Neoplasms

Heart and Blood Diseases

Blood and Lymph Conditions

Immune System Diseases

All Conditions

Rare Diseases

Multiple Myeloma

Neoplasms, Plasma Cell

Neoplasms by Histologic Type

Hemostatic Disorders

Blood Coagulation Disorders

Vascular Diseases

Paraproteinemias

Blood Protein Disorders

Hematologic Diseases

Hemorrhagic Disorders

Lymphoproliferative Disorders

Immunoproliferative Disorders

All Drugs and Chemicals

Immunomodulating Agents

Immunologic Factors

There are only collections of the samples.

Evaluation of patients resistance to immunotherapies in Multiple Myeloma

A total of 40 Multiple Myeloma (MM) patients at clinical relapse who progressed during Proteasome Inhibitors (PIs) or Immunomodulating Drugs (IMiDs)-based therapies and who are assigned to antiCD38-based salvage treatments, will be enrolled. We will collect bone marrow (BM) and peripheral blood (PB) samples from patients at specific timepoints:

* baseline (BM, PB and buccal swab)
* every 3 month (PB)
* achievement of response (≥ Very Good Partial Response (VGPR)) (BM and PB)
* relapse or refractory status to antiCD38-based treatments (BM and PB) Samples will be processed and stored in the "Hematological Laboratory" located in the University of Turin (Italy) for various proposed analyses: at specific time-points CD138+ (Plasma Cells-PCs) and marker CD138/19+ (B cells) will be immunomagnetically enriched from the BM mononuclear cells and frozen as viable cells in dimethyl sulfoxide (DMSO); PB mononuclear cells (PBMCs) will be isolated from whole blood by density-gradient centrifugation, and frozen as above; plasma fraction from PB and BM will be obtained by centrifugation and stored frozen; a buccal swab will be obtained at the time of enrollment as a source of control germline DNA and stored frozen.

Aim 1: Evaluation of cell-intrinsic mechanisms on BM.

1. Whole Genome Sequencing (WGS) and Whole Exome Sequencing (WES) will be performed on marker CD138+ purified cells to evaluate their genomic profile, and on buccal swab DNA to restrict the analysis to variants or structural abnormalities that have a clear somatic status, and are therefore specific to the tumor cells. In details:

   1.1 WGS: libraries will be prepared with TruSeq™(Kit Illumina) DNA Polymerase Chain Reaction (PCR)-Free Library Preparation Kit (Illumina, San Diego, CA) from 500ng of genomic DNA, aiming for an average target insert of 300bp. Sequencing will be performed on a 150bp-paired end protocol, at a target depth of 40x for tumor samples and 30x for normal samples.

   1.2 WES: libraries will be prepared with SureSelectXT Human All Exon V6 (Agilent technologies int., Santa Clara, CA) from 100ng of genomic DNA, aiming for an average target insert of 300bp. Sequencing will be performed on a 150bp-paired end protocol, aiming for a target depth of 200x for tumor samples and 100x for normal samples.

   1.3 Data analysis: next generation sequencing scoring system output format files (\*.FASTQ files) will be aligned to the reference genome using Burrows-Wheeler Alignment Tool (BWAmem), and deduplicated aligned Binary Alignment Map (BAM) files will be analyzed using the following published tools available at the Wellcome Trust Sanger Institute (WTSI):
   1. accurate genome-wide allele-specific copy number (ASCAT) and Battenberg for clonal and subclonal copy number changes.
   2. BRASS for structural variations (large inversions and deletions, translocations, internal tandem duplication).
   3. Caveman and Pindel for Single Nucleotide Variants (SNVs) and small insertion-deletions (indels).

   The clonal composition of the sample and the genomic evolution of myeloma over time will be inferred from the adjusted cancer cell fraction of the variants identified, clustered and analyzed using a hierarchical bayesian Dirichlet process.

   The mutational processes operative at various phases of MM will be analyzed using a Non-Negative Matrix Factorization (NNMF) approach to extract mutational signatures from the array of substitutions in their 5' and 3' context.

