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Thread: Clinically Significant PCa & AS / Relationship between index lesion and metastases

  1. #1

    Clinically Significant PCa & AS / Relationship between index lesion and metastases

    I don't want to clutter up the main Forum page with threads, so I'm combining topics in this one.

    Defining clinically significant prostate cancer on the basis of pathological findings [2018, Full Text, J. Epstein co-author]

    (Added to the Subforum today)

    Abstract

    The definition of clinically significant prostate cancer is a dynamic process that was initiated many decades ago, when there was already evidence that a great proportion of patients with prostate cancer diagnosed at autopsy never had any clinical symptoms. Autopsy studies led to examinations of radical prostatectomy (RP) specimens and the establishment of the definition of significant cancer at RP: tumour volume of 0.5 cm3, Gleason grade 6 [Grade Group (GrG) 1], and organ‐confined disease. RP studies were then used to develop prediction models for significant cancer by the use of needle biopsies. The first such model was used to delineate the first active surveillance (AS) criteria, known as the ‘Epstein’ criteria, in which patients with a cancer Gleason score of 3 + 3 = 6 (GrG1) involving fewer than two cores, and <50% of any given core, and a prostate‐specific antigen density of <0.15 ng/ml per cm3 had a minimal risk of significant cancer at RP. These were adopted as components of the ‘very‐low‐risk category’ of the National Comprehensive Cancer Network guidelines, in which AS is supported as a management option. With the increase in the popularity of AS, much research has been carried out to better define significant/insignificant cancer, in order to be able to safely offer AS to a larger proportion of patients without the risk of undertreatment. Research has focused on allowing higher volume tumours, focal extraprostatic extension, and a limited amount of Gleason pattern 4, and the significance of different morphological patterns of Gleason 4. Other areas of research that will probably impact on the field but that are not covered in this review include the molecular classification of tumours and imaging techniques.
    (see Full Text, which includes a summary table of AS-protocol criteria)


    I added this study to the Subforum today. It's a genomics study that includes a caveat about focal therapy. All emphasis is mine.

    Frequent clonal relations between metastases and non-index prostate cancer lesions [2019, Full Text]


    Abstract

    Primary prostate cancer lesions are clonally heterogeneous and often arise independently In contrast, metastases were reported to share a monoclonal background.. Because prostate cancer mortality is the consequence of distant metastases, prevention of metastatic outgrowth by primary tumor ablation is the main focus of treatment for localized disease. Focal therapy is targeted ablation of the primary index lesion, but it is unclear whether remaining primary lesions metastasize at a later stage. In this study, we compared copy number aberration profiles of primary prostate cancer lesions with matching pelvic lymph node metastases of 30 patients to establish clonality between a lymph node metastasis and multiple primary lesions within the same patient. Interestingly, in 23.3% of the cases, the regional metastasis was not clonally linked to the index primary lesion. These findings suggest that focal ablation of only the index lesion is potentially an undertreatment of a significant proportion of prostate cancer patients.

    Introduction

    Prostate cancer (PCa) has the highest incidence of all cancers in men worldwide (1). The majority of patients present with a tumor confined to the prostate and can be treated with curative intent. Prevention of metastatic outgrowth by local treatment of the prostate is a key objective of PCa treatment, as systemic metastatic spread is the main cause of mortality. For primary local treatment, a choice is made between radiotherapy (RT) and radical prostatectomy (RP), which are considered equally effective (2). However, both types of treatment are associated with significant adverse side effects, including urinary incontinence, impotence, and bladder and rectum dysfunction (3).

    A more focal treatment of identified tumors in the prostate could spare men the toxicity of whole-gland treatments. However, PCa is often multifocal (4). In approximately 60% of patients, multiple subclones with distinct clinicopathological features are identified in the prostate at the time of diagnosis (5). Conventionally, the largest primary tumor with the highest grade is defined as the index lesion (6, 7). There is limited evidence that progression of the disease into disseminated PCa is linked to the index lesion (8, 9). Several approaches to focal therapy (FT) have been developed in recent years, aimed at ablating the index lesion and maintaining the oncological benefit of active treatments while preserving genitourinary and other organ functions (10).

