• Gemcitabine
• Deoxycytidine/analogs & derivatives
• Deoxycytidine/pharmacology
• Deoxycytidine/therapeutic use
• Humans
• TNF-Related Apoptosis-Inducing Ligand/pharmacology
• TNF-Related Apoptosis-Inducing Ligand/metabolism
• Pancreatic Neoplasms/pathology
• Pancreatic Neoplasms/drug therapy
• Pancreatic Neoplasms/metabolism
• Mesenchymal Stem Cells/metabolism
• Mesenchymal Stem Cells/drug effects
• Animals
• Cell Line, Tumor
• Mice
• Carcinoma, Pancreatic Ductal/pathology
• Carcinoma, Pancreatic Ductal/drug therapy
• Carcinoma, Pancreatic Ductal/metabolism
• Carcinoma, Pancreatic Ductal/therapy
• Xenograft Model Antitumor Assays
• Cancer-Associated Fibroblasts/metabolism
• Cancer-Associated Fibroblasts/drug effects
• Cancer-Associated Fibroblasts/pathology
• Adenocarcinoma/pathology
• Adenocarcinoma/drug therapy
• Adenocarcinoma/metabolism

• LC3
• Tumor growth
• adenomatous polyp
• caspase
• colon
• cytokine

To investigate the effect of the casein kinase 2 interacting protein 1 (CKIP-1) on the apoptosis of the intestinal type of gastric cancer (GC).

The levels of CKIP-1 protein and the rates of apoptosis were measured in tissue samples of the intestinal type of GC and human GC cell lines. The rate of apoptosis and the protein levels of B cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), cleaved cysteinyl aspartate specific protease 3 (cleaved caspase-3), cleaved caspase-9, rat sarcoma (Ras), extracellular signal-regulated kinase 1 and 2 (ERK1/2) and phosphorylated extracellular signal-regulated kinase 1 and 2 (p-ERK1/2) were analysed in SGC7901 cells expressing CKIP-1 short hairpin RNA (shRNA; knockdown) and SGC7901 cells overexpressing CKIP-1.

The levels of CKIP-1 protein were significantly lower in the intestinal type of GC tissues compared with the samples of intestinal metaplasia. Both the levels of CKIP-1 protein and the levels of apoptosis decreased gradually with decreasing cell differentiation in the intestinal type of GC tissue and cell lines; and they were positively correlated. In the CKIP-1 shRNA group, the rate of apoptosis and the levels of Bax, cleaved caspase-3 and cleaved caspase-9 were decreased; and the levels of Bcl-2, Ras and the ratio of p-ERK/ERK were increased, compared with the control group. Opposite results were observed in the CKIP-1 overexpression group.

High levels of CKIP-1 protein may promote apoptosis in the intestinal type of GC, possibly via the downregulation of the Ras/ERK signalling pathway.

• Casein kinase 2 interacting protein 1
• apoptosis
• intestinal type of gastric cancer

The cytotoxic and apoptotic effects of turmeric (Curcuma longa) on colon cancer have been well documented but specific structural modifications of curcumin have been shown to possess greater growth-suppressive potential on colon cancer than curcumin. Therefore, the aim of this study is to identify the anti-cancer properties of curcumin analogue-MS13, a diarylpentanoid on the cytotoxicity, anti-proliferative and apoptotic activity of primary (SW480) and metastatic (SW620) human colon cancer cells. A cell viability assay showed that MS13 has greater cytotoxicity effect on SW480 (EC₅₀: 7.5 ± 2.8 µM) and SW620 (EC₅₀: 5.7 ± 2.4 µM) compared to curcumin (SW480, EC₅₀: 30.6 ± 1.4 µM) and SW620, EC₅₀: 26.8 ± 2.1 µM). Treatment with MS13 at two different doses 1X EC₅₀ and 2X EC₅₀ suppressed the colon cancer cells growth with lower cytotoxicity against normal cells. A greater anti-proliferative effect was also observed in MS13 treated colon cancer cells compared to curcumin at 48 and 72 h. Subsequent analysis on the induction of apoptosis showed that MS13 treated cells exhibited morphological features associated with apoptosis. The findings are also consistent with cellular apoptotic activities shown by increased caspase-3 activity and decreased Bcl-2 protein level in both colon cancer cell lines. In conclusion, MS13 able to suppress colon cancer cell growth by inhibiting cell proliferation and induce apoptosis in primary and metastatic human colon cancer cells.

