Neoplasms

Urinary Tract, Sexual Organs, and Pregnancy Conditions

All Conditions

Symptoms and General Pathology

Prostatic Neoplasms

Hyperplasia

Genital Neoplasms, Male

Urogenital Neoplasms

Genital Diseases

Genital Diseases, Male

Urogenital Diseases

Prostatic Diseases

Male Urogenital Diseases

10 diagnosed men in age 60 - 90 with Prostate Cancer

Nina Kucherski, MD

Yihia Johari, MD

Early detection of prostrate cancer and development of metastases. The research will attempt to match the SCM test (structuredness of the cytoplasmic matrix) in lymphocytes as an early cancer detection test using Florescent Activated Cell Sorting (FACS) as a replacement for the CellScan instrument. The test is based on measurement of cellular changes in response to the specific prostate antigen, PSA.

Early Detection of Prostate Cancer by FACS

Ziv Hospital

Mouth and Tooth Diseases

Rare Diseases

Carcinoma

Mouth Neoplasms

Precancerous Conditions

Leukoplakia

Leukoplakia, Oral

Erythroplasia

Head and Neck Neoplasms

Mouth Diseases

Stomatognathic Diseases

Pathological Conditions, Anatomical

Oral Cancer

Erythroplakia

Lip and Oral Cavity Cancer

Oral Leukoplakia

Hypoglycemic Agents

All Drugs and Chemicals

Metformin

Patients receive extended-release metformin hydrochloride PO QD for 2 weeks and then BID for 10-12 weeks. Treatment continues in the absence of disease progression or unacceptable toxicity.

Laboratory Biomarker Analysis

Metformin Hydrochloride

Scott M Lippman

This phase IIa trial studies how well metformin hydrochloride works in preventing oral cancer in patients with an oral premalignant lesion (oral leukoplakia or erythroplakia). Oral premalignant lesions look like red or whitish plaques or lesions in the mouth that do not rub off and can be associated with a higher risk of cancer. Metformin hydrochloride may help prevent oral cancer from forming in patients with an oral premalignant lesion.

PRIMARY OBJECTIVES:

I. To determine the clinical response of oral premalignant lesions to 12-14 weeks of metformin (metformin hydrochloride) intervention.

SECONDARY OBJECTIVES:

I. Histologic response to metformin intervention in the target lesion. II. Tissue-based biomarkers: metformin effect on cell proliferation and its molecular targets in the target lesion and in the normal tissue (marker of cell proliferation, Ki67, molecular targets of metformin, including, in order of priority, phosphorylated ribosomal protein S6 kinase \[pS6\], phosphorylated v-akt murine thymoma viral oncogene homolog 1 \[pAKT\]S473, phosphorylated eukaryotic translation initiation factor 4E-binding protein 1 \[p4EBP\], phosphorylated acetyl-CoA carboxylase alpha \[pACC\]).

III. Tissue-based biomarkers: expression of dysregulated molecular mechanisms and organic cation transporter 3 (OCT 3) in the target lesion and in the normal tissue, including, in order of priority, epidermal growth factor receptor (EGFR), phosphorylated (p)EGFR, tumor protein 53 (p53), phosphatase and tensin homolog (PTEN), phosphorylated mitogen-activated protein kinase 1 (pERK), cyclin-dependent kinase inhibitor 2A (p16), and OCT3.

IV. Tissue-based biomarkers: targeted analysis of cancer-associated genes in the target lesion and blood deoxyribonucleic acid (DNA).

V. Serum and saliva based biomarkers: metformin effect on serum metabolic markers (C-peptide, glycosylated hemoglobin \[HbA1c\]).

VI. Serum and saliva based biomarkers: metformin concentrations in serum and saliva.

VII Serum and saliva based biomarkers: metformin effect on serum and saliva inflammatory and angiogenic cytokines, including interleukin (IL)-6, IL-8, growth-related oncogene-1 (GRO-1), and vascular endothelial growth factor (VEGF).

EXPLORATORY OBJECTIVES:

I. To characterize changes in the saliva microbiome before and after metformin intervention, including both the absolute microbial load and taxonomic composition.