    However, a number of small reports indicated that metastatic disease does not uniformly originate from the index lesion but can also derive from small, obscure non-index primary lesions. Reports linking non-index lesions with metastases used fluorescence in situ hybridization analyses in 23 cases (11), targeted next-generation sequencing in a single patient case (12), and deep whole-genome sequencing in a cohort study of 10 cases (6). However, because most of these studies are statistically underpowered or used technologies that prevented a comprehensive interpretation of genomic data, it remains to be determined which percentage of lymph node (LN) metastases is clonally derived from a non-index lesion. Structural genomic rearrangements (SGRs) are common in PCa (13), and all SGRs cumulatively constitute a copy number alteration (CNA) profile. Profiling tumors for clonal SGRs reveals tumor evolutionary trajectories, and therefore CNA profiling can be applied to reveal clonality between primary lesions and metastases (12, 14, 15).

    In this study, we used low-coverage whole-genome sequencing (LC-WGS) to uncover CNA profiles of matched primary lesions and local metastases. In total, we have interrogated CNA profiles of 70 primary lesions and matched them with 30 local metastases from 30 patients. By comparing CNA profiles in patients, we aim to shed light on the primary clonal origins of local metastases of PCa. Interestingly, in 23.3% of cases, the index lesion was not the clonal origin of the local metastasis. This suggests that focal ablation of only the index lesion might be an undertreatment of a significant proportion of PCa patients.
    (See also Figure 1)



    There has been discussion on other threads about lesion progression. This is a complex topic, but, if you have access, this is a good paper on the clonal nature of lesion progression:

    The Heterogeneity of Prostate Cancer: A Practical Approach [2018]

    Abstract

    Prostate cancer is a paradigm tumor model for heterogeneity in almost every sense. Its clinical, spatial, and morphological heterogeneity divided by the high-level molecular genetic diversity outline the complexity of this disease in the clinical and research settings. In this review, we summarize the main aspects of prostate cancer heterogeneity at different levels, with special attention given to the spatial heterogeneity within the prostate, and to the standard morphological heterogeneity, with respect to tumor grading and modern classifications. We also cover the complex issue of molecular genetic heterogeneity, discussing it in the context of the current evidence of the genetic characterization of prostate carcinoma; the interpatient, intertumoral (multifocal disease), and intratumoral heterogeneity; tumor clonality; and metastatic disease. Clinical and research implications are summarized and serve to address the most pertinent problems stemming from the extreme heterogeneity of prostate cancer.
    From the Full Text:

    Crucial for the understanding of intratumoral genetic heterogeneity is tumor clonality (Fig. 2). This term means that, within 1 tumor focus, the evolution of the cancer is a step-wise and branched process from the early parent clones that arise from the normal epithelium and constantly progress to a higher-grade tumor via the accumulation of “driver” genetic alterations [54, 57, 58] which, in turn, provide the “fitness” advantage to a new clone (namely, a change in the birth/death balance of tumor cells towards birth). Many other genetic alterations, which have no influence on the birth/death balance are called “passengers” and are being accumulated in the tumor clones as well [59]. The positive “driver” alterations could occur anywhere in the tumor bulk within the preexisting clone and give the start to a new, more survivable clone [60]. Importantly, this also implies that all tumor clones in 1 tumor focus have a common ancestor (with the exclusion of specific circumstances, e.g., collision tumors, when 2 independent tumors coalesce during growth and form 1 focus).
    [Emphasis mine]

    Djin

  2. #2
    Top User garyi's Avatar
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    Always an interesting read, Jared.

    A primary reason I didn't have focal therapy after surgery, even with a once inch primary lesion remaining on my prostate cavity wall, was the concern of smaller tumors, not even identified via PET scan, floating around waiting to do their thing.

    I knew there was a high probability of my ulcerative colitis flaring due to SRT radiation, which happened, and just now seemingly, and slowly, is going into remission. And my PSA is still stirring around. I should know early next week what the latest reading is. It's always something.
    72...LUTS for the past 7 years
    TURP 2/16,
    G3+4 discovered
    3T MRI 5/16
    MRI fusion guided biopsy 6/16
    14 cores; four G 3+3, one G3+4,
    CIPRO antibiotic = C. Diff infection 7/16
    Cured with Vanco for 14 days
    Second 3T MRI 1/17
    Worsened bulging of posterior capsule
    Oncotype DX GPS 3/17, LFP risk 63%, Likelihood of Low
    Grade Disease 81%, Likelihood of Organ Confined 80%
    RALP 7/13/17 Dr. Gonzaglo @ Univ of Miami
    G3+4 Confirmed, Organ confined
    pT2c pNO pMn/a Grade 2
    PSA 0.32 to .54 over 3 months
    DCFPyl PET & ercMRI Scans - 11/17
    A one inch tumor remains in prostate bed = failed surgery
    All met scans clear
    SRT, 2ADT, IMGT 70.2 Gys @1.8 per, completed 5/18
    PSA <.006 9/18, .054 11/18, .070 12/18, .067 2/19, .078 5/19
    We'll see....what is not known dwarfs what is thought to be fact

