Kymera Therapeutics to Present Preclinical Data Demonstrating Potent Antitumor Activity by a Selective STAT3 Degrader in Hematologic Malignancies at the American Society of Hematology Annual Meeting

On December 9, 2019 Kymera Therapeutics Inc., a biotechnology company pioneering targeted protein degradation to discover breakthrough medicines for patients, reported the company will present new preclinical data showing the further characterization of novel, highly selective and potent degraders of STAT3 with activity across multiple hematologic malignancies including ALK-positive anaplastic large cell lymphoma (ALK+ ALCL), acute myelogenous leukemia (AML) and diffuse large B cell lymphoma (DLBCL) (Press release, Kymera Therapeutics, DEC 9, 2019, View Source [SID1234552161]). Data will be shared during a poster presentation (Abstract #3803) at the American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting in Orlando on Monday, Dec. 9 at 6:00 PM EST in Orange County Convention Center, Hall B, Level 2.

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STAT3 is an oncogenic transcription factor downstream of multiple signaling events including the IL-6/JAK and ALK pathways. Activating mutations and aberrant activation of STAT3 drive a subset of tumors via induction of autocrine factors that promote tumor proliferation and survival, as well as induction of proteins that contribute to a tumor permissive microenvironment. Degrading STAT3 has been shown to disrupt downstream signaling and induce antitumor responses in STAT3-dependent hematologic malignancies.

"As Kymera advances our STAT3 degraders into the clinic, we continue to expand the characterization of the biological impact of STAT3 degradation in liquid and solid tumors including the pharmacodynamic effect required to achieve complete tumor regression in a mouse xenograft model of ALK+ ALCL," said Jared Gollob, MD, CMO of Kymera Therapeutics. "These data highlight the potential for STAT3 degraders to treat STAT3-dependent lymphomas and leukemias, and enable the rational development of a treatment regimen that maximizes the probability of success in patients. We plan to select a lead STAT3 degrader for IND-enabling studies in 2020."

ASH Study Highlights
ABSTRACT #3803, "Small Molecule-Induced, Selective STAT3 Degradation Leads to Anti-Tumor Activity in STAT3-Dependent Heme Malignancies," presented by Fred Csibi, PhD, Associate Director, Oncology Biology at Kymera Therapeutics.

KYM-003 treatment resulted in rapid, potent and highly selective STAT3 degradation with similar activity against both mutant and wild-type STAT3.
KYM-003 repressed the growth in vitro of multiple ALK+ ALCL cell lines as well as AML and DLBCL.
Sustained STAT3 degradation of 90% or greater led to apoptosis induction and cancer cell death within 48hr in vitro and in vivo.
Intermittent dosing of KYM-003 achieved complete tumor regression in an ALK+ ALCL mouse xenograft model.

Nektar Therapeutics Announces Presentation of New Preclinical Data for its IL-15 Agonist, NKTR-255, at the American Society of Hematology (ASH) 2019 Annual Meeting

On December 9, 2019 Nektar Therapeutics (NASDAQ: NKTR) reported three presentations at the 61st American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting & Exposition for its IL-15 agonist and investigational candidate, NKTR-255 (Press release, Nektar Therapeutics, DEC 9, 2019, View Source [SID1234552160]). Data were presented from a number of preclinical studies conducted in collaboration with researchers from the Dana-Farber Cancer Institute and the Fred Hutchinson Cancer Research Center.

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NKTR-255 is an interleukin-15 (IL-15) receptor agonist, which is currently being evaluated in a Phase 1 clinical study in patients with multiple myeloma (MM) and non-Hodgkin’s lymphoma (NHL). NKTR-255 is designed to work by selectively targeting the IL-15 pathway to expand both natural killer (NK) cells and memory CD8 T cell populations.

"The preclinical data being recognized at ASH (Free ASH Whitepaper) demonstrate NKTR-255’s promise in hematological malignancies through its potential to restore both NK cell and memory CD8 T cell compartments in patients," said Loui Madakamutil, Ph.D., Senior Vice President and Head of Discovery and Research at Nektar Therapeutics. "In studies presented by the laboratory of Dr. Nikhil Munshi at Dana-Farber, NKTR-255 enhanced the number and function of NK and CD8+ effector memory T cell populations in peripheral blood and bone marrow from patients with multiple myeloma and, also increased expression of activating receptors found on those NK cells. Separately, researchers from the laboratory of Dr. Cameron Turtle at Fred Hutchinson demonstrated NKTR-255 prevented tumor growth and increased survival of CAR T cells when added to a CD19-targeted CAR T cell regimen in models of B cell lymphoma. This preclinical data reinforces the basis of our ongoing clinical trial evaluating the potential of NKTR-255 in patients with multiple myeloma and non-Hodgkin’s lymphoma."