II. To evaluate the potential microbiome signatures that are correlated with treatment response.

OUTLINE:

Patients receive extended-release metformin hydrochloride orally (PO) once daily (QD) for 2 weeks and then twice daily (BID) for 10-12 weeks. Treatment continues in the absence of disease progression or unacceptable toxicity.

After completion of study treatment, patients are followed up for 2-4 weeks.

Metformin Hydrochloride in Preventing Oral Cancer in Patients With an Oral Premalignant Lesion

M4OC-Prevent: Metformin for Oral Cancer Prevention

This will characterize changes in the saliva microbiome before and after metformin intervention, including both the absolute microbial load and taxonomic composition. Will first evaluate changes in alpha diversity among matched pairs using non-parametric analogous Wilcoxon rank-sum test (Mann-Whitney test). To test for significant differences in beta diversity (e.g. if pretreatment and post-treatment samples cluster in principle coordinates analysis space), permutational multivariate analysis of variance (PERMANOVA) will be used.

Will first evaluate changes in alpha diversity among matched pairs using non-parametric analogous Wilcoxon rank-sum test (Mann-Whitney test). To test for significant differences in beta diversity (e.g. if pretreatment and post-treatment samples cluster in principle coordinates analysis space), PERMANOVA will be used.

Number of participants with complete and partial clinical response to metformin intervention.

Criteria for complete and partial clinical response are:

Complete Response (CR): Disappearance of all evidence of lesion(s). Partial Response (PR): Greater than or equal to 50% reduction in the sum of the products of diameters of lesion(s) measurable at baseline. Non-measurable lesion(s) may not increase greater than or equal to 25% in size and no new lesion may appear.

Number of participants with complete and partial histologic response to metformin intervention.

Criteria for complete and partial histologic response are:

Complete Response (CR): Complete reversal of dysplasia or hyperplasia to normal epithelium in the target lesion.

Partial Response (PR): Improvement of the degree of dysplasia or hyperplasia in the target lesion.

Nonparametric methods, e.g. signed rank test, will be performed to evaluate each of the changes in tissue, serum, and saliva markers.

Nonparametric methods, e.g. signed rank test, will be performed to evaluate each of the changes in tissue, serum, and saliva markers. A univariate logistic regression model with the clinical response as the outcome variable will be fitted to explore if any of the expression of frequent dysregulated mechanisms and OCT3 level are associated with the clinical response to metformin hydrochloride.

Nonparametric methods, e.g. signed rank test, will be performed to evaluate each of the changes in tissue, serum, and saliva markers. A univariate logistic regression model with the clinical response as the outcome variable will be fitted to explore if any genomic alterations are associated with the clinical response to metformin hydrochloride.

National Cancer Institute (NCI)

Patients receive extended-release metformin hydrochloride PO QD for 2 weeks and then BID for 10-12 weeks. Treatment continues in the absence of disease progression or unacceptable toxicity.

Laboratory Biomarker Analysis: Correlative studies

Metformin Hydrochloride: Given PO

Prevention (Extended-release Metformin Hydrochloride)

Age, Continuous

Sex: Female, Male

Ethnicity (NIH/OMB)

Race (NIH/OMB)

Canada

United States

Region of Enrollment

Dr. Sherry Chow

Clinical Response to Metformin Intervention

Histologic Response to Metformin Intervention

Changes in Cell Proliferation and Its Molecular Targets

Changes in Frequent Dysregulated Molecular Mechanisms and OCT Expression

Impact of Genomic Alterations on the Biological and Biochemical Consequences and Clinical Response to Metformin Hydrochloride

Change in Measurements of Metformin Hydrochloride Concentrations in Serum and Saliva

Change in Serum Metabolic Markers

Change in Serum and Saliva Inflammatory and Angiogenic Cytokines

Change in Saliva Microbiome Analyzed Using Flow Cytometry

Microbiome Signatures Correlated With Treatment Response

Overall Study

Skin and Connective Tissue Diseases

Keratosis

No dysplasia, mild, moderate, severe dysplasia, CIS

Assessment for risk of progression to oral cancer

STRATICYTE™ Test

Jody Filkowski, BSc, MSc, PhD

Jason TK Hwang, HBSc, MSc, PhD

Andrew G Sikora, MD, PhD

Simon W Young, DDS, MD, PhD

The purpose of this study is to validate the ability of the STRATICYTE™ predictive model to predict the transformation of oral potentially malignant disorders (OPMDs) to oral squamous cell carcinoma (OSCC) in a retrospective cohort of patients who received biopsies.