  3. #3
    Quote Originally Posted by DjinTonic View Post
    The mythological monster Hydra coming to mind. Chop off one head to see two of them regrow.
    --------------
    DOB 1965
    PM me for PSA graphing service & detailed story
    PSA 6.8 11/17
    PSA 7.5 04/18
    MRI 05/18 inconclusive, PI-RADS3?
    PSA 11.8 01/19
    PSA 10.1 02/19
    12 core random biopsy 02/19 (4+3)=7 suspicion of vascular invasion, grade 4 cribriform pattern, no PTEN loss 02/19
    Bone scan negative 04/19
    Symptoms: slight burning when urinating, at times some stinging in bladder region, frequent urination on many days.
    Some ED
    PSA 13.3 04/01/19
    RRP 04/04/19
    pT2c pN0 (0 of 7 lymph nodes positive) pL0 pV0 R0(local) Pn1
    Perineural growth predominantly on right hand side, tumour diameter 15mm 90% G4 10% G3
    Prostatic parenchyma with glandular hyperplasia and chronic granular, partly purulent inflammation.
    PSA 0.14 04/30/19
    PSA 0.02 05/13/19
    PSA 0.008 06/04/19

  4. #4
    Quote Originally Posted by KarlEmagne View Post
    The mythological monster Hydra coming to mind. Chop off one head to see two of them regrow.
    Yes, indeed. On the "good" side, PCa is, for most, slow growing. But its multifocal and heterogeneous nature can make it formidable. Couple that with the finding in the 2nd paper above that in about 1/4 of men with metastases, the metastases did not come from the index lesion (the largest lesion with the highest grade). That should give pause to all but (perhaps) low-risk men considering focal therapy and stress the active part of AS. In addition, it highlights the role that genomic testing can play, whether before or after primary treatment.

    We see evidence of multifocality and heterogeneity in the results of first-time biopsies in Forum Brother's signature. I would a single positive core is the exception. Likewise, Gleason scores often differ among the cores.

    From the Full Text of the Heterogeneity paper above:

    Prostate cancer has an almost unique infiltration pattern, characterized by a relatively nondestructive growth of intervening stroma between benign preexisting glands, creating irregular tongues of tumor tissue that may extend quite far from the main focus of origin. This is in stark contrast to many other solid tumors (e.g., breast cancer, lung cancer, hepatocellular carcinoma, etc.), that often show a locally destructive yet cohesive growth pattern that results in a round tumor nodule, that can be more easily assessed by radiology and/or biopsy. In this sense, prostate cancer is a very ungrateful target indeed, and this has made it the only neoplasm to be diagnosed by random sampling at biopsy.
    It's not so much a question of a single, well-defined lesion progressing in toto, but rather that individual tumor cells can produce clones with different genetic properties, eventually giving rise to a higher Gleason lesion, or a lesion that now has the ability to metastasize. The above-described infiltration doesn't mean a brand new lesion can't just form ex novo in another part of the prostate. What's a fellow to do?

