagnosis of salivary gland-like breast carcinomas were included.
RESULTS: In this period, 6384 patients were diagnosed with breast cancer at our institution; salivary gland-like carcinomas were found in 7 patients (0.1%), adenoid cystic carcinoma was diagnosed in 5 patients (0.07%), acinic cell carcinoma in 1 patient (0.015%) and mucoepidermoid carcinoma in 1 patient (0.015%). The triple-negative subtype was found in all of the tumors. Median follow-up was 66.3 months (range, 1-108 months). No patient developed local or distant recurrence.
CONCLUSIONS: Salivary gland-like breast tumors are extremely rare. We found a global incidence of 0.1%. Adenoid cystic, acinic cell and mucoepidermoid carcinomas were the three histologic types diagnosed. Although the triple-negative subtype is mainly found, good prognosis is expected.

PMID: 27667558 [PubMed - indexed for MEDLINE]

Permalink for 'High grade transformation of salivary gland acinic cell carcinoma with emphasis on histological diagnosis and clinical implications.'

High grade transformation of salivary gland acinic cell carcinoma with emphasis on histological diagnosis and clinical implications.

Fetched: March 19th, 2017, 1:00am EDT

High grade transformation of salivary gland acinic cell carcinoma with emphasis on histological diagnosis and clinical implications.

Pathol Res Pract. 2016 Nov;212(11):1059-1063

Authors: Bury D, Dafalla M, Ahmed S, Hellquist H

Abstract
Acinic cell carcinoma (ACC) is commonly thought of as a low grade malignant salivary neoplasm, and possibly has the best prognosis of all salivary malignancies with a 10-year survival of almost 90%. High grade transformation (HGT) in these tumours is a relatively rare event but is increasingly being reported. HGT (formerly referred to as dedifferentiation) in acinic cell carcinoma has shown to drastically reduce the survival rates and its recognition is imperative as more aggressive clinical management is needed. We report a case of parotid acinic cell carcinoma in a 82-year old woman where the fine needle aspirate suggested either pleomorphic adenoma or the possibility of carcinoma ex pleomorphic adenoma. Per-operatively it became clear that the facial nerve was involved and the tumour mass was debulked only. The histology showed an acinic cell carcinoma with foci of high grade differentiation (ACC-HGT). We describe the histology of HGT in ACC and the most common differential diagnoses. We emphasise the need of very generous sampling of the tumour, as to recognise any area of high grade transformation, some of which can be very small. A literature review of ACC-HGT as well as HGT in other salivary gland neoplasms is presented. HGT of ACC greatly thus influences the macroscopical and microscopical evaluation of the specimen but also, given the high incidence of metastases and morbidity, carries significant treatment implications.

PMID: 27623207 [PubMed - indexed for MEDLINE]

Permalink for 'MET exon 14 skipping mutation in triple-negative pulmonary adenocarcinomas and pleomorphic carcinomas: An analysis of intratumoral MET status heterogeneity and clinicopathological characteristics.'

MET exon 14 skipping mutation in triple-negative pulmonary adenocarcinomas and pleomorphic carcinomas: An analysis of intratumoral MET status heterogeneity and clinicopathological characteristics.

Fetched: March 15th, 2017, 1:00am EDT

MET exon 14 skipping mutation in triple-negative pulmonary adenocarcinomas and pleomorphic carcinomas: An analysis of intratumoral MET status heterogeneity and clinicopathological characteristics.

Lung Cancer. 2017 Apr;106:131-137

Authors: Kwon D, Koh J, Kim S, Go H, Kim YA, Keam B, Kim TM, Kim DW, Jeon YK, Chung DH