   The possible driver mutation role of all extracted missense mutation will be evaluated by the recently published dN/dS algorithm.
2. RNA-seq on marker CD138+ purified cells to evaluate transcriptomic profile will be performed using TruSeq Stranded Messanger RiboNucleic Acid (mRNA) Library Prep Kit (Illumina, San Diego, CA) on 500 ng total RNA, followed by sequencing, aiming for 100x106 total reads per sample. DNA excision repair protein (ERCC) spike-in mix will be added to facilitate normalization of the expression levels between samples. Reads will be aligned with Tophat2 to call SNVs, indels, and detect gene fusions. Cufflinks2 will be used to profile gene expression and detect novel transcript isoforms. Overall gene transcript expression levels will be quantified using the Reads Per Kilobase Million (RPKM) metric based on uniquely mapping reads.
3. Flow cytometry analysis will be performed on BM samples to examine potential determinants of immunotherapy sensitivity/resistance and the expression of specific targets including marker Cluster of Differentiation 38 (CD38), B-cell maturation antigen (BCMA), marker Cluster of Differentiation 33 (CD33), Programmed death-ligand 1 (PDL1), and marker Cluster of Differentiation 19 (CD19) prior to treatment, at response and at relapse. We will evaluate MM percent positive cells and Mean Fluorescence Intensity (MFI) in order to monitor the antigen expression during the evolution of the disease. Receptor density will also be performed. Moreover the European cytoflow consortium of International Myeloma Foundation (EuroFlow-IMF) MM minimal residual disease (MRD) panel will be applied to monitor MRD in particular by using a multiepitope (ME) antiCD38 to detect possible determinants of resistance. Moreover this panel will allow us to monitor the phenotype evolution of the clonal population, looking in particular at the shift towards more immature cells, which has been suggested as a mechanism of resistance to bortezomib.
4. Storage of viable marker CD138-: we will evaluate distribution of marker CD38 also on marker CD138- cells and we will determine if genomic or immunophenotypic lesions responsible for resistance could be present also in the marker CD138- fraction.

Aim 2: Evaluation of cell-extrinsic mechanism on BM and PB.

1. Flow Cytometry analysis of lymphocyte subpopulations will be performed in the same BM and PB to evaluate T-cells population (marker CD38+, marker Cluster of Differentiation 4 (CD4+), marker Cluster of Differentiation 8 (CD8+), Tregs cells) and other regulatory and suppressive immune populations like Myeloid-Derived Suppressor Cells (MDSCs). T cells will be measured at baseline, response and at relapse, and they could help in evaluating the interaction between B and T cell compartments in patients receiving immunotherapies. Moreover, evaluation of some immune checkpoints on T cells at baseline and post-treatment will be performed.
2. RNA-seq of lymphocyte subpopulations will be performed to identify the frequencies of the various helper and effector lymphocyte populations, and correlate those with response to treatment or lack thereof. We will also perform RNA-seq on different marker CD4+ T-lymphocytic subpopulations in responsive and non-responsive MM to identify potential suppressive signatures in the latter group. The same lymphocyte subpopulations will be analyzed in BM samples from 10 healthy subjects (BM biopsy in lymphoma negative staging).
3. Measurement of a broad spectrum of cytokines produced and secreted by MM and other cells within the BM microenvironment: cytokines and chemokines related to MM bone and microenvironment will be measured in BM and PB plasma from patients at each time-point. The laboratory assays will be performed by using an enzyme-linked immunosorbent assay (ELISA) kit.
4. BM biopsy: bone biopsies from MM patients at baseline and after Monoclonal Antibody Therapy (mAbs therapy) will be evaluated for the expression of suppressive molecules such as, marker Cluster of Differentiation 80/86 (CD80/86), marker Cluster of Differentiation 40 (CD40) in the tumor cells and in the BM lymphoid population by immunohistochemistry.

Aim 3: After comprehensively characterizing the genomic, transcriptomic and immunophenotypic features of CD138+ cells, and having a clear picture of the effector/suppressive immune population in MM, we will then correlate these features with clinical data. In detail, we will create a database including the following columns:

* Baseline clinical characteristics
* Prognostic factors: International Staging System (ISS), Revised International Staging System (R-ISS), Lactate Dehydrogenase (LDH), cytogenetic analysis by Fluorescence In Situ Hybridization test (FISH)
* Prior therapies and relevant clinical results
* Best response: responses will be defined according to the International Uniform Response Criteria. Responders are defined as subjects with at least a VGPR.
* Duration of Response (DOR), Progression Free Survival (PFS), Overall survival (OS) and Time to Progression (TTP) data In this aim, we will look for correlation between biological features and disease response or lack thereof, to understand which cell-intrinsic and cell-extrinsic features are better predictors of response. Because of the time needed before disease response can be assessed, this analysis will be performed after at least 1 year of treatment or at earlier progression. In a first analysis, biological features will be associated with best response to treatment, PFS and other baseline clinical, prognostic and treatment variables using linear models. Subsequently, starting from year 3, when enough follow-up will allow a meaningful analysis of PFS and OS, Kaplan-Meier and Coxregression models will be fitted to identify possible independent prognostic factors.