    Djin

    (There is a great title for a pathology paper in the above: Prostate Cancer, the Ungrateful Target.)
    Last edited by DjinTonic; 05-02-2019 at 12:51 PM.
    69 yr at Dx, BPH x 20 yr, 9 (!) neg. biopsies, PCA3 -
    2013 TURP (90→30 g) path. neg. for cancer; then 6-mo. checkups
    6-06-17 DRE: nodule R and PSA rise, on finasteride: 3.6→4.3
    6-28-17 Biopsy #10: 2/14 cores: G10 (5+5) 50% RB, G9 (4+5) 5% RLM
    Bone scan, CTs, X-rays: negative
    8-7-17 Open RP, neg. frozen sections, Duke Regional
    SM EPE BNI LVI SVI LNI(16): negative, PNI+, nerves spared
    pT2c pN0 bilat. acinar adenocarcinoma G9 (4+5) 5% of prostate (4.5 x 5 x 4 cm, 64 g)
    11-10-17 Decipher 0.37 Low Risk: 5-yr met risk 2.4%; 10-yr PCa-specific mortality 3.3%
    Dry; ED OK with sildenafil
    9-16-17 (5 weeks) PSA <0.1
    LabCorp uPSA (Roche ECLIA):
    11-28-17 (3 mo. ) 0.010
    02-26-18 (6 mo. ) 0.009
    05-30-18 (9 mo. ) 0.007
    08-27-18 (1 year) 0.018
    09-26-18 (13 mo) 0.013 (checking rise)
    11-26-18 (15 mo) 0.012
    02-25-19 (18 mo) 0.015
    05-22-19 (21 mo) 0.015

  5. #5
    Top User garyi's Avatar
    Join Date
    Apr 2017
    Posts
    1,174
    You and Karl had me rethinking both our history's, Djin, especially the possibility of a TURP or biopsey unleashing cancer cells outside the prostate. I don't suspect the medical world would have that on the top of their research priority list, nor would they easily admit the possibility, for fear of liability.

    Or so my cynical self suspects.
    72...LUTS for the past 7 years
    TURP 2/16,
    G3+4 discovered
    3T MRI 5/16
    MRI fusion guided biopsy 6/16
    14 cores; four G 3+3, one G3+4,
    CIPRO antibiotic = C. Diff infection 7/16
    Cured with Vanco for 14 days
    Second 3T MRI 1/17
    Worsened bulging of posterior capsule
    Oncotype DX GPS 3/17, LFP risk 63%, Likelihood of Low
    Grade Disease 81%, Likelihood of Organ Confined 80%
    RALP 7/13/17 Dr. Gonzaglo @ Univ of Miami
    G3+4 Confirmed, Organ confined
    pT2c pNO pMn/a Grade 2
    PSA 0.32 to .54 over 3 months
    DCFPyl PET & ercMRI Scans - 11/17
    A one inch tumor remains in prostate bed = failed surgery
    All met scans clear
    SRT, 2ADT, IMGT 70.2 Gys @1.8 per, completed 5/18
    PSA <.006 9/18, .054 11/18, .070 12/18, .067 2/19, .078 5/19
    We'll see....what is not known dwarfs what is thought to be fact

  6. #6
    Quote Originally Posted by garyi View Post
    You and Karl had me rethinking both our history's, Djin, especially the possibility of a TURP or biopsey unleashing cancer cells outside the prostate. I don't suspect the medical world would have that on the top of their research priority list, nor would they easily admit the possibility, for fear of liability.

    Or so my cynical self suspects.
    For non-metastatic PCa I would say that transfer of cells within the prostate is the concern, since circulating tumor cells that we know are in the bloodstream can't establishes themselves elsewhere. If a lesion is metastasis-capable, then the spread outside the prostate by other procedures like a TURP is a valid question.

    Speaking for myself, had I been on AS for PCa and found I needed a procedure for BPH, whether invasive or not, I'd pull the trigger on RP for two reasons: I would worry about the effect of the procedure on the cancer, and I could permanently solve both conditions at once. (Even though I had a very successful TURP for BPH, my prostate had grown back half the removed amount at the time of my RP four years later. My doc had told me that some men need a 2nd BPH procedure in time.)

    Djin
    Last edited by DjinTonic; 05-02-2019 at 02:33 PM.
    69 yr at Dx, BPH x 20 yr, 9 (!) neg. biopsies, PCA3 -
    2013 TURP (90→30 g) path. neg. for cancer; then 6-mo. checkups
    6-06-17 DRE: nodule R and PSA rise, on finasteride: 3.6→4.3
    6-28-17 Biopsy #10: 2/14 cores: G10 (5+5) 50% RB, G9 (4+5) 5% RLM
    Bone scan, CTs, X-rays: negative
    8-7-17 Open RP, neg. frozen sections, Duke Regional
    SM EPE BNI LVI SVI LNI(16): negative, PNI+, nerves spared
    pT2c pN0 bilat. acinar adenocarcinoma G9 (4+5) 5% of prostate (4.5 x 5 x 4 cm, 64 g)
    11-10-17 Decipher 0.37 Low Risk: 5-yr met risk 2.4%; 10-yr PCa-specific mortality 3.3%
    Dry; ED OK with sildenafil
    9-16-17 (5 weeks) PSA <0.1
    LabCorp uPSA (Roche ECLIA):
    11-28-17 (3 mo. ) 0.010
    02-26-18 (6 mo. ) 0.009
    05-30-18 (9 mo. ) 0.007
    08-27-18 (1 year) 0.018
    09-26-18 (13 mo) 0.013 (checking rise)
    11-26-18 (15 mo) 0.012
    02-25-19 (18 mo) 0.015
    05-22-19 (21 mo) 0.015