Details of the preclinical data presentations at ASH (Free ASH Whitepaper) are as follows and are available on the scientific section of Nektar’s website at View Source

Abstract 2866: "Combination of NKTR-255, a polymer conjugated human IL-15, with CD19 CAR T cell immunotherapy in a preclinical lymphoma model," Chou, C., et al. (This study was conducted in collaboration with the Turtle Laboratory in the Fred Hutchinson Cancer Research Center.)

Session: 625. Lymphoma: Pre-Clinical – Chemotherapy and Biologic Agents: Poster II
Date: Sunday, December 8, 2019, 6:00 p.m. – 8:00 p.m. Eastern Standard Time
CAR T cells treated with NKTR-255 demonstrate increased proliferation and survival both in vitro and in vivo which may in part be due to increased expression of bcl-2.
Tumor bearing mice treated with NKTR-255 and CAR T cells have decreased tumor burden and increased survival compared to mice treated with CAR T cells alone.
Tumor-bearing mice previously treated with NKTR-255 and CAR T cells are able to reject tumor re-challenge supporting persistence of functional CAR T cells.
Abstract 4398: "Restoring innate and adaptive immune repertoire in multiple myeloma for therapeutic application," Fernandez, R., et al. (This study was conducted in collaboration with Dr. Nikhil C. Munshi at the Jerome Lipper Multiple Myeloma Center at Dana-Farber Cancer Institute.)
Note: Dr. Rafael Fernandez was recognized with a 2019 ASH (Free ASH Whitepaper) Abstract Achievement Award for this abstract.

Session: 652. Myeloma: Pathophysiology and Pre-Clinical Studies, Excluding Therapy: Poster III
Date: Monday, December 9, 2019, 6:00 p.m. – 8:00 pm. Eastern Standard Time
Multiple myeloma patients are known to experience impaired innate immunity and a decline in function of NK cells along with lower expression of activating receptors found on these cells.
Treatment with NKTR-255 enhanced the number and function of both NK and CD8+ effector memory T cell populations in peripheral blood from healthy donors and MM patients in a dose dependent manner.
NKTR-255 was also able to revert the inhibitory status of NK cells from MM patients and showed synergy with daratumumab and elotuzumab to significantly increase status of NK susceptibility of the MM cells.
Findings suggest NKTR-255 delivers a significant impact on the activation of effector cell function to efficiently target MM cells.
Details of the Trials in Progress poster presentation are as follows:

Abstract 4459: "A Phase 1, Open-Label, Multi-Center, Dose Escalation and Dose Expansion Study of NKTR-255 As a Single Agent in Relapsed or Refractory Hematologic Malignancies and in Combination with Daratumumab As a Salvage Regimen for Multiple Myeloma," Shah, N., et al.

Session: 704. Immunotherapies: Poster III
Date: Monday, December 9, 2019; 6:00 p.m. – 8:00 p.m. Eastern Standard Time
About the Phase 1 Study of NKTR-255 (NCT04136756)

NKTR-255 is currently being evaluated in an open-label Phase 1, dose escalation and dose expansion study in patients with select hematological malignancies (relapsed or refractory NHL or MM). The dose escalation phase of the study will evaluate the safety and tolerability of NKTR-255 as monotherapy in approximately 40 patients in order to establish a recommended Phase 2 dose (RP2D) for NKTR-255. The dose expansion phase of the study will enroll patients with MM or NHL (relapsed/refractory salvage) to evaluate the NKTR-255 RP2D in combination with targeted antibodies, including anti-CD38 monoclonal antibody, daratumumab in MM and anti-CD20 monoclonal antibody, rituximab in NHL. These studies are designed to assess pharmacokinetic and pharmacodynamic effects, anti-tumor activity and a range of biomarker assessments associated with NK and memory T cell populations.