Although the relatively small size of the cohort will limit statistical power and the possibility to perform subgroup analysis, this attempt to identify biomarkers could improve the clinical management of the patient, by prioritizing the vast array of salvage treatments in MM and thus decreasing costs.

Genomic and Phenotypic Determinants of Resistance to Immunotherapies in Multiple Myeloma

The patients' response to new drugs administration will be evaluated identifying genomic aberrations (e.g. TRAF3 deletion/mutation and Cereblon mutation) or impaired cellular surface molecules expression (eg CD38, CD55, CD59 expression).

The analysis will include T-cells population (eg. CD38+, CD4+, CD8+, Tregs cells), regulatory and suppressive immune populations (MDSCs) and cytokines (eg Activin-A, IL-3, IL-6, RANKL, OPG, MIP-1α, MIP-3α and DKK-1) characterization.

Response measured through cytofluorimetric analysis. Results will be integrated by statistical models (e.g. univariate, multivariate analysis) and then correlated to mutational results and patients' available clinical data in order to predict outcome.

Response measured through mutational analysis. Results will be integrated by statistical models (e.g. univariate, multivariate analysis) and then correlated to cytofluorimetric results and patients' available clinical data in order to predict outcome.

University of Turin, Italy

Principal Investigator

Symptoms and General Pathology

Digestive System Diseases

Carcinoma

Neoplasm Metastasis

Colonic Neoplasms

Colorectal Neoplasms

Intestinal Neoplasms

Gastrointestinal Neoplasms

Digestive System Neoplasms

Gastrointestinal Diseases

Colonic Diseases

Intestinal Diseases

Herbal and Botanical

Cola

Blood and surgical specimen sampling the day of surgery

Sampling

Thomas Aparicio, Pr

Jérôme Lambert, Pr

Diane Goéré, Pr

Colorectal cancer (CRC) is the 3rd most common cancer in France. Treatment of CRC relies primarily on surgical removal of the primary tumor and chemotherapy is the current standard of care for synchronous metastatic disease. Overall survival remains strongly correlated with the tumor stage at the time of surgery, from 90% at five years for localized disease (stages 1 and 2), to around 20% for metastatic forms of the disease (stage 4). Recent research in cancer highlights the role of the immune system in the development, evolution and fate of tumors. Understanding the nature of interactions between different immune cells infiltrating the tumor is important for the development of innovative therapies. Recently, the consensus molecular classification of CRC confirmed the importance of the immune response in CRC by showing that a "high immune response" is a good prognostic indicator for patients with this pathology. However, immunotherapies are effective for only a minority of patients with metastatic CRC. Indeed, anti Programmed cell Death 1 (anti-PD-1), -PD-L1 immune checkpoint blocking antibodies have only shown effectiveness in patients with microsatellite instability (MSI), which only represents 5% of metastatic CRCs.

Thus, the aim of this study is to better understand the role of the immune system on the development of CRC and its possible modulation to treat or prevent metastatic recurrences.

Blood and surgical specimen sampling the day of surgery (primary tumor and metastases if applicable)

Study and Modulation of Immune Responses in Primary and Metastatic Colon Cancers

Etude et Modulation de la réponse Immunitaire Dans Les Cancers COlorectaux Primaires et METastatiques

Characterize effective immunotherapies in colorectal cancers by demonstrating their effectiveness in a co-culture model between cancer cells and autologous T cells.

Evaluation of transcriptomic differences between tissues or cells from the healthy mucosa compared to those from the primary or metastatic tumor: sequencing of mRNA in the two types of mucosa and comparison of mRNA expression profiles between the latter.