  7. #7
    Also worth noting is that the TULSA-PRO device, which is a HIFU variant and expected to receive FDA certification this year, is for whole gland treatment.

    While there are focal therapy providers and advocates, there seems to be a lot of recurrences and do-overs. Zapping only the index lesion with maybe a 75 percent chance of stopping the cancer may be OK with a few older patients, but there is too much evidence of heterogenity in PCa for it to assure the majority of prospective patients.
    DOB: May 1944
    In Active Surveillance program at Johns Hopkins
    Strict protocol of tests, including PHI, DRE, MRI, and biopsy.
    Six biopsies from 2009 to 2019. Numbers 1, 2, and 5 were negative. Numbers 3,4, and 6 were positive with 5% Gleason(3+3) found. Last one was Precision Point transperineal.
    PSA 4.4, fPSA 24, PHI 32
    Hopefully, I can remain untreated. So far, so good.

  8. #8
    Quote Originally Posted by garyi View Post
    .....my ulcerative colitis flaring due to SRT radiation, which happened, and just now seemingly, and slowly, is going into remission. And my PSA is still stirring around. I should know early next week what the latest reading is. It's always something.
    Good luck Brother garyi!!!

    May both your UC subside and your PSA wane permanently!!!

    Maintain strength & optimism as always!

    MF
    Last edited by Michael F; 05-02-2019 at 05:26 PM.
    PSA: Oct '09 = 1.91, Oct '11 = 2.79, Dec '11 = 2.98 (PSA, Free = 0.39ng/ml, % PSA Free = 13%)
    Referred to URO MD
    Jan '12: DRE = Positive: "Left induration"
    Jan '12: Biopsy = 6 of 12 Cores were Positive: 1 = Gleason 7 (3+4) and 5 = Gleason 6
    Referred to URO Surgeon
    March '12: Robotic RP: Left Positive Margins + EPEs. MD waited in surgery for preliminary Path Report then excised substantial left adjacent tissue(s) down to negative margins and placed 2 Ti clips for SR guidance, if needed in future.
    Pathology: Gleason (3+4) pT3a pNO pMX pRO / Prostate Size = 32 grams; Tumor = Bilateral; 20% / Perineural invasion: present
    3 month Post Op standard PSA = <0.1 ng/ml
    1st uPSA at 7 months Post Op = 0.018 ng/ml
    uPSA remains "stable" at 84 Months Post Op: Mean = 0.021 (20x uPSAs: Range 0.017 - 0.026) LabCorp: Ultrasensitive PSA: Roche ECLIA
    Continence = Very Good (≥ 99%)
    ED = present

  9. #9
    Top User garyi's Avatar
    Join Date
    Apr 2017
    Posts
    1,174
    [QUOTE=Michael F;381787]Good luck Brother garyi!!!

    May both your UC subside and your PSA wane permanently!!!

    Maintain strength & optimism as always!

    Thank you Michael, and lets not overlook my unique sense of humor

    Had my uPSA draw at LabCorp this morning. It's the first test since my journey began whose results I'm anxious, not worried, just interested, in seeing.

    Also had an appointment with my VA PCP today. It's like kissing your sister. I just use them for back up, and with an old and undeserved Purple Heart, I seem to get expedited service, not that it's significant. Seems all the good VA docs, at least in the Southeast are retiring...being pushed out. Not unlike senior Air Force pilots a few years ago, the same time we were reading about military pilot shortages.

    So feeling good this morning, we went for lunch at a very good Chinese restaurant. I ate carefully, and still exploded shortly thereafter. It was ugly. Ulcerative colitis...part of Behcet's Disease. A gift from SEA, we think.