• 1,5-bis(4-hydroxy-3-methoxyphenyl)-1,4-pentadiene-3-one
• Bcl-2
• Caspase-3
• apoptosis
• cell proliferation
• colon cancer
• curcumin analogue
• diarylpentanoid (DAP)

• colitis
• colon
• inflammatory bowel diseases

• apoptosis
• cell death
• colorectal cancer
• curcumin

• Cell Line, Tumor
• Cell Proliferation/drug effects
• Cell Survival/drug effects
• Colorectal Neoplasms/drug therapy
• Colorectal Neoplasms/genetics
• Curcumin/pharmacology
• Gene Expression Regulation, Neoplastic/drug effects
• Gene Regulatory Networks/drug effects
• Humans
• Signal Transduction/drug effects

• Cell proliferation
• Ki-67 marker
• angiogenesis
• apoptosis
• colorectal neoplasms

• Adult
• Aged
• Apoptosis/genetics
• Biomarkers, Tumor/genetics
• Cell Proliferation/genetics
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/pathology
• Disease-Free Survival
• Endoglin/genetics
• Female
• Follow-Up Studies
• Humans
• Ki-67 Antigen/genetics
• Male
• Middle Aged
• Neovascularization, Pathologic/epidemiology
• Neovascularization, Pathologic/genetics
• Neovascularization, Pathologic/pathology
• Prognosis

Neurotoxicity is a major side effect of platinum derivatives both during and after treatment. In the absence of effective pharmacological compounds, the opportunity to identify safe adjuvant treatments among medicinal plants seems appropriate. Astragali radix is an adaptogenic herbal product recently analyzed in platinum-treated cancer patients. With the aim of evaluating the anti-neuropathic profile of Astragali radix, a previously characterized aqueous (Aqu) and two hydroalcoholic (20%HA and 50%HA) extracts were tested in a rat model of oxaliplatin-induced neuropathy. Repeated administrations significantly reduced oxaliplatin-dependent hypersensitivity with 50%HA, the most effective, fully preventing mechanical and thermal hypersensitivity. Ex vivo, 50%HA reduced morphometric and molecular alterations induced by oxaliplatin in peripheral nerve and dorsal-root-ganglia. In the spinal cord and in brain areas, 50%HA significantly decreased activation of microglia and astrocytes. Furthermore, 50%HA prevented the nephro- and hepato-toxicity induced by the anticancer drug. The protective effect of 50%HA did not alter oxaliplatin-induced apoptosis in colon tumors of Pirc rats, an Apc-driven model of colon carcinogenesis. The hydroalcoholic extract (50%HA) of Astragali radix relieves pain and promotes the rescue mechanisms that protect nervous tissue from the damages triggering chronic pain. A safe profile strongly suggests the usefulness of this natural product in oxaliplatin-induced neuropathy.

Apc-mutated Pirc rats, spontaneously developing intestinal tumours, are resistant to 1,2-dimethylhydrazine- (DMH-) induced colon apoptosis. To understand this phenomenon, we analyzed the expression of genotoxic stress-related genes Mgmt, Gsta1, and Gstp1 in the colon of wt and Pirc rats in basal conditions and 24 h after DMH; plasmatic oxidant/antioxidant status was also evaluated. After DMH, Mgmt expression was increased in both genotypes but significantly only in wt rats; Gsta1 expression was significantly increased in both genotypes. Gstp1 expression did not vary after DMH but was lower in Pirc rats. Moreover, for each genotype, we studied by microarray technique whole gene expression profile after DMH. By unsupervised cluster analysis, 28 genes were differentially modulated between the two genotypes. Among them were interferon-induced genes Irf7, Oas1a, Oasl2, and Isg15 and the transcription factor Taf6l, overexpressed in DMH-treated wt rats and unchanged in Pirc rats. RT-PCR confirmed their overexpression in DMH-treated wt rats and showed a slighter variation in DMH-treated Pirc rats. Taken together, despite a blunted induction of Irf7, Oas1a, and Mgmt, defective apoptosis in Pirc rats 24 h after DMH is not mirrored by major differences in gene expression compared with wt rats.

