Primary cutaneous plasmacytoma should be in the differential diagnosis in case of solitary or multiple erythematous–violaceous nodules or papules. The diagnosis relies on clinical, histological, and immunochemical findings, without underlying evidence of multiple myeloma. Treatment should be individualized, and agents such as bortezomib or lenalidomide have shown to be effective. Multiple myeloma (MM) is a malignant hematological disease characterized by the proliferation of clonal plasma cells in the bone marrow with monoclonal immunoglobulin production leading to anemia, renal impairment, hypercalcemia, and bone lesions 1, 2. Dissemination to the skin (secondary cutaneous plasmacytomas) is usually associated with advanced stages of the disease. By contrast, primary cutaneous plasmacytoma (PCP) is a very rare skin tumor characterized by the absence of bone marrow myeloma infiltration as well as absence of organ damage 1, 3, 4. A 76-year-old man was referred to our hospital in January 2013 by his general practitioner because of asymptomatic skin lesions that had appeared 1 month earlier. The physical examination revealed erythematous–violaceous papules and nodules, measuring 0.5–2 cm on the face (Fig. 1A–C), upper chest, back (Fig. 1D), upper extremities, and legs. Ten years before the patient had been diagnosed having a solitary extramedullary plasmacytoma (SEP) located at the left inferior nasal concha without bone marrow infiltration as well as absence of any other sign of myeloma dissemination including the lack of monoclonal M-component. He achieved and maintained complete remission after treatment with surgical excision and local radiotherapy. Complete remission was confirmed through a new nasal biopsy after treatment. He was followed up during this period of 10 years with physical examination, evaluation of the monoclonal component by serum and urine protein electrophoresis and immunofixation serum-free light-chain (FLC) measurement and annual computed tomography (CT). The only relevant finding during this period of time was the emergence of a monoclonal IgG-Kappa band, with a normal FLC ratio in 2011, that reached 0.7 mg/dL in 2013. At the moment of appearance of the cutaneous lesions, an excisional skin biopsy was performed that revealed a diffuse-pattern proliferation of neoplastic plasma cells in the superficial and deep dermis reaching the subcutaneous tissue with dissection of reticular dermis collagen (Fig. 2A and B). Epidermis and papillary dermis were not affected (Fig. 2C). Cells showed an enlarged size, basophilic cytoplasm, atypical nucleus with clumped chromatin and small nucleolus (Fig. 2D). Immunohistochemical analysis revealed positivity for CD79A (Fig. 3A), CD138 (Fig. 3B), CD56, BCL2 (Fig. 3C), MUM1 (Fig. 3D), as well as negativity for CD3, CD5, CD10, CD20, CD23, CD43, PAX5, BCL6, ciclyne D1, EMA, EBER (EBV). Restriction for Kappa light chains was demonstrated. Proliferative index for Ki67 was approximately 15%. Therefore, it was concluded that the biopsy's skin was infiltrated by a plasma cell neoplasm that was compatible with a primary multiple cutaneous plasmacytoma. The initial nasal biopsy was revised, and it was concluded that both samples were morphologically and immunohistochemically identical. A thorough search for underlying MM was conducted using imaging techniques (skeletal survey and CT scan), serum and urine protein electrophoresis, FLC, and bone marrow aspirate. The absence of myeloma-related symptomatology or findings excluded symptomatic MM from the diagnostic possibilities. Considering the extensive dissemination of the cutaneous involvement, and according to the age of the patient, good performance status and lack of comorbidities, the patient received systemic therapy with a regimen including bortezomib, adriamycin, melphalan, and prednisone (VAMP). After the first six cycles, complete disappearance of the skin lesions and monoclonal component was noticed, and thus, complete response (CR) was obtained. Induction treatment was well tolerated, and the patient received consolidation for six additional cycles with an alternating scheme including the previous regimen (VAMP), alternating with thalidomide, cyclophosphamide, and low-dose dexamethasone (TaCyDex). Although a relapse of primary multiple cutaneous plasmacytoma was detected 2 years after end of treatment, the patient is still alive and remains CR under continuous lenalidomide and dexamethasone treatment. Monoclonal gammopathies constitute a heterogeneous group of diseases characterized by the presence of a single clone proliferation of plasma cells, typically producing a monoclonal immunoglobulin. These entities include a wide spectrum of disorders, from monoclonal gammopathy of uncertain significance to multiple myeloma, plasma cell leukemia, solitary bone plasmacytoma (SBP), or extramedullary plasmacytoma (EMP) 3, 5. Solitary plasmacytoma (SP) is a rare neoplasm defined by localized clonal plasma cell (PC) infiltration without systemic tumor dissemination. Both the skeletal survey and the bone marrow are normal, and no related organ or tissue impairment is observed. Localized clonal PC infiltrates may arise either in the bone (SBP) or extramedular (EMP). Approximately 50% of patients with SBP and 15% with