About NKTR-255

NKTR-255 is an IL-15 receptor agonist designed to activate the IL-15 pathway and expand NK cells and promote the survival and expansion of memory CD8+ T cells without inducing suppressive regulatory T cells. Through optimal engagement of the IL-15Rα/IL-2Rβγ receptor complex, NKTR-255 enhances functional NK cell repopulation and formation of long-term immunological memory, which may lead to sustained anti-tumor immune response. NKTR-255 is uniquely designed to overcome the challenges of recombinant IL-15 and other IL-15 agonists, which are rapidly cleared from the body and have shown diminishing response to successive doses.1 Designed using Nektar’s polymer conjugation technology to extend circulating half-life, NKTR-255 can be dosed every 14 or 21 days.

CTI BioPharma Announces Presentation of Data Supporting Pacritinib’s Benefit in Myelofibrosis Patients with Severe Thrombocytopenia at the 61st American Society of Hematology Meeting

On December 9, 2019 CTI BioPharma Corp. (Nasdaq: CTIC) reported the presentation of data from the Company’s pacritinib development program, including results from the PAC203 Phase 2 clinical trial, at the 61st American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting being held December 7-10 in Orlando, Florida (Press release, CTI BioPharma, DEC 9, 2019, View Source [SID1234552159]).

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"The data presented at ASH (Free ASH Whitepaper) underscore the clinical and scientific rationale for our ongoing PAC203 Phase 3 PACIFICA trial evaluating pacritinib at 200 mg BID in severely thrombocytopenic myelofibrosis patients," said Adam R. Craig, M.D., Ph.D. "Pacritinib has now been demonstrated to provide clinical benefit in treating severely thrombocytopenic myelofibrosis (platelet counts less than 50,000 per microliter) in three clinical trials, including two prior randomized Phase 3 studies. Further, the PAC203 Phase 2 results from the 200 mg BID cohort demonstrate a favorable risk-benefit profile for pacritinib when treating patients with advanced disease that have high mutational risk and long durations of prior ruxolitinib exposure. The totality of the data presented at ASH (Free ASH Whitepaper) reinforces our belief that pacritinib has the potential to be an important therapy for severely thrombocytopenic myelofibrosis patients, a population for whom available therapeutic options are limited and often ineffective."

"While currently available treatments for myelofibrosis convey clinical benefit to a majority of the population, patients who are severely thrombocytopenic, and are therefore considered high-risk, continue to lack safe and efficacious therapies," said Claire N. Harrison, M.D., Consultant Haematologist and Professor of Myeloproliferative Neoplasms in London, as well as Chair of the PACIFICA steering committee and Principal Investigator of the PAC203 Phase 2 trial. "Myelofibrosis patients with platelet counts of less than 50,000 per microliter have a median survival of approximately 8 months after discontinuation of first line ruxolitinib therapy. In the PAC203 Phase 2 trial, which represents one of the most advanced and heavily pre-treated myelofibrosis patient populations studied to date as demonstrated by a median prior exposure to ruxolitinib of 1.7 years and the high risk mutational profiles, pacritinib at 200 mg BID achieved an impressive response rate in the severely thrombocytopenic patient population of 17% with a promising safety profile, demonstrating its potential to change the treatment paradigm in this area of serious unmet medical need."

All posters and presentation materials will be available at ctibiopharma.com following the presentations.

Results of PAC203: A Randomized Phase 2 Dose-Finding Study and Determination of the Recommended Dose of Pacritinib

Results from the PAC203 Phase 2 trial are being presented today, Monday, December 9, at 10:30 AM ET, in an oral presentation session.

Abstract: No. 667

Summary: PAC203 enrolled patients with myelofibrosis who were intolerant of or who had not benefitted from prior treatment with ruxolitinib. Patients were randomized in equal measure across 3 dosing arms: 200mg twice-daily (BID), 100mg BID, and 100mg daily (QD), with randomization stratified by baseline platelet count. Patients were mostly thrombocytopenic and anemic at baseline, with a median platelet count was 55,000, and 44% of patients having baseline platelet counts of less than 50,000. Patients had been heavily pre-treated with ruxolitinib, with a median 1.7 years of prior exposure. The study endpoint was broadly defined as an analysis of safety and efficacy data across dosing arms based on data after all patients either reached week 24 or stopped study treatment.