The study objectives are to:

1. Evaluate STRATICYTE™ sensitivity and specificity in a cohort of patients that meet the inclusion/exclusion criteria.
2. Identify patient and clinical characteristics influencing the sensitivity and specificity of the STRATICYTE™ model.
3. Estimate the correlation between STRATICYTE™ outcome and time to a positive diagnosis of oral cancer.

FFPE specimens immunohistochemically stained with S100A7

Evaluation of Oral Potentially Malignant Disorders (OPMDs) With STRATICYTE™

Standard measures of accuracy calculated using cross-tabulation of predicted risk category and confirmed cancer progression over a 5-year period from biopsy

Kaplan-Meier analyses to compare time to a positive diagnosis of oral cancer between patients/biopsies with a STRATICYTE™ classification of Low- and Elevated-Risk.

From all possible pairs of patients, compute the number of concordant and discordant pairs. Compute C-index as the proportion of all possible pairs that are concordant.

The University of Texas Health Science Center, Houston

Loma Linda University

Minnesota Oral & Facial Surgery

University of Alabama at Birmingham

Proteocyte Diagnostics Inc.

Breast Neoplasms

Breast Diseases

Skin Diseases

Bone Density Conservation Agents

Micronutrients

Antirheumatic Agents

Vitamins

Vitamin D

Cholecalciferol

Trace Elements

Hormones

Calcium

Calcium, Dietary

Vitamin D3

Calciferol

oral capsules, 10,000 IU per week for 6 months

vitamin D3

Carol Fabian, MD

The overall goal of this project is to determine if high dose vitamin D3 given to premenopausal women at high risk for development of breast cancer, who initially have insufficient levels of 25-hydroxy vitamin D (\<30 ng/ml), will raise 25(OH)D levels above 50 ng/ml. If so, will certain risk biomarkers for development of breast cancer be reliably and favorably modulated?

Protocol Objectives:

To determine if high dose vitamin D3 given to premenopausal women who initially have insufficient levels of 25-hydroxy vitamin D (\<30 ng/ml) will raise 25(OH)D levels above the 50 ng/ml level considered to be required for breast health. If so, will certain risk biomarkers for development of breast cancer be reliably and favorably modulated? The primary endpoint will be a decrease in mammographic breast density (percent area considered at increased density). Change in proliferation (a decrease as assessed by Ki-67) will also be examined. Modulate of expression of genes important in breast cancer risk or reflective of vitamin D's mechanism of action will be studied using quantitative real time polymerase chain reaction (qRT-PCR).

Study Design:

The study is a single-arm open label clinical trial. Women who are high risk for development of breast cancer on the basis of family or personal history will undergo random periareolar fine needle aspiration (RPFNA) to acquire breast cells for assessment of gene expression by qRT-PCR. Women with mammographic density \>10% will be eligible for enrollment. All subjects will receive high dose vitamin D3 (3 capsules of 10,000 IU of vitamin D3 every week for 6-8 months). At that time, a repeat RPFNA and mammogram will be performed. Measurement of serum levels of 25(OH)D will be performed at baseline, 3 months, and 6 months.

Modulation of Breast Cancer Risk Biomarkers by High Dose Vitamin D

Change in the percent of the breast area that is considered to be at higher density on mammogram.

Change in percent of cells expressing staining for Ki-67 antibody in breast epithelial cell specimens acquird by Random Periareolar Fine Needle Aspiration.

Assessment of 25(OH)D levels as a measure of circulating vitamin D.

BTR Group

Professor, Director Breast Cancer Prevention Unit

Group/Cohort Label vitamin D3

vitamin D3: oral capsules, 10,000 IU per week for 6 months

High Dose Vitamin D3 (10,000 IU Weekly)

Female

Sex/Gender, Customized

Gail model is an algorithm to calculate a predicted probability of developing breast cancer within the next 5 years.

Gail Risk 5-year Probability of Cancer Development

Single arm pilot trial so all comparisons are within subject for change over the course of the study.

Bruce F. Kimler, Ph.D.

