glycogen and Carcinoma--Renal-Cell

The majority of kidney cancers are clear-cell carcinomas (ccRCC), characterized by the accumulation of cholesterol, cholesterol esters, other neutral lipids and glycogen. Rather than being a passive bystander, the clear-cell phenotype is suggested to be a biomarker of deregulated cholesterol and lipid biosynthesis, which plays an important role in development of the disease. One clue to this relationship has come from the elucidation of the hereditary kidney cancer gene, TRC8, which functions partly to degrade key regulators of endogenous cholesterol and lipid biosynthesis. In addition, deregulation of the mevalonate pathway has been shown to play a key role in cellular transformation and invasion. These findings are supported by considerable epidemiologic data linking obesity and the deregulation of lipid biosynthesis to ccRCC.

Topics: Animals; Carcinoma, Renal Cell; Cholesterol; Cholesterol Esters; Glycogen; Humans; Kidney Neoplasms; Lipids; Mevalonic Acid; Obesity; Receptors, Cell Surface

Clear cell tumors of the lower respiratory tract comprise a diverse group of lesions. The prototypical lesion is the benign clear cell tumor or "sugar tumor," a tumor of enigmatic histogenesis, whose name derives from the high glycogen content of the cells. Analogous to the salivary gland lesion of the same name, acinic cell tumors may also occur in the tracheobroncheal tree. The topic of "clear cell carcinoma" is discussed, which in the opinion of the authors does not constitute a distinct tumor entity. A discussion of potential lesion metastatic to the lung with clear cell histology is also presented. Histological details of the various entities are discussed, as well as the significant histochemical, immunohistological, and electron microscopic features; in particular, such findings that are relevant to differential diagnosis are stressed, including the distinction of primary and metastatic lesions.

Topics: Adenocarcinoma, Clear Cell; Adolescent; Adult; Aged; Biomarkers, Tumor; Carcinoma, Acinar Cell; Carcinoma, Renal Cell; Child; Diagnosis, Differential; Female; Glycogen; Humans; Immunohistochemistry; Lung Neoplasms; Male; Middle Aged

The primary subtypes of renal cell carcinoma (RCC) include clear cell, papillary and chromophobe RCC. RCC occurs often due to loss of von Hippel‑Lindau (VHL) and accumulation of lipids and glycogen, and RCC cells may exhibit sensitivity to the disruption of normal metabolism or homologous recombination gene defect. Although the application of molecular‑targeted drugs (tyrosine kinase inhibitors) and immune checkpoint inhibitors has been recommended for the treatment of advanced RCC, more targets of DNA damage repair (DDR) signaling pathway involved in the synthetic lethal effect have been investigated. However, although achievements has been made in the exploration of the roles of DDR genes on RCC progression, their association has not been systematically summarized. Poly (ADP‑ribose) polymerase (PARP) 1 inhibitors are used in tumors with BRCA1/2 DNA repair‑associated mutations. PARP family enzymes perform post‑translational modification functions and participate in DDR and cell death. Inhibitors of PARP, ataxia telangiectasia mutant gene and polymerase θ serve key roles in the treatment of specific RCC subtypes. PARP1 may serve as an important biological marker to predict the therapeutic effect of immune checkpoint inhibitors and evaluate the prognosis of patients with ccRCC with polybromo 1 mutation. Therefore, the roles of DDR pathway on RCC progression or treatment may hold promises for the treatment of certain specific types of RCC.

Topics: Adenosine Diphosphate; Carcinoma, Renal Cell; DNA Damage; DNA Repair; Glycogen; Humans; Immune Checkpoint Inhibitors; Kidney Neoplasms; Lipids; Poly(ADP-ribose) Polymerase Inhibitors; Poly(ADP-ribose) Polymerases; Protein Kinase Inhibitors; Ribose

Glycogen accumulation is a highly consistent, distinguishable characteristic of clear cell renal cell carcinoma (ccRCC)

Topics: Carcinoma, Renal Cell; Cell Proliferation; Disease Progression; Gene Expression Regulation, Neoplastic; Glycogen; Glycogen Synthase; Humans; Kidney Neoplasms; Tumor Microenvironment

Metabolism reprogramming is a hallmark of many cancer types. We focused on clear cell renal carcinoma (ccRCC) which is characterized by its clear and glycogen-enriched cytoplasm with unknown reasons. The aim of this study was to identify the clinical significance, biological function, and molecular regulation of glycogen synthase 1 (GYS1) in ccRCC glycogen accumulation and tumor progression.