Colon cancer is caused by multiple genomic alterations which lead to genomic instability (GI). GI appears in molecular pathways of microsatellite instability (MSI) and chromosomal instability (CIN) with clinically observed case shares of about 15–20% and 80–85%. Radiation enhances the colon cancer risk by inducing GI, but little is known about different outcomes for MSI and CIN. Computer-based modelling can facilitate the understanding of the phenomena named above. Comprehensive biological models, which combine the two main molecular pathways to colon cancer, are fitted to incidence data of Japanese a-bomb survivors. The preferred model is selected according to statistical criteria and biological plausibility. Imprints of cell-based processes in the succession from adenoma to carcinoma are identified by the model from age dependences and secular trends of the incidence data. Model parameters show remarkable compliance with mutation rates and growth rates for adenoma, which has been reported over the last fifteen years. Model results suggest that CIN begins during fission of intestinal crypts. Chromosomal aberrations are generated at a markedly elevated rate which favors the accelerated growth of premalignant adenoma. Possibly driven by a trend of Westernization in the Japanese diet, incidence rates for the CIN pathway increased notably in subsequent birth cohorts, whereas rates pertaining to MSI remained constant. An imbalance between number of CIN and MSI cases began to emerge in the 1980s, whereas in previous decades the number of cases was almost equal. The CIN pathway exhibits a strong radio-sensitivity, probably more intensive in men. Among young birth cohorts of both sexes the excess absolute radiation risk related to CIN is larger by an order of magnitude compared to the MSI-related risk. Observance of pathway-specific risks improves the determination of the probability of causation for radiation-induced colon cancer in individual patients, if their exposure histories are known.

• Adenoma/genetics
• Carcinoma/genetics
• Chromosome Aberrations/radiation effects
• Colonic Neoplasms/genetics
• Colonic Neoplasms/pathology
• Female
• Gamma Rays
• Genomic Instability/genetics
• Genomic Instability/radiation effects
• Humans
• Male
• Models, Biological
• Neoplasms, Radiation-Induced/genetics
• Sex Characteristics

AIM: To evaluate the expression of Bcl-xL, Bak, and Bax proteins in correlation with particular clinico-histopathological parameters, including tumor invasion front, in patients with colorectal cancer.

METHODS: The expression of these proteins was evaluated with the use of the immunohistochemical method in 50 primary tumors.

RESULTS: According to observations, a low expression of Bax and Bak proteins is related to the localization of the tumor in the rectum (P < 0.05 and P < 0.05 respectively), which may explain an increased incidence of colorectal cancer in this area. A positive expression of Bax protein also correlates with the presence of cancer cell infiltration to lymph and blood vessels (P < 0.05), which may suggest the participation of this protein in the early stages of colorectal cancer progression. Moreover, a positive expression of Bcl-xL protein correlated with a positive expression of Bak protein. This may suggest a greater participation of Bcl-xL protein in the inhibition of the proapoptotic Bak protein, but not the Bax protein.

CONCLUSION: Bax protein is probably very significant in the cancerogenesis mechanism in the large intestine.

• Bak
• Bax
• Bcl-xL
• Cancer cell infiltration
• Colorectal cancer

• Biomarkers, Tumor/analysis
• Colorectal Neoplasms/chemistry
• Colorectal Neoplasms/pathology
• Disease Progression
• Female
• Humans
• Immunohistochemistry
• Male
• Neoplasm Invasiveness
• bcl-2 Homologous Antagonist-Killer Protein/analysis
• bcl-2-Associated X Protein/analysis
• bcl-X Protein/analysis

• crypt morphogenesis
• growth dynamics
• stem cells
• tissue mechanics

Alterations to apoptosis are a common occurrence in human tumours. The aim of our study was to determine the influence of apoptotic variations on the carcinogenesis and prognosis of colorectal carcinomas (CRCs).

A TUNEL assay was performed on archival material from 103 colorectal carcinomas, 26 adenomas and 20 samples of normal epithelia.

The number of apoptotic cells was higher in CRCs (1.09 ± 0.13) than in adenomas (0.38 ± 0.23, p = 0.059) and normal epithelium (0.06 ± 0.04, p = 0.001). In addition, the apoptotic index (AI) was greater in metastatic disease (stage IV) than in other stages (p = 0.017). No relationship was found between apoptotic rates and age, gender or tumour grade. However, patients with tumours that showed higher AI values had a significantly lower disease-free survival (DFS) and overall survival (OS) than those with tumours that had lower AIs (p = 0.020 and p = 0.027). In a multivariate Cox proportional hazards model, AI remained a significant independent predictor of survival.