Change in Mammographic Breast Density Over Course of Study

Change in Proliferation (as Assessed by Ki-67) Examined in Breast Epithelial Cells.

OH Vitamin D Levels in Serum

Disease Progression

This study will analyze blood samples to identify substances that are associated with the development of breast cancer. It will determine if:

* Women who are diagnosed with a benign breast condition that is related to a considerably increased risk of breast cancer are more likely to have certain gene variants than women diagnosed with conditions related to very little increased breast cancer risk
* Women with benign breast conditions who subsequently develop breast cancer are more likely to have certain gene variants than women with similar benign conditions who do not develop breast cancer.

This study will examine blood samples from premenopausal women who underwent breast biopsy (removal of a small piece of breast tissue for microscopic examination) at four hospitals in Grand Rapids, MI, from 1977 to 1987 and were found to have benign breast disease. The women, who agreed to participate in a study of markers for breast cancer, also provided a blood sample and were interviewed for information on their breast cancer risk factors, family history of breast cancer, use of medications, and history of medical conditions.

This study will retrieve the biopsy reports for these women, determine which of them later developed breast cancer, and perform genotyping on their blood samples.

The information from this study may help in future diagnosis and treatment of breast cancer.

Prevention and treatment of intraepithelial neoplasia and benign pre-malignant conditions has become an important focus of the NCI's 2015 goal of eliminating suffering and death due to cancer, although very little is known about the factors that influence development of frank malignancy in those with high risk benign/precursor conditions. The Radiation Epidemiology and Biostatistics Branches of the NCI propose to evaluate the contribution of inherited genetic variation to benign pre-malignant breast conditions, and to subsequent breast cancer risk in women diagnosed with such conditions, in the Breast Cancer Serum Bank, a unique biospecimen resource housed at NCI since 1995. Premenopausal participants (N=2632) biopsied at an average age of 27 in 1977-1987, (many diagnosed with high risk benign breast conditions (moderate/florid breast hyperplasia and atypia)) were interviewed and provided a blood sample. Participant biopsy reports will be obtained for review and recoding, and participants will be traced for vital status and breast cancer development (expected n = 240 cases). Variants in genes related to hormone metabolism and cell signaling, processes implicated in the development of premalignant breast conditions, and in genes associated with cell cycle control and apoptosis, and thus possibly related to progression to breast cancer among women with premalignant breast conditions will be assessed at the NCI Central Genotyping Facility. We have a remarkable opportunity in this study to address scientific questions regarding breast carcinogenesis mechanisms at relatively little cost. Greater comprehension of the influence of inherited factors on distinct steps in the biological pathway, first from normal tissue to benign high risk breast tumors, and then hence the breast cancer, should contribute to our understanding of the molecular mechanisms that shape breast cancer development, and holds promise for the discovery and delivery of sound risk-adapted interventions for women with high risk premalignant conditions.

Markers for Breast Cancer

Risk of Breast Cancer and Hyperplastic Conditions in the Breast Cancer Serum Bank in Relation to Inherited Genetic Variants

Carcinoma in Situ

Carcinoma, Squamous Cell

Squamous Cell Carcinoma of Head and Neck

Neoplasms, Glandular and Epithelial

Neoplasms by Histologic Type

You will be given a higher dose of Avmacol® each month, taking 2 Avmacol® tablets per day the first month (Cycle 1), 4 Avmacol® tablets per day the second month (Cycle 2), and 8 Avmacol® tablets per day the third month (Cycle 3). Investigators will study how Avmacol® affects your body by collecting three different tissues: 1) your cheek cells (buccal cells); 2) your urine; and 3) your blood. After you have finished three months of Avmacol®, you will return one month later for an end-of-study visit.

Avmacol is a dietary supplement available over the counter

Avmacol

Dan P Zandberg, MD

Avmacol is an over-the-counter dietary supplement containing broccoli seed and sprout extracts in tablet form, hypothesized to activate protective cellular pathways including detoxication. In this study, participants who have been curatively treatment for head and neck cancer, will take Avmacol twice a day for 3 months.

The broccoli seed preparation, Avmacol®, results in acute and/or sustained induction of NRF2 target gene transcripts in the oral mucosa of patients who have been curatively treated for a tobacco-related head and neck squamous cell carcinoma (HNSCC), including high grade dysplasia, carcinoma in situ, or invasive carcinoma. This study is not designed to examine the therapeutic or reparative effects of Avmacol® on premalignant lesions of the oral cavity.