Topics: Animals; Carcinoma, Renal Cell; Cell Line, Tumor; Cell Proliferation; Disease Progression; Glycogen; Glycogen Synthase; Humans; Immunohistochemistry; Kidney Neoplasms; Male; Metabolome; Mice; Mice, Inbred BALB C; NF-kappa B; Prognosis; Signal Transduction

Topics: Biopsy, Needle; Carcinoma, Renal Cell; Cell Nucleus; Diagnosis, Differential; Glycogen; Humans; Intranuclear Inclusion Bodies; Kidney; Kidney Neoplasms; Male; Middle Aged; Thyroid Cancer, Papillary; Thyroid Neoplasms

Patients with von Hippel-Lindau (VHL) disease harbor a germline mutation in the VHL gene leading to the development of several tumor types including clear cell renal cell carcinoma (ccRCC). In addition, the VHL gene is inactivated in over 90% of sporadic ccRCC cases. 'Clear cell' tumors contain large, proliferating cells with 'clear cytoplasm', and a reduced number of cilia. VHL inactivation leads to the stabilization of hypoxia inducible factors 1a and 2a [HIF1a and HIF2a (HIF2a is also known as EPAS1)] with consequent up-regulation of specific target genes involved in cell proliferation, angiogenesis and erythropoiesis. A zebrafish model with a homozygous inactivation in the VHL gene (vhl(-/-)) recapitulates several aspects of the human disease, including development of highly vascular lesions in the brain and the retina and erythrocytosis. Here, we characterize for the first time the epithelial abnormalities present in the kidney of the vhl(-/-) zebrafish larvae as a first step in building a model of ccRCC in zebrafish. Our data show that the vhl(-/-) zebrafish kidney is characterized by an increased tubule diameter, disorganized cilia, the dramatic formation of cytoplasmic lipid vesicles, glycogen accumulation, aberrant cell proliferation and abnormal apoptosis. This phenotype of the vhl(-/-) pronephros is reminiscent of clear cell histology, indicating that the vhl(-/-) mutant zebrafish might serve as a model of early stage RCC. Treatment of vhl(-/-) zebrafish embryos with a small-molecule HIF2a inhibitor rescued the pronephric abnormalities, underscoring the value of the zebrafish model in drug discovery for treatment of VHL disease and ccRCC.

Topics: Animals; Apoptosis; Basic Helix-Loop-Helix Transcription Factors; Carcinoma, Renal Cell; Cell Proliferation; Cytoplasmic Vesicles; Embryonic Development; Glycogen; Humans; Kidney Neoplasms; Kidney Tubules; Larva; Neoplasm Staging; Phenotype; Pronephros; Tumor Suppressor Proteins; Zebrafish; Zebrafish Proteins

Activation of the PI3K/AKT/mTOR pathway is a crucial molecular event in human clear cell renal cell carcinoma (ccRCC), and is also upregulated in diabetic nephropathy. In diabetic rats metabolic changes affect the renal distal tubular epithelium and lead to glycogen-storing Armanni-Ebstein lesions (AEL), precursor lesions of RCC in the diabetes induced nephrocarcinogenesis model. These lesions resemble human sporadic clear cell tubules (CCT) and tumor cells of human ccRCC.Human sporadic CCT were examined in a collection of 324 nephrectomy specimen, in terms of morphologic, metabolic and molecular alterations, and compared to preneoplastic CCT and RCC developed in the rat following streptozotocin-induced diabetes or N-Nitrosomorpholine administration. Diabetic and non-diabetic rats were subjected to the dual PI3K/mTOR inhibitor, NVP/BEZ235.Human sporadic CCT could be detected in 17.3% of kidney specimens. Human and rat renal CCT display a strong induction of the PI3K/AKT/mTOR pathway and related metabolic alterations. Proteins involved in glycolysis and de novo lipogenesis were upregulated. In in vivo experiments, dual inhibition of PI3K and mTOR resulted in a reduction of proliferation of rat diabetes related CCT and increased autophagic activity.The present data indicate that human sporadic CCT exhibit a pattern of morphologic and metabolic alterations similar to preneoplastic lesions in the rat model. Activation of the PI3K/AKT/mTOR pathway in glycogenotic tubuli is a remarkable molecular event and suggests a preneoplastic character of these lesions also in humans.