EMP will evolve into MM 6. Within the EMP group, solitary extramedullary plasmacytomas (SEP) are usually localized in the upper respiratory tract and constitute around 3–5% of all plasma cell neoplasms 7, 8. Some patients have a small monoclonal protein, in the serum or urine, that disappears after treatment 3, 4, 9. In our patient, no monoclonal component was detected at the time of the nasal plasmacytoma; however, it was detected 2 years before the second episode. In some patients with SP, clonal plasma cells can be detected in the bone marrow using sensitive techniques such as flow cytometry and this finding is associated with higher risk of progression to active disease 6. However, in our patient, no clonal plasma cells infiltration was observed by high-sensitive flow cytometry investigation neither at diagnosis of nasal EMP nor currently. When only the skin is affected, EMP is referred to as cutaneous plasmacytoma, which is divided into primary cutaneous plasmacytoma (PCP) when there is no evidence of underlying disease, or secondary when it is the result of cutaneous involvement of a hematological systemic disease (approximately in 10% of MM cases) 1, 3, 4, 8. PCP are infrequent tumors, comprising <5% of all primary extramedullary plasmacytomas, and show considerable overlap with the plasmacytic variant of the primary cutaneous marginal zone B-cell lymphoma (PCMZL) included in the World Health Organization-European Organization for Research and Treatment of Cancer classification 10, 11. Diagnosis is based on clinical, histological, and immunochemical findings. Clinically, PCP patients develop solitary or multiple erythematous–violaceous subcutaneous papules, nodules, and/or plaques with a diameter from 1 to 5 cm, with a predilection for the face, trunk, and extremities 4, 9, as was our patient's case. However, some authors state that there are no predilection sites 8, 10. It seems to be more frequent in elderly male population 4. From a histological point of view, a dense monomorphic plasmacytic infiltrate is usually found in the superficial dermis with the epidermis generally spared 4. Atypia, binucleation, and increase in the mitotic activity can be present. Immunohistochemical study usually features positivity for CD79 4, CD138 9, CD38, CD56 8, and MUM1/IRF4 7, 8 and CD20 negativity 4, 7. This technique also allows distinguishing reactive plasma cell proliferation by infections or inflammatory processes from PCP 4, 8. Diagnostic criteria include cytoplasmic expression of immunoglobulins restricted to one immunoglobulin chain and exclusion of underlying myeloma through laboratory, radiological, and bone marrow investigations 9. All of these criteria were met in our patient's case. Therapy options range from surgical excision plus radiotherapy in the case of solitary plasmacytomas 1, 6, to systemic therapy in the case of multiple lesions, as occurred in our case 4, 9. Novel agents, such as proteasome inhibitors and immunomodulatory drugs, have been recently introduced in the treatment of patients with MM, and they have showed to be also effective in EMP, especially for proteasome inhibitors 15, 16. In this patient, our first choice was to combine the proteasome inhibitor bortezomib with conventional agents such as melphalan and prednisone. This combination has demonstrated to be effective in patients with MM. Due to the presence of multiple PCP, we added adryamicine to enhance the synergistic effect. Our patient achieved complete remission after six cycles, and this response was consolidated with six additional cycles of VAMP, but alternating them with an immunomodulatory drug-based combination (TaCyDex) to upgrade the response and avoid the selection of resistant clones. After the last relapse, continuous lenalidomide in combination with dexamethasone was chosen. Treatment was well tolerated and effective, achieving a sustained CR. On the one hand, although our patient had a previous SEP, no circulating aberrant plasma cells were identified in peripheral blood using flow cytometry assessment. Although the sensitivity of the flow cytometry is high, assessments of higher sensitivity would be required to identify the clonal plasma cells. Regarding this, it is important to take into account that it is hypothesized that clonal plasma cells are able to circulate 12-14 resulting in multiple plasmacytomas 6. On the other hand, regardless the fact that diagnosis of primary cutaneous plasmacytoma was performed after excluding the presence of both myeloma and plasmacytoma of any other organ system, it is important to note that the review of the initial nasal biopsy concluded that both samples were morphologically and immunophenotypically identical. Therefore, it is impossible to elucidate whether the latest malignant plasma neoplasm constitutes a late relapse, or instead both episodes are not related with the patient presenting a multiple PCP after an ESP. We present the case of a patient with a multiple cutaneous plasma cell neoplasm with a dermatopathology analysis that favors the option of a common origin of the latest episodes and the previous nasal plasmacytoma. To our knowledge, this is the first case of a multiple PCP with such a long history of previous ESP and good response to treatment. None declared.