We will systematically assess the clinical chemopreventive potential of Avmacol® administration to patients with tobacco-related HNSCC at high risk for second primary tumor by:

1. Conducting this phase 0 clinical study to evaluate the pharmacodynamic range of NRF2 pathway activation in the oral mucosa of HNSCC patients, in response to two tolerable and bioactive doses of Avmacol®;
2. Determining whether the level of NRF2 pathway activation achieved in human oral epithelium is chemopreventive in the NQO1 murine model of environmental carcinogenesis; and
3. Analyzing specimens from the Phase 0 trial to determine whether Avmacol® induces changes in alternative biomarkers of SF chemopreventive efficacy identified in the laboratory.

Thirty-six individuals who have previously been treated for tobacco-related, HPV-negative HNSCC will be recruited for this study.

After being deemed eligible, subjects will be assigned a patient number and be registered into the CTMA database.

At registration, they will be randomized to receive either 4 tablets/day in Cycle 1 or 8 tablets/day in Cycle 1 (and the other dose in Cycle 2). This randomization is not blinded. Randomization will be stratified by history of head and neck radiation therapy (yes or no).

Effects of Avmacol® in the Oral Mucosa of Patients Following Curative Treatment for Tobacco-related Head and Neck Cancer

A Phase 0 Study Evaluating the Systemic Bioavailability and Pharmacodynamic Effects of Avmacol® in the Oral Mucosa of Patients Following Curative Treatment for Tobacco-related Head and Neck Cancer

Quantitative changes in NRF2 target gene transcripts expression (i.e. NQO1 and GCLC) in oral mucosa (buccal cytobrush) by quantitative polymerase chain reaction (qPCR) according to a linear mixed model framework.

Changes in NRF2 target proteins in buccal punch biopsies by immunoblotting.

Change in NRF2 target gene transcripts, between the two doses of Avmacol® by immunoblotting.

Changes in Peripheral Blood Mononuclear Cells (PBMC) gene expression and flow cytometry patterns in NK cells.

Changes in Peripheral Blood Mononuclear Cells (PBMC) gene expression and flow cytometry patterns in T cells.

Change in serum cytokine levels, as determined by multiplexed bead-based cytokine assays.

Measurement of urinary metabolites of SF using isotope dilution mass spectrometry.

Patients will receive a diary for daily logging of adverse events. This will tabulated by Avmacol dose and type and grade of adverse events. The mean frequency and grade of events will be calculated by dose, and between-dose differences compared by means

Genomic alterations in primary tumors will be characterized and the proportion determined by number of patients with NRF2 related genes per the total number of patients studied.

University of Arizona

University of Pittsburgh

Principal Investigator

Hemorrhage

Endometrial Hyperplasia

Endometrial Neoplasms

Uterine Hemorrhage

Uterine Neoplasms

Genital Neoplasms, Female

Uterine Diseases

Genital Diseases, Female

Female Urogenital Diseases

Pregnancy Complications

Female Urogenital Diseases and Pregnancy Complications

Women in one large U.S. health care plan. Cases will consist of women who developed endometrial carcinoma or censored complex atypical hyperplasia at least 1 year after receiving a diagnosis of endometrial hyperplasia.

Women in one large U.S. health care plan. Controls will consist of individually matched women who received a diagnosis of endometrial hyperplasia at the same age and date as the cases and were cancer-free and hysterectomy-free until the date at which the index cases were diagnosed with endometrial carcinoma or censored complex atypical hyperplasia.

Nicolas Wentzensen, M.D.

This study, conducted jointly by the National Cancer Institute and the Kaiser Permanente Center for Health Research Northwest (KPCHRN) in Portland, Oregon, will lay the groundwork for a future study to identify precursors of endometrial cancer; that is, conditions that precede development of cancer of the lining of the uterus. The diagnosis of endometrial hyperplasia (a condition of abnormal proliferation of endometrial tissue) includes most precursors of endometrial cancer, as well as many benign conditions. Currently, three methods of classifying endometrial cancer precursors have been suggested based on endometrial hyperplasia findings, but it is not known which classification best predicts cancer risk.