Topics: Animals; Carcinoma, Renal Cell; Cell Line, Tumor; Cell Proliferation; Diabetes Mellitus, Experimental; Glycogen; Humans; Immunohistochemistry; Kidney Neoplasms; Male; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Rats; Rats, Inbred Lew; Signal Transduction; TOR Serine-Threonine Kinases

Topics: Animals; Basic Helix-Loop-Helix Transcription Factors; Carcinoma, Renal Cell; Gene Expression Regulation, Neoplastic; Glycogen; Humans; Kidney Neoplasms; Kidney Tubules

Renal cell carcinoma (RCC) is the most common primary cancer arising from the kidney in adults, with clear cell renal cell carcinoma (ccRCC) representing approximately 75% of all RCCs. Increased expression of the hypoxia-induced factors-1α (HIF1α) and HIF2α has been suggested as a pivotal step in ccRCC carcinogenesis, but this has not been thoroughly tested. Here, we report that expression of a constitutively activated form of HIF2α (P405A, P530A, and N851A, named as HIF2αM3) in the proximal tubules of mice is not sufficient to promote ccRCC by itself, nor does it enhance HIF1αM3 oncogenesis when coexpressed with constitutively active HIF1αM3. Neoplastic transformation in kidneys was not detected at up to 33 months of age, nor was increased expression of Ki67 (MKI67), γH2AX (H2AFX), or CD70 observed. Furthermore, the genome-wide transcriptome of the transgenic kidneys does not resemble human ccRCC. We conclude that a constitutively active HIF2α is not sufficient to cause neoplastic transformation of proximal tubules, arguing against the idea that HIF2α activation is critical for ccRCC tumorigenesis.

Topics: Animals; Basic Helix-Loop-Helix Transcription Factors; Carcinoma, Renal Cell; Cell Proliferation; Cell Transformation, Neoplastic; Gene Expression Regulation, Neoplastic; Glycogen; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; Kidney; Kidney Neoplasms; Kidney Tubules; Mice; Mice, Inbred C57BL; Mice, Transgenic; Mutation

Clear cell carcinoma (CCC) is a histologically distinct carcinoma subtype that arises in several organ systems and is marked by cytoplasmic clearing, attributed to abundant intracellular glycogen. Previously, transcription factor hepatocyte nuclear factor 1-beta (HNF1B) was identified as a biomarker of ovarian CCC. Here, we set out to explore more broadly the relation between HNF1B and carcinomas with clear cell histology. HNF1B expression, evaluated by immunohistochemistry, was significantly associated with clear cell histology across diverse gynecologic and renal carcinomas (P<0.001), as was hypomethylation of the HNF1B promoter (P<0.001). From microarray analysis, an empirically-derived HNF1B signature was significantly enriched for computationally-predicted targets (with HNF1 binding sites) (P<0.03), as well as genes associated with glycogen metabolism, including glucose-6-phophatase, and strikingly the blood clotting cascade, including fibrinogen, prothrombin and factor XIII. Enrichment of the clotting cascade was also evident in microarray data from ovarian CCC versus other histotypes (P<0.01), and HNF1B-associated prothrombin expression was verified by immunohistochemistry (P = 0.015). Finally, among gynecologic carcinomas with cytoplasmic clearing, HNF1B immunostaining was linked to a 3.0-fold increased risk of clinically-significant venous thrombosis (P = 0.043), and with a 2.3-fold increased risk (P = 0.011) in a combined gynecologic and renal carcinoma cohort. Our results define HNF1B as a broad marker of clear cell phenotype, and support a mechanistic link to glycogen accumulation and thrombosis, possibly reflecting (for gynecologic CCC) derivation from secretory endometrium. Our findings also implicate a novel mechanism of tumor-associated thrombosis (a major cause of cancer mortality), based on the direct production of clotting factors by cancer cells.