Evaluation of proteomic differences between tissues or cells from the healthy mucosa in comparison to those from the primary tumor by:

multiplexed immunodetection in situ in tissues detection and dosage of proteins in culture supernatants (ELISA), in a co-culture model between cancer cells and autologous T cells, with or without modulation of a pathway targeting the T lymphocyte response by immunotherapy.

Evaluation of the TCR repertoire by sequencing, carried out from:

patient blood, DNA from cancerous tissues and healthy mucosa DNA from the co-culture between cancer cells and autologous T cells, with or without modulation of a pathway targeting the T lymphocyte response by immunotherapy

Assistance Publique - Hôpitaux de Paris

Skin and Connective Tissue Diseases

Recurrence

Melanoma

Neuroendocrine Tumors

Neuroectodermal Tumors

Neuroectodermal Tumors, Primitive

Neoplasms, Germ Cell and Embryonal

Neoplasms, Nerve Tissue

Nevus, Pigmented

Nevus

Nevi and Melanomas

Skin Neoplasms

Skin Diseases

Disease Attributes

Neuroendocrine Tumor

Neuroepithelioma

BRAF-mutated metastatic patients treated with 1st line targeted therapy

Metastatic patients treated with 1st line immunotherapy

BRAF-mutated patients treated with adjuvant targeted therapy

Patients treated with adjuvant immunotherapy

Blood samples at each protocol visit, T and NK cell analysis

Blood samples

Skin biopsy

Eve Maubec, PhD

Zahia Ben Abdesselam, Project M

Cutaneous melanoma is a tumor with a serious evolution if its initial diagnosis is late. Since 2011, the treatment of advanced forms involves two therapeutic approaches : targeted therapies (BRAF and MEK inhibitors) if the tumor carries a BRAF mutation or immunotherapies (anti-PD1, anti-CTLA-4) regardless of tumor BRAF mutation status. Current data support the hypothesis that combinations of agents targeting the tumor and its environment will be required for durable responses in the majority of patients. Investigators will study the role of NK lymphocytes in tumor immunosurveillance in patients undergoing first-line innovative therapy with metastatic melanoma or at high-risk of recurrence.

Natural Killer (NK) lymphocytes are cytotoxic effectors of the innate immune response that are involved in different phases of tumor immunosurveillance. These lymphocytes are activated upon contact with tumor cells and exert direct cytotoxic activity without prior immunization. Activated NK lymphocytes produce cytokines, including IFN-γ and TNF-α, which induce and maintain an activation of the adaptive immune response by CD8+ lymphocytes. Numerous studies in various experimental tumor models highlight the role of NK cells in the control of metastasis.

Our previous work has shown that NK cells infiltrate primary melanomas, that metastatic patients have altered blood NKs, and furthermore, that chemotherapy modulates their functional status. Investigators also observed a particular distribution of gene polymorphisms encoding NK activating receptors of stage IV melanoma patients compared to healthy donors. Finally, the investigator described a novel population of NK lymphocytes in metastatic lymph nodes draining melanoma NK cell activation is regulated by a balance between activating receptors (NKG2D, NCR) and inhibitory receptors that bind to modulatory classical and non-classical HLA-I molecules (HLA-E and G). More recently it has been shown that Lc NKs also express checkpoint receptors including CD96/TIGIT, NKG2A, TIM3 and PD-1 (the latter 2 are present on LcTs) that negatively modulate NK activation. The possibility of activating the lytic and secretory function of Lc NKs by interfering with these receptors may represent an alternative yet to be explored in immunotherapy treatments.

More recently, th investigator have developed a program to understand the interactions between tumor mutational profile, treatment with targeted therapies and NK immunogenicity. the investigator have a panel of melanoma lines with and without the BRAF V600E mutation and vemurafenib resistant variants have been obtained from some mutated lines. the investigator evaluated the impact of treatment and resistance to BRAF inhibition on Lc NK recognition and lysis. yhe investigator showed that a BRAF inhibitor, vemurafenib, decreased membrane and soluble expression of MICA/B and ULBP2, ligands for NKG2D, an activating receptor present on Lc NKs and certain populations of Lc T cells, in all BRAF mutated lines treated. For 6 of the 7 mutated lines, modulations of NK ligands expression by vemurafenib correlated with a slight decrease in NK cytotoxic functions.