Pacritinib was shown to be generally well tolerated across dosing cohorts, with the most common treatment-emergent non-hematologic adverse events (AEs) being gastrointestinal, including diarrhea (20.5%; Grade 3: 3.1%) and nausea (20%; Grade 3: 0.6%), distributed similarly across arms. The most common hematologic AEs were thrombocytopenia and anemia, both occurring at higher frequencies at the 200 mg dose BID (32% and 22% respectively); this did not, however, lead to higher rates of Grade 3/4 hemorrhage at higher doses (200 mg BID: 5.6%; 100 mg BID: 0%; 100 mg QD: 5.8%; all Grade 3). Similarly, the highest dose saw no excess in Grade 3/4 cardiac (200 mg BID: 3.7%; 100 mg BID: 7.3%; 100 mg QD: 3.7%; all Grade 3) or infectious (200 mg BID: 15%; 100 mg BID: 11%; 100 mg QD: 12%) AEs. In this cohort of advanced MF patients, there were 7 Grade 5 (fatal) AEs: 2 at 200 mg BID (sepsis, subdural hematoma), 3 at 100 mg BID (disease progression, subdural hematoma, heart failure), and 2 at 100 mg QD (sepsis, tuberculosis).

The 200 mg BID arm had the highest observed rates of SVR ≥35% (200 mg BID: 9.3%; 100 mg BID: 1.8%; 100 mg QD: 0.0%). Of the 5 patients with SVR ≥35% at the 200 mg BID dose, 4 had platelet counts <50,000/mL, representing a 17% (4/24) response rate among patients with severe thrombocytopenia. Though a dose response relationship was not observed in total symptom score (TSS) based on the threshold of 50% reduction in symptom score, as 4 patients achieved this endpoint on all arms, the median reduction in TSS was greatest for patients treated at 200 mg BID (200 mg BID: 27%%; 100 mg BID: 16%; 100 mg QD: 3%).

The data from PAC203 support the Phase 3 PACIFICA trial, currently underway to compare the safety and efficacy of 200 mg BID of pacritinib to Physician’s Choice in 180 adult myelofibrosis patients with severe thrombocytopenia (platelet counts of less than 50,000 per microliter).

The Oral JAK2/IRAK1 Inhibitor Pacritinib Demonstrates Spleen Volume Reduction in Myelofibrosis Patients Independent of JAK2V617F Allele Burden

Results from a retrospective analysis from two Phase 3 studies, PERSIST-1 and PERSIST-2, of pacritinib in myelofibrosis patients were presented in a poster session on Saturday, December 7.

Abstract: No. 1674

Summary: A retrospective analysis of PERSIST-1 and PERSIST-2 was performed in which outcomes were stratified by JAK2 V617F mutation status and allele burden. The efficacy endpoint for this study was the percentage of patients achieving ≥35% SVR at week 24 based on an intention-to-treat analysis. Analysis was based on pooled results across the two studies for patients treated with pacritinib and those treated with best available therapy (BAT), and assessed patients with JAK2 V617F for possible relationship between allelic burden and SVR at 24 weeks. The analysis showed pacritinib was associated with a significantly higher rate of SVR response than BAT among patients with low JAK2 allele burden (<50%), while no SVR response was observed for patients treated with BAT (including ruxolitinib) who had low JAK2 allele burden or JAK2 V617F-negative disease. This data suggests that pacritinib, a JAK2/IRAK1 inhibitor, may provide benefit over a wider range of patients with myelofibrosis compared to other JAK inhibitors, specifically patients with low JAK2 allele burden who were shown to have lower baseline platelet counts, more severe anemia and smaller spleen size.

Pacritinib Demonstrates Efficacy Versus Best Available Therapy in Myelofibrosis Patients with Severe Thrombocytopenia in Two Phase 3 Studies

Results from a retrospective analysis of PERSIST-1 and PERSIST-2 will be presented in a poster session today, Monday, December 9 at 6:00 PM ET.

Abstract: No. 4195

Summary: This analysis was performed in patients treated on PERSIST-1 and PERSIST-2 with a baseline platelet count <50,000/μL. At 24 weeks, significantly more patients achieved ≥35% SVR with pacritinib compared with BAT (P-values <0.01). Although not statistically significant, TSS reductions ≥50% nearly doubled for those receiving pacritinib versus BAT. The safety profile in patients with severe thrombocytopenia was generally manageable and consistent with the overall study populations from the two Phase 3 trials. This retrospective analysis represents the largest population of patients with MF and severe thrombocytopenia to be studied in clinical trials, a population with a serious unmet medical need, and the results illustrate the clinical activity of pacritinib in the treatment of these patients.

Molecular Analysis in the Pacritinib Dose-Finding PAC203 Study in Patients with Myelofibrosis Refractory or Intolerant to Ruxolitinib

Results from a baseline mutational analysis of patients enrolled in the Phase 2 PAC203 study of pacritinib in patients with myelofibrosis will be presented in a poster session today, December 9, 2019 at 6:00 PM ET.