We conclude that disregulated apoptosis is an important event during CRC development and progression. Higher AIs are associated with more aggressive tumours and a poorer prognosis for patients with CRC.

• Adult
• Aging/pathology
• Apoptosis
• Carcinogenesis
• Cell Proliferation
• Child
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/pathology
• Colorectal Neoplasms/physiopathology
• Female
• Gene Expression Profiling
• Humans
• Intestinal Mucosa/pathology
• Male

• tumor differentiation factor
• receptor
• differentiation
• mass spectrometry

• Animals
• Cell Differentiation/physiology
• Humans
• Neoplasms/metabolism
• Neoplasms/pathology
• Nerve Tissue Proteins/metabolism
• Pituitary Gland/metabolism

FAS/FASL altered expression may cause tumor protecting immunomodulation, with a direct impact on patient prognosis. FAS expression was studied in 60 squamous cell carcinomas of the oral cavity. FAS expression did not show a significant association with tumor histopathological characteristics, but was significantly associated with lymph node positivity. FAS expression was significantly associated with disease specific death and negative FAS expression was an independent risk factor, increasing risk 4 times when compared to positive expression. When FAS and FASL expression results were combined, we were able to define high, intermediate and low risk profiles. Disease-free and disease-specific survival were significantly correlated with FAS/FASL expression profiles. The high risk category was an independent marker for earlier disease relapse and disease-specific death, with approximately 4- and 6-fold increased risk, respectively, when compared to the low risk profile. Risk profiles based on FAS/FASL expression showed that high risk was significantly associated with increased disease relapse and death, as well as shorter disease-free or disease-specific survival. This categorization, added to patient clinical data, may facilitate the choice of therapy, minimizing treatment failure and increasing disease control.

The primary aim was to determine the prognostic significance of apoptosis in colorectal tumour cells and tumour-associated stroma. A secondary aim was to determine whether apoptosis was related to immune surveillance.

Immunohistochemistry was performed using monoclonal antibodies recognising cleaved caspase-3 (CC3), cleaved poly (ADP-ribose) polymerase (PARP), p53, Bcl2, MHC-II, B cells (CD16), macrophages (CD68) and T cells (CD3), on a tissue microarray of 462 colorectal tumours.

Kaplan–Meier analysis demonstrated that patients with high expression of CC3 in the tumour or CC3 or cleaved PARP in tumour-associated stroma have a good prognosis. This suggests that tumour stroma is promoting tumourigenesis and that high levels of death within the stroma breaks this link. CC3 levels in the tumour correlated with cleaved PARP and MHC-II expression but not with CD16, CD68, CD3, p53 or Bcl2 expression. CC3 levels on tumour-associated stroma also correlated with cleaved PARP and MHC-II expression but not with CD16, CD68, CD3, p53 or Bcl2 expression. Tumour cells express MHC-II in response to IFN-γ, suggesting that this may be one of the initiators of apoptosis within the good prognosis tumours. Although 73% of the MHC-II-positive tumour had high levels of apoptosis, many tumours had high levels of apoptosis in the absence of MHC-II, implying that this is only one of many causes of apoptosis within tumours. On multivariate analysis, using Cox's proportional hazards model, tumour stage, vascular invasion and expression of CC3 in tumour-associated stroma were shown to be independent markers of prognosis.

This study shows that a high level of apoptosis within colorectal tumour-associated stroma is an independent marker of good prognosis.

The discovery of microRNA, a group of regulatory short RNA fragments, has added a new dimension to the diagnosis and management of neoplastic diseases. Differential expression of microRNA in a unique pattern in a wide range of tumor types enables researches to develop a microRNA-based assay for source identification of metastatic disease of unknown origin. This is just one example of many microRNA-based cancer diagnostic and prognostic assays in various phases of clinical research.

Since colorectal cancer (CRC) is a phenotypic expression of multiple molecular pathways including chromosomal instability (CIN), micro-satellite instability (MIS) and CpG islands promoter hypermethylation (CIMP), there is no one-unique pattern of microRNA expression expected in this disease and indeed, there are multiple reports published, describing different patterns of microRNA expression in CRC.

The scope of this manuscript is to provide a comprehensive review of the scientific literature describing the dysregulation of and the potential role for microRNA in the management of CRC. A Pubmed search was conducted using the following MeSH terms, "microRNA" and "colorectal cancer". Of the 493 publications screened, there were 57 papers describing dysregulation of microRNA in CRC.