Topics: Adenocarcinoma, Clear Cell; Blood Coagulation; Blood Coagulation Factors; Carcinoma, Renal Cell; Computational Biology; DNA Methylation; Endometrial Neoplasms; Female; Gene Expression Regulation, Neoplastic; Glucose-6-Phosphatase; Glycogen; Hepatocyte Nuclear Factor 1-beta; Humans; Immunohistochemistry; Kidney Neoplasms; Oligonucleotide Array Sequence Analysis; Ovarian Neoplasms; Risk; Venous Thrombosis

Papillary renal cell carcinoma (PRCC) includes two different morphological subtypes. The differences of genetics and ultrastructure of the two subtypes have been rarely reported. Also, new biomarkers related to the diagnosis and prognosis of PRCC have still not been well elucidated. Immunohistochemistry, fluorescence in situ hybridization (FISH) and transmission electron microscopy were used systematically to determine the characteristics of 56 cases of PRCC and to reveal new diagnostic and prognostic information. Type 1 PRCC presented higher expression rates of EMA and CK7, whereas type 2 presented a higher expression rate of CD10. New immunohistochemical markers, including: p504s, PAX-2, PAX-8 and CA-IX showed extensive immunostaining in PRCC. We first revealed a distinct immunostaining pattern of CA-IX, which was located in multiple foci in PRCC. All tumors had at least one chromosomal aberration including loss of Y, gains of 7 or 17. Gain of chromosome 17 was common in type 1; losses of chromosome 18, 11 and 8 appeared in type 2. Ultrastructurally, glycogen granules and secondary lysosomes were seen in type 1, mitochondria and smooth endoplasmic reticulum were scattered in type 2. Tumor subtype, nuclear grade, TNM stage, clear cell renal cell carcinoma (CCRCC) component and sarcomatoid elements, metastasis, CAIX expression, losses of chromosome 18 and 8 were related to poor outcome of PRCC. We conclude that the two subtypes of PRCC originate from different renal cells, and arise from partially common genetic pathways. EMA, CK7, CD10, p504s, PAX-2, PAX-8 and CA-IX are helpful markers in the differential diagnosis of PRCC. CA-IX expression, losses of chromosome 18 and 8 are new prognostic factors of PRCC.

Topics: Adult; Aged; Aged, 80 and over; Antigens, Neoplasm; Biomarkers, Tumor; Carbonic Anhydrase IX; Carbonic Anhydrases; Carcinoma, Renal Cell; Chromosome Aberrations; Endoplasmic Reticulum, Smooth; Female; Glycogen; Humans; In Situ Hybridization, Fluorescence; Kaplan-Meier Estimate; Kidney Neoplasms; Lysosomes; Male; Microscopy, Electron, Transmission; Middle Aged; Mitochondria; Prognosis; Survival Rate

Clear cell (CRCC) and papillary (PRCC) renal cell carcinomas (RCC) are the two most frequent subtypes of RCC. In this study, we studied RCC which displayed a hybrid morphology with areas of PRCC and CRCC or which contained papillary structures with clear cell changes (CCC). Consecutive cases of RCC collected over a 12-year period were reviewed to identify RCC with papillary structures and a possible admixture between CRCC and non-oncocytic PRCC. Special stains for glycogen and immunostaining for cytokeratin 7 were applied to sections containing both areas of classical PRCC and PRCC with CCC. Of the total of 541 RCC retrieved, there were 68 non-oncocytic RCC having papillary structures that could be grouped into: (a) group 1 (15 cases), CRCC with areas of papillary formation; (b) group 2a (9 cases), PRCC with extensive CCC with areas of foamy epithelial cells or macrophages; (c) group 2b (18 cases), RCC with areas of classical PRCC with focal CCC; and (d) group 3 (26 cases), RCC with features of groups 2a and 2b and containing areas of classical CRCC. There was a high rate (12/68) of sarcomatous transformation in the study cases. Groups 2 and 3 were associated with a higher rate of vascular invasion, distant metastasis, and mortality than classical PRCC and a higher rate of lymph node metastasis than CRCC. Our study identifies two groups of RCC (referred to as groups 2 and 3) that exhibit characteristic cytohistopathologic hybrid features that set them apart from classical RCC. This type of hybrid tumor seems to be associated with a more aggressive biologic behavior, and its recognition may facilitate the classification of RCC with ambiguous morphology.