    Life goes on, and believe it or not, I'm most appreciative and optimistic, dear brother Michael. Yes, and a bit cynical, too.
    72...LUTS for the past 7 years
    TURP 2/16,
    G3+4 discovered
    3T MRI 5/16
    MRI fusion guided biopsy 6/16
    14 cores; four G 3+3, one G3+4,
    CIPRO antibiotic = C. Diff infection 7/16
    Cured with Vanco for 14 days
    Second 3T MRI 1/17
    Worsened bulging of posterior capsule
    Oncotype DX GPS 3/17, LFP risk 63%, Likelihood of Low
    Grade Disease 81%, Likelihood of Organ Confined 80%
    RALP 7/13/17 Dr. Gonzaglo @ Univ of Miami
    G3+4 Confirmed, Organ confined
    pT2c pNO pMn/a Grade 2
    PSA 0.32 to .54 over 3 months
    DCFPyl PET & ercMRI Scans - 11/17
    A one inch tumor remains in prostate bed = failed surgery
    All met scans clear
    SRT, 2ADT, IMGT 70.2 Gys @1.8 per, completed 5/18
    PSA <.006 9/18, .054 11/18, .070 12/18, .067 2/19, .078 5/19
    We'll see....what is not known dwarfs what is thought to be fact

  10. #10
    [QUOTE=garyi;381790]
    Quote Originally Posted by Michael F View Post
    Good luck Brother garyi!!!

    May both your UC subside and your PSA wane permanently!!!

    Maintain strength & optimism as always!

    Thank you Michael, and lets not overlook my unique sense of humor

    Had my uPSA draw at LabCorp this morning. It's the first test since my journey began whose results I'm anxious, not worried, just interested, in seeing.

    Also had an appointment with my VA PCP today. It's like kissing your sister. I just use them for back up, and with an old and undeserved Purple Heart, I seem to get expedited service, not that it's significant. Seems all the good VA docs, at least in the Southeast are retiring...being pushed out. Not unlike senior Air Force pilots a few years ago, the same time we were reading about military pilot shortages.

    So feeling good this morning, we went for lunch at a very good Chinese restaurant. I ate carefully, and still exploded shortly thereafter. It was ugly. Ulcerative colitis...part of Behcet's Disease. A gift from SEA, we think.

    Life goes on, and believe it or not, I'm most appreciative and optimistic, dear brother Michael. Yes, and a bit cynical, too.
    I didn't know that enuchs had a special sense of humor


    Djin, who, wanting to be helpful, asks garyi if he's tried Coltect as add-on therapy? (I have no experience with it, I just happened upon this study looking for something else.)


    Speaking of unique/enuch, I got my (updated) Shingles vaccine shots in a Minute Clinic in a Target. Chatting with the NP, I remarked that the room was rather small, so I see why they call it a Mi-'nute Clinic.
    Last edited by DjinTonic; 05-03-2019 at 02:47 AM.
    69 yr at Dx, BPH x 20 yr, 9 (!) neg. biopsies, PCA3 -
    2013 TURP (90→30 g) path. neg. for cancer; then 6-mo. checkups
    6-06-17 DRE: nodule R and PSA rise, on finasteride: 3.6→4.3
    6-28-17 Biopsy #10: 2/14 cores: G10 (5+5) 50% RB, G9 (4+5) 5% RLM
    Bone scan, CTs, X-rays: negative
    8-7-17 Open RP, neg. frozen sections, Duke Regional
    SM EPE BNI LVI SVI LNI(16): negative, PNI+, nerves spared
    pT2c pN0 bilat. acinar adenocarcinoma G9 (4+5) 5% of prostate (4.5 x 5 x 4 cm, 64 g)
    11-10-17 Decipher 0.37 Low Risk: 5-yr met risk 2.4%; 10-yr PCa-specific mortality 3.3%
    Dry; ED OK with sildenafil
    9-16-17 (5 weeks) PSA <0.1
    LabCorp uPSA (Roche ECLIA):
    11-28-17 (3 mo. ) 0.010
    02-26-18 (6 mo. ) 0.009
    05-30-18 (9 mo. ) 0.007
    08-27-18 (1 year) 0.018
    09-26-18 (13 mo) 0.013 (checking rise)
    11-26-18 (15 mo) 0.012
    02-25-19 (18 mo) 0.015
    05-22-19 (21 mo) 0.015

 

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