This study will examine surgical specimens of hyperplasia and cancer from women diagnosed with endometrial cancer at least 2 years after a diagnosis of endometrial hyperplasia. Investigators will estimate the percentage of cases with different degrees of hyperplasia, and assess the subsequent cancers that developed. This will allow them to rank hyperplasia lesions according to cancer risk and identify lesions that represent the most immediate cancer precursors. They will also review patients medical charts for information related to cancer risk and treatment.

Study participants will include women enrolled in the KPCHRN who are 40 years of age or older and who were diagnosed with endometrial cancer at least 2 years after being diagnosed with endometrial hyperplasia.

Three systems have been proposed to classify endometrial carcinoma precursors, but it is currently unclear which system best predicts cancer risk and is most reproducible. The optimal surrogate endpoint for endometrial carcinoma is therefore unknown. The pathologic diagnosis of endometrial hyperplasia (EH) includes most suspected immediate precursors and many mild, highly reversible proliferations. We propose an exploratory study to assess the feasibility of investigating EH as a source of an endometrial carcinoma surrogate endpoint.

We are conducting a nested case-control study within a large, population-based health care plan. We will identify cases, defined as women who were diagnosed with EH at least one year before being diagnosed with endometrial carcinoma or severe atypical hyperplasia at hysterectomy, through a computerized search of plan databases. We will retrieve the slides from the matching biopsy and hysterectomy on which carcinoma was diagnosed. Women ages 40 or older who were plan members and received a biopsy or curettage diagnosis of EH between 1970 and 2002 will be eligible to be a case.

We will perform an initial histologic review of cases index biopsy slides to assess two types of misclassification known to affect the diagnosis of EH: a) false-negative endometrial carcinoma (i.e., prevalent carcinoma t the time of EH diagnosis) and b) false-positive EH (i.e., a benign, non-hyperplastic lesion). From cases physical records and linked computer records, we will collect data on histopathologic classification of EH lesions and subsequent carcinomas; descriptive data (e.g., patient weight, parity, and menopausal status); and a summary of relevant treatments and follow-up procedures (e.g., hormone therapy or additional clinical procedures).

We will select controls, defined as women who were diagnosed with EH but then did not develop endometrial carcinoma or undergo hysterectomy for a follow-up interval that is equivalent to the follow-up interval of the cases. Controls will be individually matched to cases on age at EH diagnosis, date of EH diagnosis, and duration of follow-up, and also counter-matched based on the original EH diagnosis. After selecting 3 controls per case, we will assemble the same data from controls: histologic review of original slides, descriptive data from medical records databases, and treatment and follow-up procedure data from linked databases.

These data will then be used to estimate the cancer risk associated with specific EH classifications, identify other patient or clinical factors that might modify those risks, explore predictors of EH, and explore molecular factors that might influence the probability of developing carcinoma after a diagnosis of EH.

Preliminary Study of Endometrial Hyperplasia Groundwork for a Study to Define Precursors of Endometrial Cancer

Preliminary Study of Endometrial Hyperplasia: Groundwork for a Study to Define an Optimal Classification of Endometrial Carcinoma Precursors

Formalin fixed paraffin embedded tissue blocks and pathology slides from women with endometrial cancer and women with endometrial hyperplasia with covariate data from medical records.

Oral Squamous Cell Carcinoma

No evidence of dysplasia

Mild dysplasia

Moderate dysplasia

Severe dysplasia

Assessment for mild, moderate, or severe dysplasia, and risk of progression to oral cancer

Standard of Care Histopathology

STRATICYTE Assessment

Jason Hwang, PhD

Mark Darling, MSc, MChD

Tim McGaw, DDS, MSc, MD

The purpose of this observational study is to evaluate the utility of the S100A7 immunohistochemistry signature-based assessment - STRATICYTE - in determining the risk of progression to cancer of clinically suspicious oral lesions.

Background: The standard of care for potentially premalignant oral epithelial lesion (PPOEL) risk assessment for progression to cancer is dysplasia grading by histopathology. With significant overlap between dysplasia grades and high inter- and intra-observer variations, dysplasia grading alone has been shown to be inadequate as a prognostic tool. To investigate the utility of the S100A7 immunohistochemistry signature-based assessment - STRATICYTE - in the early diagnosis of invasive oral cancer, a prospective multi-center observational study was designed with specimens obtained from community-based practices.