Abstract
OBJECTIVES: MET mutations leading to exon 14 skipping rarely occur in non-small cell lung cancer (NSCLC). Recently, small molecule inhibitors targeting MET mutations showed clinical benefit. However, the clinicopathological characteristics of NSCLC harboring MET mutations, and the correlation among mutations, protein expression, and gene copy number of MET in NSCLC remain unclear. Therefore, we address these issues.
MATERIALS AND METHODS: MET exon 14 skipping mutations were evaluated using real-time quantitative reverse-transcription-PCR (qRT-PCR) in 102 triple-negative (i.e., EGFR mutation (-)/ALK translocation (-)/KRAS mutation (-)) pulmonary adenocarcinomas, and 45 pleomorphic carcinomas. MET mutation and gene copy were also examined in microdissected tissues obtained from tumor areas with heterogeneous MET immunohistochemical expression.
RESULTS: MET mutations were detected in 8.8% (9/102) of triple-negative adenocarcinomas and 20% (9/45) of pleomorphic carcinomas of the lung. Patients with MET-mutated adenocarcinomas was significantly older than those without MET mutations (P=0.015). The male to female and ever-to never-smoker ratios were 3:6 and 2:7, respectively, among patients with MET-mutated adenocarcinomas. All (9/9) of the MET-mutated adenocarcinomas showed acinar predominant histology with associated lepidic patterns. In contrast, the male to female and ever- to never-smoker ratios were 8:1 and 7:1, respectively, among patients with MET-mutated pleomorphic carcinomas. The carcinoma component of MET-mutated pleomorphic carcinomas was mostly adenocarcinoma of acinar pattern (8/9). MET mutation was detected by qRT-PCR in all samples with heterogeneous MET expression microdissected from five cases with MET-mutated adenocarcinoma, while MET gene amplification was detected in tumor areas expressing high MET protein levels among MET-mutated adenocarcinomas.
CONCLUSION: MET-mutated NSCLC is characterized by older age in patients with adenocarcinoma and by an acinar histology and variable MET expression in patients with adenocarcinoma and pleomorphic carcinomas. Moreover, MET gene amplification might occur in the tumor cells harboring the MET mutation.

PMID: 28285687 [PubMed - in process]

Patterns of lymph node metastasis of parotid cancer.

Fetched: February 28th, 2017, 5:13am EST

Patterns of lymph node metastasis of parotid cancer.

Auris Nasus Larynx. 2016 Aug;43(4):446-50

Authors: Shinomiya H, Otsuki N, Yamashita D, Nibu K

Abstract
OBJECTIVE: To define the incidence and pattern of spread of lymph node metastasis from parotid cancers and to clarify the risk factors and appropriate extent of neck dissection (ND) for individual patient with parotid cancer.
METHODS: A total of 72 patients with parotid gland cancer treated by surgery between 1994 and 2013 were analyzed retrospectively by reference to medical records. In line with our protocol, patients with clinically positive lymph nodes and/or cT3/T4 disease were generally selected to undergo ND.
RESULTS: Pathological examinations revealed mucoepidermoid carcinoma in 23 patients, carcinoma ex pleomorphic adenoma in 11, adenoid cystic carcinoma in 9, salivary duct carcinoma in 9, acinic cell carcinoma in 8, squamous cell carcinoma in 5, adenocarcinoma NOS in 4, epithelial myoepithelial carcinoma in 2, and basal cell carcinoma in 1. Thirty-three patients underwent neck dissection: modified radical ND (MRND) in 13, and elective ND (END) in 20. Postoperative RT (PORT) was performed in 33 patients. Among 13 cN+ patients, 10 were pN+ and lymph node metastasis was distributed mainly in levels I, II, III and V. Among 59 cN- patients, clinical T1, T2, T3 and T4 classifications accounted for 10, 24, 10 and 15 patients, respectively. The incidence of occult lymph node metastasis was 22%. Occult lymph node metastasis was mostly seen in the intraparotid, levels I and II of patients with cT4 disease. Among the ND group, 12 necks were pathologically negative for cancer (pN0). Relapse of neck lymph node metastasis occurred only in two patients treated by MRND with pathologically positive lymph nodes (pN+). These patients developed local and distant metastasis within 1 year after neck lymph node recurrence, and subsequently died of the cancer. pN+ was found in 19/30 high grade (63%), 1/10 intermediate grade (10%), and 3/32 low grade (9.4%). Among 33 patients who received PORT, only 1 patient relapsed neck lymph node.
CONCLUSION: For patients with clinically positive lymph nodes, ipsilateral modified radical neck dissection (levels I-V) is recommended. Elective neck dissection is strongly recommended for patients with T3N0 or T4N0 disease, and the extent of ND should include at least level I/II. PORT for patients with high-risk features may improve the outcome of good neck control.