• colorectal cancer
• microRNA

• Antibodies, Neoplasm/immunology
• Apoptosis/drug effects
• CASP8 and FADD-Like Apoptosis Regulating Protein/metabolism
• Caspase 8/metabolism
• Cell Line, Tumor
• Colonic Neoplasms/enzymology
• Colonic Neoplasms/pathology
• Death Domain Receptor Signaling Adaptor Proteins/metabolism
• Enzyme Activation/drug effects
• Humans
• Models, Biological
• Phosphatidylinositol 3-Kinases/metabolism
• Phosphoinositide-3 Kinase Inhibitors
• Pyrimidines/pharmacology
• Pyrroles/pharmacology
• Receptor, IGF Type 1/antagonists & inhibitors
• Receptor, IGF Type 1/metabolism
• Receptors, TNF-Related Apoptosis-Inducing Ligand/immunology
• Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism
• Recombinant Proteins/pharmacology
• Signal Transduction/drug effects
• TNF-Related Apoptosis-Inducing Ligand/pharmacology

• Animals
• Apoptosis
• Cardiolipins/metabolism
• Colon/metabolism
• Colon/pathology
• Crosses, Genetic
• Dietary Fats, Unsaturated/metabolism
• Fish Oils/metabolism
• Genotype
• Glutathione Peroxidase/metabolism
• Mice
• Mice, Inbred C57BL
• Mitochondria/metabolism
• Oxidative Stress
• Oxygen Consumption
• Phospholipid Hydroperoxide Glutathione Peroxidase
• Protons

• R01 CA059034 NCI NIH HHS
• CA59034 NCI NIH HHS
• R01 CA129444-04 NCI NIH HHS
• CA129444 NCI NIH HHS
• P30 ES009106 NIEHS NIH HHS
• R01 CA129444 NCI NIH HHS
• P30ES09106 NIEHS NIH HHS
• R01 CA059034-18 NCI NIH HHS

Fas Ligand (FasL) expression by cancer cells may contribute to tumour immune escape via the Fas counterattack against tumour-infiltrating lymphocytes (TILs). Whether this plays a role in colorectal carcinogenesis in Lynch syndrome was examined studying FasL expression, tumour cell apoptosis and number of TILs in colorectal neoplasms from Lynch syndrome patients (50 adenomas, 20 carcinomas) compared with sporadic cases (69 adenomas, 52 carcinomas). FasL expression was observed in 94% of Lynch syndrome adenomas and in all carcinomas. FasL expression patterns and apoptotic indices were similar in Lynch syndrome-associated neoplasms and sporadic cases. The number of TILs was higher in Lynch syndrome neoplasms than in sporadic cases. There were no correlations between FasL expression and tumour cell apoptosis or number of TILs in Lynch syndrome-associated neoplasms. So, FasL expression is an early event in Lynch syndrome and sporadic colorectal carcinogenesis, but not related to TIL number. Taken together, our data do not support a role for the Fas counterattack in colorectal carcinogenesis in Lynch syndrome.

Among diet components, some fatty acids are known to affect several stages of colon carcinogenesis, whereas others are probably helpful in preventing tumors. In light of this, our aim was to determine the composition of fatty acids and the possible correlation with apoptosis in human colon carcinoma specimens at different Duke's stages and to evaluate the effect of enriching human colon cancer cell line with the possible reduced fatty acid(s). Specimens of carcinoma were compared with the corresponding non-neoplastic mucosa: a significant decrease of arachidonic acid, PPARα, Bad, and Bax and a significant increase of COX-2, Bcl-2, and pBad were found. The importance of arachidonic acid in apoptosis was demonstrated by enriching a Caco-2 cell line with this fatty acid. It induced apoptosis in a dose- and time-dependent manner via induction of PPARα that, in turn, decreased COX-2. In conclusion, the reduced content of arachidonic acid is likely related to carcinogenic process decreasing the susceptibility of cancer cells to apoptosis.