Methods: Patients that qualify to enroll in the study will be assessed for both standard of care histopathological assessment for dysplasia grade and STRATICYTE risk assessment, and followed for up to 60 months (from initial biopsy) to determine the outcome of their oral lesion(s).

Formalin-fixed paraffin-embedded tissue sections stained with H\&E and S100A7

Early Prediction of Oral Cancer by S100A7 Immunohistochemistry Signature-based Assessment

A Multi-Centre Prospective Community-Based Observational Study on Prediction of Malignant Progression of Clinically Suspicious Oral Lesions With STRATICYTE

Cancer progression rate in patients with oral neoplasia with dysplasia and STRATICYTE Low-Risk or Elevated Risk

Cancer progression rate in patients with oral neoplasia without dysplasia and STRATICYTE Low-Risk or Elevated-Risk

Recurrence rate in patients with oral neoplasia with or without dysplasia and STRATICYTE Low-Risk or Elevated-Risk

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Early Detection of Prostate Cancer by FACS	NCT00524823	Prostate Cancer Hyperplasia		60 Years - 90 Years	Ziv Hospital
Metformin Hydrochloride in Preventing Oral Cancer in Patients With an Oral Premalignant Lesion	NCT02581137	Erythroplakia Hyperplasia Oral Cavity Car... Oral Leukoplaki...	Laboratory Biom... Metformin Hydro...	18 Years -	National Cancer Institute (NCI)
Evaluation of Oral Potentially Malignant Disorders (OPMDs) With STRATICYTE™	NCT05853783	Mouth Diseases	STRATICYTE™ Tes...	18 Years -	Proteocyte Diagnostics Inc.
Modulation of Breast Cancer Risk Biomarkers by High Dose Vitamin D	NCT01166763	Breast Cancer	vitamin D3	- 55 Years	University of Kansas Medical Center
Markers for Breast Cancer	NCT00339248	Breast Cancer		15 Years -	National Institutes of Health Clinical Center (CC)
Effects of Avmacol® in the Oral Mucosa of Patients Following Curative Treatment for Tobacco-related Head and Neck Cancer	NCT03268993	Head and Neck C... Head and Neck S... Head and Neck C... Head and Neck Tobacco-Related... Carcinoma in Si... Dysplasia Hyperplasia Premalignant Le...	Avmacol	18 Years -	University of Pittsburgh
Effects of Avmacol® in the Oral Mucosa of Patients Following Curative Treatment for Tobacco-related Head and Neck Cancer	NCT03268993	Head and Neck C... Head and Neck S... Head and Neck C... Head and Neck Tobacco-Related... Carcinoma in Si... Dysplasia Hyperplasia Premalignant Le...	Avmacol	18 Years -	University of Pittsburgh
Preliminary Study of Endometrial Hyperplasia Groundwork for a Study to Define Precursors of Endometrial Cancer	NCT00339651	Endometrial Hyp... Endometrial Can... Postmenopausal ... Vaginal Bleedin...		40 Years - 120 Years	National Institutes of Health Clinical Center (CC)
Early Prediction of Oral Cancer by S100A7 Immunohistochemistry Signature-based Assessment	NCT04622462	Oral Neoplasm	Standard of Car... STRATICYTE Asse...	15 Years - 90 Years	Proteocyte Diagnostics Inc.
Broccoli Sprout Extract in Preventing Recurrence in Patients With Tobacco-Related Head and Neck Squamous Cell Cancer	NCT03182959	HNSCC Head and Neck C... Head and Neck S... Tobacco-Related... Carcinoma in Si... Dysplasia Hyperplasia Premalignant Le...	Avmacol®	18 Years -	University of Arizona

Spots Global Cancer Trial Database for hyperplasia

Every month we try and update this database with for hyperplasia cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Spots Global Cancer Trial Database for hyperplasia

Every month we try and update this database with for hyperplasia cancer trials from around the world to help patients and their families find trials that might be right for them. We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.

Every month we try and update this database with for hyperplasia cancer trials from around the world to help patients and their families find trials that might be right for them.
We offer this 100% free of charge and do not endorse any of the trials listed here, we hope it helps you or a loved one.