Abstract Despite recent progress in its treatment, multiple myeloma (MM) remains incurable, thus necessitating identification of novel anti-MM agents. We report that the marine-derived cyclodepsipeptide Aplidin exhibits, at clinically achievable concentrations, potent in vitro activity against primary MM tumor cells and a broad spectrum of human MM cell lines, including cells resistant to conventional (e.g., dexamethasone, alkylating agents, and anthracyclines) or novel (e.g., thalidomide and bortezomib) anti-MM agents. Aplidin is active against MM cells in the presence of proliferative/antiapoptotic cytokines or bone marrow stromal cells and has additive or synergistic effects with some of the established anti-MM agents. Mechanistically, a short in vitro exposure to Aplidin induces MM cell death, which involves activation of p38 and c-jun NH2-terminal kinase signaling, Fas/CD95 translocation to lipid rafts, and caspase activation. The anti-MM effect of Aplidin is associated with suppression of a constellation of proliferative/antiapoptotic genes (e.g., MYC, MYBL2, BUB1, MCM2, MCM4, MCM5, and survivin) and up-regulation of several potential regulators of apoptosis (including c-JUN, TRAIL, CASP9, and Smac). Aplidin exhibited in vivo anti-MM activity in a mouse xenograft model. The profile of the anti-MM activity of Aplidin in our preclinical models provided the framework for its clinical testing in MM, which has already provided favorable preliminary results. [Cancer Res 2008;68(13):5216–25]
Summary The randomized phase III ELOQUENT ‐2 study ( NCT 01239797) evaluated the efficacy and safety of elotuzumab + lenalidomide/dexamethasone ( EL d) versus lenalidomide/dexamethasone (Ld) in relapsed/refractory multiple myeloma. EL d reduced the risk of disease progression/death by 30% versus Ld (hazard ratio [ HR ] 0·70). Median time from diagnosis was 3·5 years. We present extended 3‐year follow‐up data. Endpoints included progression‐free survival ( PFS ), overall response rate ( ORR ) and interim overall survival ( OS ). Exploratory post‐hoc analyses included impact of time from diagnosis and prior lines of therapy on PFS , and serum M‐protein dynamic modelling. ORR was 79% ( EL d) and 66% (Ld) ( P = 0·0002). EL d reduced the risk of disease progression/death by 27% versus Ld ( HR 0·73; P = 0·0014). Interim OS demonstrated a trend in favour of EL d ( P = 0·0257); 1‐, 2‐ and 3‐year rates with EL d versus Ld were: 91% versus 83%, 73% versus 69% and 60% versus 53%. In patients with ≥ median time from diagnosis and one prior therapy, EL d resulted in a 53% reduction in the risk of progression/death versus Ld ( HR 0·47). Serum M‐protein dynamic modelling showed slower tumour regrowth with EL d. Adverse events were comparable between arms. EL d provided a durable and clinically relevant improvement in efficacy, with minimal incremental toxicity.
Topic: 14. Myeloma and other monoclonal gammopathies - Clinical Background: Talquetamab (tal) is a G protein-coupled receptor family C group 5 member D × CD3 bispecific antibody. In the phase 1/2 MonumenTAL-1 trial (NCT03399799/NCT04636552), tal has shown an overall response rate (ORR) of ≥73% in patients (pts) with relapsed/refractory multiple myeloma (RRMM) who have received ≥3 prior lines of therapy (LOT) and are triple-class exposed (TCE). LocoMMotion (NCT04035226) and MoMMent (NCT05160584) are prospective observational studies characterizing real-world physician’s choice (RWPC) treatment and associated clinical outcomes in pts with TCE RRMM recruited between 2019 and 2022. In the absence of a control arm in MonumenTAL-1, adjusted comparisons can be performed to determine the relative effectiveness of tal vs other treatments. Aims: To contextualize the comparative effectiveness of talquetamab vs RWPC in pts with TCE RRMM. Methods: Individual pt-level data (IPD) from MonumenTAL-1 were included for pts who received tal 0.4 mg/kg subcutaneously (SC) weekly (QW) and tal 0.8 mg/kg SC every other week (Q2W) utilizing the Sept 2022 data cut-off (DCO) date. An external control arm was created using IPD from LocoMMotion and MoMMent (both DCO Oct 2022) who met MonumenTAL-1 eligibility criteria. Imbalances in baseline characteristics of prognostic variables (refractory status, ISS stage, time to progression on prior LOT, extramedullary disease, number of prior LOT, time since diagnosis, average duration of prior LOTs, age, hemoglobin, lactate dehydrogenase, creatinine clearance, ECOG performance status, sex, MM type, and prior stem cell transplant) were adjusted for using inverse probability of weighting (IPW) with average treatment effect in the treated (ATT) weights applied to the RWPC cohort to balance versus the two tal cohorts separately. Balance after adjustment was assessed using standardized mean differences (SMD). Outcomes of interest were ORR, ≥VGPR, ≥CR, DOR, PFS, time to next treatment (TTNT), and OS. Response and progression outcomes were evaluated based on IMWG criteria. For binary outcomes, a weighted logistic regression was used to estimate odds ratios and response ratios (RRs) with the respective 95% CIs. For time-to-event outcomes, a weighted Cox proportional hazards model was used to estimate hazard ratios (HRs) and 95% CIs. Sensitivity analyses evaluated the impact of alternative statistical methods (alternative weighting approaches and multivariable regression). Results: From the pooled RWPC cohort, 177 pts fulfilled the inclusion criteria. At baseline, pts received 58 different treatment regimens. After weighting, the RWPC cohort was well balanced versus both tal cohorts, with all SMD <0.20. Pts treated with tal 0.4 mg/kg QW (N=143) had superior outcomes vs RWPC (see Table): pts were 2.6, 5.3, and 95.3 times more likely to achieve response (ORR), ≥VGPR, and ≥CR, respectively, and had reduced risk for progression or death and death by 47% and 56%, respectively. Similarly, pts treated with tal 0.8 mg/kg Q2W (N=145) had superior outcomes vs RWPC (see Table): pts were 2.6, 5.0, and 106.8 times more likely to achieve response (ORR), ≥VGPR, and ≥CR, respectively, with significantly longer DOR, and had reduced risk for progression or death and death by 57% and 56%, respectively. Results were generally consistent across all sensitivity analyses. Summary/Conclusion: Both schedules of tal showed superior effectiveness compared with RWPC, highlighting its clinical benefit and novel treatment option for pts with TCE RRMM.Keywords: Bispecific, G-protein-coupled receptors, Multiple myeloma, Real world data
8033 Background: As multiple myeloma (MM) negatively affects patients’ (pts) health-related quality of life (HRQoL), assessment of patient-reported outcomes (PROs) in addition to clinical outcomes is important. Teclistamab (tec; JNJ-64007957) is an off-the-shelf bispecific antibody that redirects CD3+ T cells to mediate T-cell activation and subsequent lysis of BCMA-expressing MM cells. Initial results from the pivotal cohort of the phase 1/2 MajesTEC-1 study demonstrated that tec was well tolerated with encouraging efficacy in pts who received ≥3 prior lines of treatment (LOT; including a proteasome inhibitor, an immunomodulatory drug, and an anti-CD38 antibody). Here we report PROs from this cohort. Methods: Pts (aged ≥18 years) had documented RRMM (International Myeloma Working Group criteria), progressive/measurable disease, and had previously received ≥3 prior LOT; prior anti-BCMA treatment (tx) was not allowed. Pts received weekly subcutaneous tec at the recommended phase 2 dose (1.5 mg/kg with step-up doses of 0.06 and 0.3 mg/kg). PROs were assessed at screening and every even cycle (cycles 2–8 reported here) using the EORTC QLQ-C30 (range: 0–100; higher scores indicate better global health status [GHS] but greater symptom severity [symptom scales]) and the EuroQol 5-dimensional descriptive system (visual analog scale [VAS] range: 0 [worst imaginable health state] to 100 [best imaginable]). Tx effect was assessed by a mixed-effects model with repeated measures; the proportion of pts with meaningful improvement was defined as a change ≥10 points. Time to worsening was determined using the Kaplan-Meier estimate. Results: A total of 110 pts were included (median follow-up: 7.8 mos). Overall PRO compliance rates were high (baseline [BL]: 85–90%; cycles 2–8: 80–94%). Tec improved overall HRQoL as evidenced by improvements in GHS scores (cycles 2–8) and reduction in pain (-4.2 [cycle 2] to -15.1 [cycle 8]; Table), with no overall change in physical functioning and fatigue. The proportions of pts with meaningful improvements from BL at cycle 8 were GHS: 50%; physical functioning: 35%; pain: 65%; fatigue: 73%; 50% of pts reported meaningful improvement in their overall health (VAS). Median time to improvement from baseline was ̃1.5 months (with nausea/vomiting and fatigue taking longer to improve), while median time to worsening (all symptoms) ranged from 2 months to not estimable. Conclusions: Consistent with clinical outcomes, pts treated with tec reported rapid, clinically meaningful improvements in HRQoL. Clinical trial information: NCT04557098. [Table: see text]
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