Abstract: No. 4214

Summary: The baseline mutational analysis was performed on 105 (out of total 164 recruited, 161 treated) myelofibrosis patients in the PAC203 study. The PAC203 cohort, characterized by ruxolitinib failure and a high burden of anemia and thrombocytopenia, was shown to be a molecularly high-risk population, characterized by high incidence of HMR, TP53 and RAS mutations, high mutational burden, and low incidence of CALR mutations.

About Myelofibrosis and Severe Thrombocytopenia

Myelofibrosis is a type of bone marrow cancer that results in formation of fibrous scar tissue and can lead to severe anemia, weakness, fatigue and an enlarged spleen and liver. Patients with severe thrombocytopenia are estimated to make up more than one-third of patients treated for myelofibrosis, or approximately 18,000 people.1 Severe thrombocytopenia, defined as blood platelet counts of less than 50,000 per microliter, has been shown to result in overall survival rates of just 15 months.2 Thrombocytopenia in patients with myelofibrosis is associated with the underlying disease but has also been shown to correlate with treatment with ruxolitinib, which can lead to dose reductions, and as a result, may potentially reduce clinical benefit. Survival in patients who have discontinued ruxolitinib therapy is further compromised, with an average overall survival of seven to 14 months.3,4 There are currently no approved therapies available to treat myelofibrosis patients with severe thrombocytopenia, or patients who have failed ruxolitinib treatment, thereby making this a significant unmet medical need.

About Pacritinib

Pacritinib is an investigational oral kinase inhibitor with specificity for JAK2, FLT3, IRAK1 and CSF1R. The JAK family of enzymes is a central component in signal transduction pathways, which are critical to normal blood cell growth and development, as well as inflammatory cytokine expression and immune responses. Mutations in these kinases have been shown to be directly related to the development of a variety of blood-related cancers, including myeloproliferative neoplasms, leukemia and lymphoma. In addition to myelofibrosis, the kinase profile of pacritinib suggests its potential therapeutic utility in conditions such as acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), chronic myelomonocytic leukemia (CMML), and chronic lymphocytic leukemia (CLL), due to its inhibition of c-fms, IRAK1, JAK2 and FLT3.

STORM Therapeutics’ Collaborator Awarded ASH-BSH Abstract Achievement Award at the 61st ASH Annual Meeting & Exposition

On December 9, 2019 STORM Therapeutics, the biotechnology company focused on the discovery of small molecule therapies modulating RNA epigenetics reported, that its collaborator Dr. Konstantinos Tzelepis, Sir Henry Wellcome Fellow and visiting scientist at the Wellcome Sanger Institute, received the ASH (Free ASH Whitepaper)-BSH Abstract Achievement Award for his work on STORM Therapeutics’ lead programme, METTL3, at the 61st Annual Meeting of the American Society of Hematology (ASH) (Free ASH Whitepaper) held on 7th-10th December 2019 in Orlando, Florida (Press release, STORM Therapeutics, DEC 9, 2019, View Source;exposition-300971436.html [SID1234552158]).

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Dr. Tzelepis received the meritorious award for his abstract entitled ‘Pharmacological Inhibition of the RNA m6a Writer METTL3 As a Novel Therapeutics Strategy for Acute Myeloid Leukemia’ at the Abstract Achievement Award Ceremony which was held on Saturday, 7th December 2019 at 3:30pm (EST) at the Orange County Convention Center in Exhibit Hall B2-B4.

Dr. Tzelepis’s work, which was carried out in collaboration with the Wellcome Sanger Institute and the University of Cambridge, was presented in an oral presentation during the "802. Chemical Biology and Experimental Therapeutics: Novel Compounds and Mechanisms of Action" session on Sunday, 8th December 2019 at 9:30am-11:30am (EST) at the Orange County Convention Centre. The abstract and talk encapsulated the ground-breaking work made on targeting RNA modifying enzymes for cancer treatment and described the recent progress made with the METTL3 inhibitor.

STORM has identified small molecule inhibitors of METTL3 that are orally bioavailable and show pronounced anti-tumour efficacy in physiologically relevant, proof of concept animal models of Acute Myeloid Leukaemia (AML). The talk demonstrated that small molecule inhibition of METTL3 produces the same phenotype and effects previously described in one of STORM’s founder scientists’ publications using genetic models and validates METTL3 as a druggable target for cancer.