Vemurafenib-resistant (R) variants were generated and their characteristics were compared to those of sensitive (S) lines. The acquisition of resistance to vemurafenib induces a significant increase in NK functions (IFNg secretion and target lysis). The responsible mechanisms involve both the expression of NK receptor ligands and the modulation of death domain receptors (Fas, TRAILRII). Transcriptome analyses reveal different targets of interest in the three pairs of S/R melanoma lines carrying the BRAF V600E mutation and distinct additional mutations (submitted manuscript).

Based on our recent results our hypothesize that Lc NKs are important players in tumor immunosurveillance during current treatments of melanoma patients. Immunotherapy approaches targeting these effectors may be of interest in combinations with targeted therapies or immunotherapies. The frequency of intratumoral Lc NKs has been shown to correlate with the presence of stimulatory dendritic cells and this environment is required for a response to anti-PD1 immunotherapy. Innovative antibodies are being developed to activate the antitumor functions of NK cells

Characterization of NK Cells Under First Line Advanced Therapy Either as Curative Therapy for Metastatic Melanoma or as Adjuvant Therapy for High-risk of Recurrence

NK cells are recovered from blood samples taken before the start of treatment and after 3-4 weeks

NK cells are recovered from blood samples taken at 2-3 months to 6 of treatment Late changes from Month2-Month 3 to Month 6 in the expression of membrane or soluble markers of NK or LcT cells during treatment and according to treatment groups (targeted therapy or immunotherapy used in a curative or an adjuvant setting).

analysis of soluble or membrane markers altered during treatment as a function of responders and non-responders according to RECIST 1.1 criteria.

Tumor biopsy analysis to Identification of tumor markers or combination of tumor markers whose expression is associated with response or resistance to therapy according to RECIST 1.1. If sequential biopsies are obtained in patients with skin metastases, investigation of an association between tumor phenotype in the microenvironment at S3-S4 of treatment and response to treatment

Blood analysis evaluat soluble and membrane markers at baseline and during treatment as a function of treatment response

Cellular analysis to see modification of the expression of membrane markers (+/- 30% of expression of the marker or Mean Fluorescence) or soluble markers (+/- 20% of expression of the marker) of NK or LcT cells during the treatment and according to the treatment received: targeted therapy or immunotherapy

Cellular analysis to study modification of the expression of membrane markers (+/- 30% of expression of the marker or of the Mean Fluorescence) or soluble markers (+/- 20% of expression of the marker) of NK or LcT cells during the treatment and according to the presence or not of metastasis at the inclusion

Société de Dermatologie Française

Behaviors and Mental Disorders

Quality of Life

Antineoplastic Agents

Immune Checkpoint Inhibitors

Antineoplastic Agents, Immunological

All patients included in this study will receive approved immune-checkpoint inhibitors therapies, such as CTLA-4, PD-1, and PD-L1 inhibitors.

immune-checkpoint inhibitors therapies

Dominique GENRE, MD

Margot BERLINE, MSc, MBA

Elodie Crétel

Renaud SABATIER, MD

Pierre SOUBEYRAN, Dr

Christelle LEVY, Dr

Christelle LEVY

Leila BENGRINE-LEFEVRE

Laurence CRISTOL, MD

Michaël BRINGUIER, Dr

Emmanuelle BOURBOULOUX, MD

Loïc MOUREY, Dr

Renaud Sabatier, MD

The co-primary objectives will be to assess the safety and quality of life under treatment.

The co-primary objectives will be to assess the safety and quality of life under treatment. Secondary objectives will be evaluations of geriatric data modifications under treatment, efficacy (progression-free survival and overall survival), correlation between toxicity and efficacy, and comparison of the safety profiles between various immunotherapy regimens.

Another secondary objective will be the comparison between patients and clinicians symptom reporting. The investigators will also perform a pharmacokinetics analysis on PD1-monoclonal antibodies to improve the understanding of PD-1 inhibitors pharmacokinetics for the elderly population.

Finally, toxicity and efficacy will be compared to immunological parameters such as the description of tumor infiltrating lymphocytes, markers of immunosenescence and inflammation.

This is a national prospective phase 4, multi-centre, single arm, open-label cohort study to evaluate the safety and efficacy of immune checkpoint inhibitors-based therapies in elderly patients with advanced or metastatic melanoma or NSCLC.