PMID: 26656731 [PubMed - indexed for MEDLINE]

Permalink for 'Stereotactic Radiosurgery and Metformin Hydrochloride in Treating Patients With Borderline-Resectable or Locally-Advanced Pancreatic Cancer'

Stereotactic Radiosurgery and Metformin Hydrochloride in Treating Patients With Borderline-Resectable or Locally-Advanced Pancreatic Cancer

Posted: May 30th, 2014, 10:00am EDT

Conditions: Acinar Cell Adenocarcinoma of the Pancreas; Duct Cell Adenocarcinoma of the Pancreas; Recurrent Pancreatic Cancer; Stage I-III Pancreatic Cancer
Interventions: Drug: metformin hydrochloride; Radiation: stereotactic radiosurgery
Sponsors: Case Comprehensive Cancer Center; National Cancer Institute (NCI)
Recruiting - verified April 2017

Ultrasound-Guided Photodynamic Therapy With Photofrin & Gemcitabine for Patients With Locally Advanced Pancreatic Cancer

Posted: January 15th, 2013, 10:00am EST

Conditions: Acinar Cell Adenocarcinoma of the Pancreas; Duct Cell Adenocarcinoma of the Pancreas; Stage III Pancreatic Cancer
Interventions: Drug: porfimer sodium; Procedure: endoscopic ultrasonography; Procedure: photodynamic therapy; Drug: gemcitabine hydrochloride
Sponsors: John DeWitt; American Society for Gastrointestinal Endoscopy; Pinnacle Biologics Inc.
Recruiting - verified August 2016

Permalink for 'Genotype-guided Dosing of mFOLFIRINOX Chemotherapy in Patients With Previously Untreated Advanced Gastrointestinal Malignancies'

Genotype-guided Dosing of mFOLFIRINOX Chemotherapy in Patients With Previously Untreated Advanced Gastrointestinal Malignancies

Posted: July 16th, 2012, 10:00am EDT

Conditions: Acinar Cell Adenocarcinoma of the Pancreas; Adenocarcinoma of the Gallbladder; Adenocarcinoma of Unknown Primary; Adult Primary Cholangiocellular Carcinoma; Advanced Adult Primary Liver Cancer; Cholangiocarcinoma of the Extrahepatic Bile Duct; Cholangiocarcinoma of the Gallbladder; Diffuse Adenocarcinoma of the Stomach; Duct Cell Adenocarcinoma of the Pancreas; Intestinal Adenocarcinoma of the Stomach; Localized Unresectable Adult Primary Liver Cancer; Metastatic Carcinoma of Unknown Primary; Metastatic Extrahepatic Bile Duct Cancer; Mixed Adenocarcinoma of the Stomach; Mucinous Adenocarcinoma of the Colon; Mucinous Adenocarcinoma of the Rectum; Newly Diagnosed Carcinoma of Unknown Primary; Signet Ring Adenocarcinoma of the Colon; Signet Ring Adenocarcinoma of the Rectum; Stage III Pancreatic Cancer; Stage IIIA Colon Cancer; Stage IIIA Gallbladder Cancer; Stage IIIA Gastric Cancer; Stage IIIA Rectal Cancer; Stage IIIB Colon Cancer; Stage IIIB Gallbladder Cancer; Stage IIIB Gastric Cancer; Stage IIIB Rectal Cancer; Stage IIIC Colon Cancer; Stage IIIC Gastric Cancer; Stage IIIC Rectal Cancer; Stage IV Gastric Cancer; Stage IV Pancreatic Cancer; Stage IVA Colon Cancer; Stage IVA Gallbladder Cancer; Stage IVA Rectal Cancer; Stage IVB Colon Cancer; Stage IVB Gallbladder Cancer; Stage IVB Rectal Cancer; Unresectable Extrahepatic Bile Duct Cancer
Interventions: Drug: oxaliplatin; Drug: irinotecan hydrochloride; Drug: leucovorin calcium; Drug: fluorouracil; Other: laboratory biomarker analysis
Sponsors: University of Chicago; National Cancer Institute (NCI)
Recruiting - verified April 2017

Texans fan's big heart lands her big surprise - KTRK-TV

Posted: August 28th, 2014, 5:28pm EDT

KTRK-TV

Texans fan's big heart lands her big surprise
KTRK-TV
In 2012, Gilmore's cancer -- acinic cell carcinoma -- relapsed for a fourth time. During treatment, Sprague performed cardiac ultrasounds regularly and got to know how big Gilmore's heart really was. "It's giant. Giant heart, it's awesome," Sprague ...

Accessory parotid gland tumors: A series of 4 cases.