Keith Blundy, CEO of STORM Therapeutics, said: "STORM is progressing fast in its preclinical work with our multiple programmes to showcase the capabilities of our novel platform. STORM is a pioneer in RNA epigenetics and we are very pleased to hear that our collaborator is being recognized for the partnership research of METTL3. As the first company in the world to demonstrate in vivo activity of an RNA methyltransferase inhibitor, we are excited to be leading the field as we look to develop these highly innovative new treatment options for cancer patients."

New Menarini CELLSEARCH Studies to be Presented at San Antonio Breast Cancer Symposium

On December 9, 2019 Menarini Silicon Biosystems, the pioneer of liquid biopsy and rare cell technologies, reported that new research utilizing the company’s CELLSEARCH Circulating Tumor Cell (CTC) test will be featured at the upcoming 2019 San Antonio Breast Cancer Symposium (SABCS) (Press release, Menarini Silicon Biosystems, DEC 9, 2019, View Source [SID1234552157]).

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Researchers from Northwestern University will present the results of three studies that used the FDA-cleared CELLSEARCH system to conduct CTC testing in a total of 463 breast cancer patients. The poster presentations provide preliminary insight into the use of liquid biopsy and CTC enumeration to help clinicians better understand the metastatic process and facilitate management of patients with metastatic breast cancer (MBC).

"Liquid biopsies enable us to monitor the disease over time and more fully understand the complexity, heterogeneity and evolution of the disease, which is critical to selecting better treatments," said Massimo Cristofanilli, M.D., F.A.C.P., Associate Director for Translational Research, Robert H. Lurie Comprehensive Cancer Center of Northwestern University. "While we need to expand these data to further prospective studies for validation, this new research marks an important step towards potentially expanding the role of liquid biopsy — particularly enumeration of CTCs and molecular analysis for accurate and real-time prediction and prognostic monitoring the metastatic process."

Dr. Cristofanilli co-authored all three CELLSEARCH studies being presented at SABCS**.

CELLSEARCH is the first and only clinically validated blood test cleared by the FDA for detecting and enumerating CTCs as an aid for physicians to manage patients with metastatic breast, prostate and colorectal cancers. The test is also approved by the Chinese National Medical Products Administration (NMPA) for use as an aid in monitoring metastatic breast cancer patients.

"There is a large body of research supporting the longstanding value of CTCs, which is one of the reasons many physicians are using CELLSEARCH in their clinics," said Fabio Piazzalunga, President and CEO of Menarini Silicon Biosystems, Inc. "Studies like these help to increase understanding of the value of liquid biopsy and CTC enumeration and play an important role in advancing precision medicine for metastatic breast cancer."

Poster Presentation Details:

Poster Session 3 – Thursday, December 12, 5:00 pm – 7:00 pm, Hall 1

Title:

Liquid biopsy methods and machine learning modeling to understand organ tropism and metastization behavior of metastatic breast cancer – P3-01-05

Authors:

Gerratana L et al.
Northwestern University, Chicago, IL; IRCCS CRO Aviano National Cancer Institute, Aviano, Italy.

Poster Session 4 – Friday, December 13, 7:00 am – 9:00 am, Hall 1

Title:

Clinical relevance of CK+/CD45+, dual-positive circulating cells (DPCells) in patients with metastatic breast cancer (MBC) – P4-01-07

Authors:

Reduzzi et al.
Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, IL.

Title:

Anatomical staging and value of CTCs in locally advanced breast cancer (LABC) and metastatic breast cancer (MBC) – P4-01-08

Authors:

Zhang Q et al.
Department of Medicine, University of Udine, Uniud, Italy; Department of Medicine, Northwestern University, Chicago, IL; Department of Pathology, Northwestern University, Chicago, IL.

The CELLSEARCH System is the most extensively studied CTC technology, with research published in more than 650 peer-reviewed publications. Providing valuable information to help physicians make patient-management decisions along with other clinical monitoring methods, the CELLSEARCH CTC test is performed at a reference laboratory using the CELLSEARCH System. The testing can be used throughout a given therapy for metastatic breast, colorectal, and prostate cancer to monitor a patient’s status by showing if their prognosis is favorable.

To learn more about the CELLSEARCH System, SABCS attendees can visit Menarini Silicon Biosystems at Booth #909.

SABCS will be held at the Henry B. Gonzalez Convention Center, San Antonio, Texas, Dec. 10-14, 2019.