• Adult
• Aged
• Aged, 80 and over
• Apoptosis
• Cell Proliferation
• Colon/pathology
• Colonic Polyps/pathology
• Demography
• Endoscopy
• Female
• Humans
• Kinetics
• Male
• Middle Aged

• Adult
• Age Factors
• Aged
• Antineoplastic Combined Chemotherapy Protocols/therapeutic use
• Apoptosis/drug effects
• Biomarkers, Tumor/metabolism
• Caspase 3/metabolism
• Chemotherapy, Adjuvant
• Colonic Neoplasms/drug therapy
• Colonic Neoplasms/enzymology
• Colonic Neoplasms/pathology
• Disease-Free Survival
• Female
• Fluorouracil/administration & dosage
• Humans
• Male
• Middle Aged
• Neoplasm Staging
• Odds Ratio
• Predictive Value of Tests
• Proportional Hazards Models
• Prospective Studies
• Recurrence
• Risk Assessment
• Risk Factors
• Sex Factors
• Time Factors
• Treatment Outcome

• Adenocarcinoma/metabolism
• Adenocarcinoma/pathology
• Aged
• Apoptosis
• Cell Proliferation
• Colorectal Neoplasms/blood
• Colorectal Neoplasms/pathology
• Cytokines/blood
• Female
• Humans
• Interferon-gamma/blood
• Interleukin-10/blood
• Ki-67 Antigen/metabolism
• Male
• Neoplasm Invasiveness/pathology
• Survival Rate
• Tumor Necrosis Factor-alpha/metabolism

• Base Pair Mismatch/genetics
• Chromosomal Instability/genetics
• Colorectal Neoplasms/genetics
• Gene Silencing
• Genes, Neoplasm/genetics
• Genomic Instability
• Humans
• Immunohistochemistry/methods
• Microsatellite Repeats/genetics
• Polymerase Chain Reaction/methods
• Prognosis

• Adenocarcinoma/genetics
• Apoptosis/genetics
• Biomarkers, Tumor/analysis
• Cell Transformation, Neoplastic
• Colonic Neoplasms/genetics
• Electron Transport Complex IV/biosynthesis
• Electron Transport Complex IV/genetics
• Gene Expression Profiling
• Humans
• Immunohistochemistry
• Intestinal Mucosa/pathology
• Risk Assessment

• CA23074 NCI NIH HHS
• CA72008 NCI NIH HHS
• P50CA95060-01 NCI NIH HHS

• Adenoma/prevention & control
• Anti-Inflammatory Agents, Non-Steroidal/administration & dosage
• Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
• Aspirin/administration & dosage
• Aspirin/therapeutic use
• Calcium/administration & dosage
• Calcium/therapeutic use
• Calcium, Dietary/administration & dosage
• Calcium, Dietary/therapeutic use
• Colorectal Neoplasms/prevention & control
• Drug Synergism
• Female
• Humans
• Male
• Middle Aged
• Multicenter Studies as Topic
• Randomized Controlled Trials as Topic

• R01 CA059005 NCI NIH HHS

• Apoptosis/physiology
• Apoptosis Regulatory Proteins
• Biomarkers, Tumor/biosynthesis
• Biomarkers, Tumor/metabolism
• Carcinoma, Squamous Cell/metabolism
• Carcinoma, Squamous Cell/pathology
• Cell Growth Processes/physiology
• Cervix Uteri/metabolism
• Fas Ligand Protein
• Female
• Humans
• Immunohistochemistry
• Ki-67 Antigen/metabolism
• Membrane Glycoproteins/biosynthesis
• Membrane Glycoproteins/metabolism
• Neoplasm Staging
• Receptors, TNF-Related Apoptosis-Inducing Ligand
• Receptors, Tumor Necrosis Factor/biosynthesis
• Receptors, Tumor Necrosis Factor/metabolism
• TNF-Related Apoptosis-Inducing Ligand
• Tumor Necrosis Factor-alpha/biosynthesis
• Tumor Necrosis Factor-alpha/metabolism
• Uterine Cervical Neoplasms/metabolism
• Uterine Cervical Neoplasms/pathology
• fas Receptor/biosynthesis
• fas Receptor/metabolism
• Uterine Cervical Dysplasia/metabolism
• Uterine Cervical Dysplasia/pathology

• Adenocarcinoma/diagnosis
• Adenocarcinoma/enzymology
• Adenocarcinoma/pathology
• Adult
• Aged
• Aged, 80 and over
• Case-Control Studies
• Colorectal Neoplasms/diagnosis
• Colorectal Neoplasms/enzymology
• Colorectal Neoplasms/pathology
• Feces/enzymology
• Female
• Humans
• Male
• Middle Aged
• Sphingomyelin Phosphodiesterase/isolation & purification
• Sphingomyelin Phosphodiesterase/metabolism