logo
    Abstract P1-08-06: SToRM: A prospective clinical trial of 1502 metastatic breast cancer (mBC) patients with detail of clinical presentation, molecular subtype, treatment modalities, prognosis and GWAS genotyping
    0
    Citation
    0
    Reference
    10
    Related Paper
    Abstract:
    Abstract Background: Due to better molecular classification and new treatment options, epidemiology and prognosis of mBC is rapidly changing. Clinical data extracted from randomized studies are only relevant to specific subpopulations and retrospective studies are prone to selection bias. SToRM is a prospective clinical trial that aims to create a cohort of 1500 mBC patients, with the ultimate goal of identifying germ line polymorphisms associated with prognosis of breast cancer (BC) and response to treatment in the metastatic phase. Material and methods: Any newly (within 1 year) diagnosed mBC patients were eligible. Whole blood samples were drawn and germline DNA extracted for genetic analysis. Extensive epidemiologic data, disease history from primary diagnosis to metastatic spread, pathological characteristics and ER, PR and HER2 status were collected. Patients are prospectively followed until death. Genotyping using the HumanCoreExome chipset from Illumina is currently underway and will be completed in early summer 2015. Results: 1502 patients were included from March 2012 to May 2014 from 71 French institutions. Median age at metastatic relapse was 60 years (range 26-93). Median time from primary diagnosis to metastatic relapse was 30 months (range 0-473) with 24% of patients already metastatic at initial diagnosis. 78% of patients were ER+, 18% were HER2+ and only 16% were triple negative. Molecular subtype classification derived from pathological data following St Gallen consensus recommendations is presented below: n (%)Luminal A like261 (22.2%)Luminal B like HER2 negative476 (40.5%)Luminal B like HER2 positive134 (11.4%)HER2 positive non Luminal (ER-)111 (9.5%)Triple negative193 (16.4%)Missing data327 64% of the patients had received previous adjuvant treatment, among which 81% received adjuvant chemotherapy and 9% trastuzumab. At metastatic relapse, loco-regional progression, liver, lung and bone metastasis were documented in 301 (20%), 494 (33%), 410 (27%) and 1017 (68%) patients respectively. 313 patients (21%) had bone only metastatic disease. First line treatment included: chemotherapy (71%), endocrine therapy (50%) and anti-HER2 treatments (17%). Survival data will be presented at the meeting. Conclusion: Despite a theoretically better prognosis and widespread use of adjuvant hormonal treatment, ER+/HER2- breast cancer still account for more than 60% of mBC. The proportion of patients with HER2+ disease (18%) and triple negative disease (16%) is consistent with percentages observed in early BC populations. In comparison with a cohort of "cured", localized cancer, such as the SIGNAL/PHARE study, GWAS analysis will allow for the identification of genetic polymorphisms correlated with treatment resistance. Fundamentally, such variants will provide insight into the molecular mechanisms responsible for host-genetic influence on BC progression. From a clinical perspective, genetic variants that predispose to metastatic disease can serve as stratification variables in future clinical trials, particularly as the development of new treatment options for resistant BC is needed. Citation Format: Bachelot T, Lavergne E, Romieu G, Rios M, Heudel P-E, Roemer-Becuwe C, Jouannaud C, Tredan O, Chaigneau L, Arnedos M, Orfeuvre H, Petit T, Quenel-Tueux N, Jacquin J-P, Ferrero J-M, Moullet I, Abadie-Lacourtoisie S, Penault-Llorca F, Blanc E, Cox D. SToRM: A prospective clinical trial of 1502 metastatic breast cancer (mBC) patients with detail of clinical presentation, molecular subtype, treatment modalities, prognosis and GWAS genotyping. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-08-06.
    Keywords:
    Clinical endpoint
    Objective : To evaluate the distributing and expression of insulin-like growth,factor-1 receptor of LN( - ) breast cancer, UN( + ) breast cancer and normal breast tissue. Methods: The IGF-1R expression on LN( - )breast cancer, LN( + ) breast cancer and normal breast tissue was tested by im-munohistochemistry. Results: The positive rateon LN( - ) breast cancer was 94.12%o(16/17), on LN/( + )breast cancer was 91.30%o(21/23) ,and on normal breast tissue was 58.33% (7/12) . The number of strongstein was 12 on LN( - )breast cancer(strong stein rayte70.59%) , and 8 on LN( + ) breast cancer(strong stein rate 34.78% ) . The positive rate on the LN( - )breast cancer and LN( + ) breast cancer was higer than it on the normal breast tissue( P 0.05) , the overexpression rate on the LN ( - ) breast cancer was higher than it on LN ( + ) breast cancer( P 0.05 ) . Conclusion : These data suggested that IGF-1R play an important role in pathogenesis and development of breast cancer. IGF-1R maybe a adjuvant indexfor diagnosing to breast cancer and estimating prognosis.