Topics: Adenocarcinoma, Clear Cell; Adenocarcinoma, Papillary; Biomarkers, Tumor; Canada; Carcinoma, Renal Cell; Glycogen; Humans; Immunoenzyme Techniques; Keratin-7; Kidney Neoplasms; Survival Rate

Clear cell tumour or "sugar tumour" of the lung is a rare primary neoplasm with unique histologic and electron microscopic features that may resemble those of metastatic renal cell carcinoma. An immunohistochemical studies are useful in a differential diagnosis these tumours: HMB45 in combination with a panel of various antibodies. The authors present a benign clear cell tumour of the lung, diagnosed on the base of its morphological, immunohistochemical and ultrastructural features.

Topics: Adenocarcinoma, Clear Cell; Adult; Antigens, Neoplasm; Carcinoma, Renal Cell; Cytoplasm; Diagnosis, Differential; Glycogen; Humans; Immunohistochemistry; Lung Neoplasms; Male; Melanoma-Specific Antigens; Neoplasm Proteins

Clear cell adenocarcinoma of salivary glands (CCASG) is a relatively rare tumor, composed entirely of clear cells of putative ductal origin. It bears striking morphologic similarities to renal cell carcinoma (RCC) of clear cell type on hematoxylin and eosin stains. Differentiation between CCASG and metastatic RCC to the salivary glands has been considered problematic or even impossible on morphologic grounds. We examined three cases of CCASG and 12 cases of RCC (6 primary and 6 metastatic) by hematoxylin and eosin staining, immunohistochemistry, and electron microscopy. Two distinctive immunohistochemical and ultrastructural patterns emerged from this analysis. CCASG showed positivity for high molecular weight cytokeratin and carcinoembryonic antigen and ultrastructurally showed prominent squamoid differentiation, glycogen pools, and absence of lipid. In contrast, RCC was characterized by positivity for vimentin and complete absence of staining for high molecular weight cytokeratin and carcinoembryonic antigen. On ultrastructural studies, RCC lacked any squamoid differentiation, and the tumor cells contained abundant cytoplasmic lipid in addition to glycogen. Thus, based on the consistent differences on the immunohistochemical staining patterns and their characteristic subcellular morphology, CCASG and RCC can be distinguished on pathologic evaluation. The different direction of differentiation of the cells in CCASG and RCC (i.e., ductal in the former and renal tubular and mesodermal in the latter) results in their distinctive immunophenotypical and ultrastructural features.

Topics: Adenocarcinoma, Clear Cell; Adult; Aged; Carcinoembryonic Antigen; Carcinoma, Renal Cell; Diagnosis, Differential; Female; Glycogen; Humans; Immunoenzyme Techniques; Keratins; Kidney Neoplasms; Lipids; Male; Middle Aged; Salivary Gland Neoplasms; Vimentin

Renal clear cell tubules and clear/acidophilic cell tumors were induced in male Sprague-Dawley rats by 7 weeks oral administration (stop model) of N-nitrosomorpholine (NNM) at a concentration of 12 mg/100 ml in the drinking water. Twelve, 23 and 34 weeks after withdrawal of NNM serial cryostat sections of the kidneys were histochemically analyzed for the following parameters: glucose transporter proteins (GLUT1, GLUT2), glycogen content and the activities of glycogen synthase (SYN), glycogen phosphorylase (PHO), glucose-6-phosphatase (G6Pase), glucose-6-phosphate dehydrogenase (G6PDH), hexokinase (HK), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), pyruvate kinase (PK), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), alkaline phosphatase (ALP), acid phosphatase (ACP) and gamma-glutamyltransferase (GGT). Clear cell (glycogenotic) tubules first appeared at 23 weeks, and clear/acidophilic cell tumors at 34 weeks after withdrawal of the carcinogen. G6Pase, ALP, GGT and GLUT2 were absent in clear cell tubules, clear/acidophilic cell tubules, and clear/acidophilic cell tumors indicating a sequential origin of all these types of lesions from the collecting duct system, in line with previous morphological findings. In comparison to the collecting duct epithelium, glycogenotic tubules demonstrated an increased activity of PHO and reduced activities of glycolytic and mitochondrial enzymes, which were accompanied by a strongly reduced expression of GLUT1. Moderately increased activities of glycolytic and mitochondrial enzymes were observed in the clear cells of clear/acidophilic cell tubules and tumors compared with those in glycogenotic tubules. They had slightly increased activities of the glycolytic enzymes GAPDH and PK compared with normal collecting duct epithelium, while most of them were nearly lacking in GLUT1. Our findings suggest that glycogen storage is not due to an increased uptake of glucose from the blood, but results from a disturbance in intracellular flux of metabolites. The development of clear cell tubules from the normal collecting duct epithelium is accompanied by a markedly decreased expression of GLUT1 along with a reduction in glycolytic and mitochondrial enzymes. This reduction of enzyme activities is replaced by an increase in enzyme activities in clear/acidophilic cell tumors indicating a fundamental shift in carbohydrate metabolism during progression from preneoplastic to neoplastic lesions.