Elderly Cancer PatIents, Safety and qualiTy of Life Under immunOtheraPies

Elderly Cancer PatIents Treated for Advanced or Metastatic Melanoma or NSCLC, Safety and qualiTy of Life Under immunOtheraPies: a Phase IV Trial

Description of adverse events' type, incidence, severity (CTCAE v.5.0), timing, seriousness, and relatedness. This endpoint will be based on the rate of grade ≥ 3 adverse events 18 weeks after treatment initiation, defined as medical assessment of safety including adverse events' type, incidence, severity (graded by the CTCAE\] v. 5.0), timing, seriousness, and relatedness. This will include clinical as well as biological toxicities such as liver and endocrine dysfunctions. All high grade adverse events will be taken into account.

Quality of life will be evaluated using the EORTC QLQ-C30 and QLQ-ELD14 questionnaires collected at inclusion and at every treatment cycles during the first 6 weeks, then every 6 weeks until treatment discontinuation. The proportion of patients with a decrease superior or equal to 10% for their global score between baseline and at 24 weeks after treatment initiation will be estimated.

Geriatric data assessment will be done at inclusion and every 6 weeks until treatment discontinuation. Exhaustive data will be collected at inclusion. The investigators will also assess the G-CODE (Geriatric Core Dataset), a recently described minimum geriatric data set (see SOFOG guidelines). G-CODE assessment will be repeated every 6 weeks during treatment and at treatment discontinuation. These data will be collected either by the geriatrician or trained clinical research nurses during geriatric consultation as part of geriatric follow-up, an integral part of the patient management.

Reminder of CTCAE version 5.0 will be completed by clinicians before every treatment cycle. Patients will also complete a language adapted version of patient-reported outcome PRO-CTCAE questionnaire. For all symptoms, the investigators will measure the proportion of pairs for which clinicians and patients gave an identical grade. The investigators will also measure the proportion of pairs that will disagree for each symptom by one point (e.g., patient grade 2 and clinician grade 1), and the proportion that will disagree by two or more points (e.g., patient grade 2 and clinician grade 4). The investigators will also record the number of symptoms for which each pair agreed.

Evaluation of Progression-free Survival (PFS) will be defined as the time from treatment beginning to radiological (according to the RECIST 1.1 criteria) or clinical progression of the disease as declared by the investigators, or death of any cause. Radiological evaluations will be performed every 6 weeks.

Overall Survival (OS) will be defined as the time from treatment beginning to death of any cause.

Correlation between occurrence of auto-immune adverse events (with a landmark time at week 18) and efficacy (PFS).

Safety profiles comparison according to treatment regimen (PD1-inhibitor monotherapy vs PD1- inhibitor/CTLA4-inhibitor combination vs CTLA-inhibitor monotherapy vs PDL1-inhibitor if available at time of trial beginning) will be performed by looking at the rate of grade 3 to 5 adverse events 18 weeks after treatment initiation for each therapy.

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Genomic and Phenotypic Determinants of Resistance to Immunotherapies in Multiple Myeloma	NCT03848676	Multiple Myelom...	Evaluation of p...	18 Years -	University of Turin, Italy
Study and Modulation of Immune Responses in Primary and Metastatic Colon Cancers	NCT06435689	Colon Cancer Peritoneal Carc...	Sampling	18 Years -	Assistance Publique - Hôpitaux de Paris
Characterization of NK Cells Under First Line Advanced Therapy Either as Curative Therapy for Metastatic Melanoma or as Adjuvant Therapy for High-risk of Recurrence	NCT05062096	Melanoma	Blood samples Skin biopsy	18 Years -	Assistance Publique - Hôpitaux de Paris
Characterization of NK Cells Under First Line Advanced Therapy Either as Curative Therapy for Metastatic Melanoma or as Adjuvant Therapy for High-risk of Recurrence	NCT05062096	Melanoma	Blood samples Skin biopsy	18 Years -	Assistance Publique - Hôpitaux de Paris
Elderly Cancer PatIents, Safety and qualiTy of Life Under immunOtheraPies	NCT03673332	Advanced or Met... Advanced or Met...	immune-checkpoi...	70 Years -	Institut Paoli-Calmettes
Study and Modulation of Immune Responses in Primary and Metastatic Colon Cancers	NCT06435689	Colon Cancer Peritoneal Carc...	Sampling	18 Years -	Assistance Publique - Hôpitaux de Paris

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