    CA 15-3
    Citations (0)
    We aimed to estimate the 15-year and lifetime risks of contralateral breast cancer in breast cancer patients according to the age of diagnosis of the first cancer and the history of breast cancer in the mother. The risks of contralateral breast cancer were estimated for all 78,775 breast cancer patients in the Swedish Family-Cancer Database (age at diagnosis of first breast cancer <70 years). The risk of experiencing a contralateral breast cancer within 15 years of diagnosis was 8.4% [95% confidence interval (CI): 8.1-8.7%] for women with an unaffected mother, was 12% (95%CI: 11-13%) for a woman with a mother with unilateral breast cancer and was 13% (95%CI: 9.5-17%) for women with a mother with bilateral breast cancer. In early-onset diagnosed women (<50 years) with an unaffected mother, the risk of contralateral breast cancer until age 80 was 23% (95%CI: 20-26%) and for late-onset (50-69 years) diagnosed women it was 17% (95%CI: 14-21%). In a woman with a mother with an early-onset unilateral breast cancer, risk of contralateral breast cancer by age 80 was 35% (95%CI: 25-46%). Women with a mother with early-onset bilateral breast cancer had 31% (95%CI: 12-67%) lifetime risk of contralateral breast cancer. The risk of contralateral breast cancer is higher for daughters of breast cancer patients than for daughters of women without breast cancer. Maternal cancer history and age at onset of first breast cancer in women should be taken into account when counseling breast cancer patients about their risk of contralateral breast cancer.
    Citations (11)
    The authors evaluated 5623 cases of primary breast cancer followed for 1 to 21 years. Overall and breast cancer death rates were determined and compared to expected rates. Breast cancer patients showed overall and breast cancer death rates significantly higher than expected and which persisted at long-term follow-up. The observed/expected overall death ratios for follow-up periods of 0-5, 6-10, 11-15 or 16-20 years were 3.61, 2.55, 1.60 and 2.11, respectively. Death rates from breast cancer at 5, 10, 15 and 20 years were 20%, 32%, 40% and 48% respectively. The evidence of a persistent excess mortality even after long-term follow-up suggests the hypothesis that breast cancer is a systemic disease when clinically diagnosed. This study provided no evidence of a "clinical" cure for breast cancer patients. Even for N- patients the 5, 10, 15 and 20 year death rates from breast cancer were 12%, 20%, 28% and 38%, respectively. N- breast cancer, which is currently considered as a localized disease cured by surgery in most cases, would be better regarded to as a slow-growing metastatic disease, although "personal" cure may be achieved in many subjects dying of causes other than breast cancer.
    MRI breast is designed to diagnose breast cancer in female.MRI has a great role in diagnosis of early breast cancer.MRI has a great role in differentiation between postoperative scar and post-operative recurrence in cases of surgically removed cancer breast.MRI also used in follows up the response of chemotherapy in cases of advanced breast cancer.Few literatures explain the use of MRI in male breast cancer.In this case report we present a case of male breast cancer and demonstrate MRI characters, enhancement and diffusion patterns similar to that occur in female breast cancer.In our case report we concluded that MRI morphologic features of cancer breast in male were the same MRI morphologic features of cancer breast in female.Cancer breast in male showed the same enhancement kinetic similar to that occurred in female with cancer breast.Cancer breast in male showed a similar enhancement curves like that in female with breast cancer.Cancer breast in male has the same diffusion patterns that occur in female with cancer breast.
    Breast MRI
    Male Breast Cancer
    Abstract Altered interaction between CD 200 and CD 200R represents an example of “checkpoint blockade” disrupting an effective, tumor‐directed, host response in murine breast cancer cells. In CD 200R1 KO mice, long‐term cure of EMT 6 breast cancer, including metastatic spread to lung and liver, was achieved in BALB /c mice. The reverse was observed with 4 THM tumors, an aggressive, inflammatory breast cancer, with increased tumor metastasis in CD 200R1 KO . We explored possible explanations for this difference. We measured the frequency of circulating tumor cells ( CTC s) in peripheral blood of tumor bearers, as well as lung/liver and draining lymph nodes. In some cases mice received infusions of exosomes from nontumor controls, or tumor bearers, with/without additional infusions of anticytokine antibodies. The measured frequency of circulating tumor cells ( CTC s) in peripheral blood was equivalent in the two models in WT and CD 200R1 KO mice. Increased metastasis in EMT 6 tumor bearers was seen in vivo following adoptive transfer of serum, or serum‐derived exosomes, from 4 THM tumor bearers, an effect which was attenuated by anti‐ IL ‐6, and anti‐ IL ‐17, but not anti‐ TNF α , antibody. Anti‐ IL ‐6 also attenuated enhanced migration of EMT 6 cells in vitro induced by 4 THM serum or exosomes, or recombinant IL ‐6. Exosome cytokine proteomic profiles responses in 4 THM and EMT 6 tumor‐bearing mice were regulated by CD 200: CD 200R interactions, with attenuation of both IL ‐6 and IL ‐17 in 4 THM CD 200 tg mice, and enhanced levels in 4 THM CD 200R1 KO mice. We suggest these cytokines act on the microenvironment at sites within the host, and/or directly on tumor cells themselves, to increase metastatic potential.
    Exosome
    Tumor M2-PK
    Adoptive Cell Transfer
    Primary tumor
    Circulating tumor cell
    Citations (24)