Topics: Animals; Carcinoma, Renal Cell; Glycogen; Immunohistochemistry; Kidney Neoplasms; Kidney Tubules, Collecting; Male; Monosaccharide Transport Proteins; Nitrosamines; Rats; Rats, Sprague-Dawley

The study was concerned with evaluating the quantitative histochemical and histoenzymatic peculiarities of renal cell carcinoma of various grade of malignancy. It involved measuring levels of lipids, glycogen, protein, nucleic acids and sugar as well as the activities of dehydrogenases, phosphatases, non-specific esterase and lipase in tumor cells. Grade I neoplasms were found to be associated with low proliferative activity matched by relatively high energy production thus causing excessive synthesis of lipids and glycogen to occur. Higher cell proliferative activity in grade II and III tumors accounts for a significantly lower level of lipids and glycogen. Those metabolic peculiarities appeared to correlate with prognosis.

Topics: Carcinoma, Renal Cell; Esterases; Glycogen; Histocytochemistry; Kidney; Kidney Neoplasms; Lipase; Lipids; Nucleic Acids; Oxidoreductases; Phosphoric Monoester Hydrolases; Prognosis; Proteins

This paper reports on 32 chromophobe cell renal carcinomas observed in 697 renal cell cancers (RCC) of adults (peak in the sixth decade of life). The chromophobe cell-type differs from other types of RCC macroscopically, the cut-surface being predominantly of grey-beige colour. Histologically, there are two variants: one is the typical (light) variant (n = 22) and the other is eosinophilic (n = 10). Both variants have in common (a) reaction of the cytoplasm with Hale's acid iron colloid; (b) electron microscopic detection of cytoplasmic microvesicles (150-300 nm), frequently with 'inner vesicles', and (c) low glycogen content in comparison with the clear cell carcinoma. Immunocytochemical investigations on the intermediate filaments show a positive reaction for cytokeratins No. 18 (uniformly) and Nos. 7 and 19 (to varying extents) for both variants, whereas vimentin was not found in any of these carcinomas, in contrast to the clear-cell type. The cytomorphological grading revealed predominantly G II tumours. A lymph node metastasis was found in one patient. On the basis of the mortality curves determined, the prognosis for patients with chromophobe cell carcinomas is more favourable than that of the clear-cell type. In terms of differential diagnosis, on the one hand, the typical (light) variant of the chromophobe cell RCC must be delimited from the clear-cell RCC, and on the other hand, the eosinophilic variant must be distinguished from the chromophilic or 'granular' RCC. Microscopic, histological, histochemical, electron microscopic, and intermediate filament analysis results document that the chromophobe cell type of RCC is a distinct entity. The implications for the nomenclature of RCC, especially with regard to the 'granular' type, are discussed.

Topics: Adult; Aged; Carcinoma, Renal Cell; Eosine Yellowish-(YS); Female; Glycogen; Humans; Intermediate Filaments; Keratins; Kidney Neoplasms; Male; Microscopy, Electron; Middle Aged; Prognosis; Staining and Labeling; Vacuoles; Vimentin

112 cases of renal cell carcinoma were studied histologically and histochemically. Variants of renal cell carcinoma were found to have certain histochemical peculiarities: accumulation of neutral fat and cholesterol esters in the clear-cell tumor variant and bound lipids and proteins in the tumors of granular cell, sarcoma-like and glandular variants. These characteristics become less distinct with decrease of differentiation degree of tumor cells. These features can be used for differential diagnosis of renal cell carcinoma.

Topics: Adult; Aged; Carcinoma, Renal Cell; Cholesterol; Glycogen; Histocytochemistry; Humans; Kidney Neoplasms; Lipid Metabolism; Middle Aged; Neoplasm Proteins; Sulfhydryl Compounds