Martha Mims

From the 2026 National Summit on Hematologic Cancers

Background/Objectives: Lymphoma-associated hemophagocytic lymphohistiocytosis (LA-HLH) is a fatal hyperinflammatory syndrome. Non-Hodgkin lymphoma (NHL) is the established primary trigger, while Hodgkin lymphoma (HL) is considered a rare cause. This exploratory study aimed to characterize the features of LA-HLH in a predominantly Hispanic patient population to generate novel pathophysiological hypotheses. Methods: We conducted a retrospective, multicenter analysis of adult patients diagnosed with HLH between 2000 and 2024. Using HLH-2004 criteria, we identified a final cohort of 20 patients with LA-HLH for analysis. Results: In our cohort (70% Hispanic, reflecting the catchment populations of the partic-ipating centers), the most common underlying malignancy was HL (60%), contradicting established literature. Stratification by HIV status suggested two distinct profiles: the HIV-negative group (n=13) was younger and driven almost exclusively by HL (85%), whereas the HIV-positive group (n=7) was older, driven by NHL (86%), and presented with more extreme hyperferritinemia and higher soluble IL-2 receptor (sIL-2R) levels. The overall mortality rate was 57.9%. Conclusions: The unexpected predominance of HL-driven HLH in this cohort suggests a need to re-evaluate the differential diagnosis in specific demographic contexts. Our findings are hypothesis-generating and suggest differing clinicopathological patterns by HIV status and lymphoma subtype; further studies are required to determine whether distinct biological pathways underlie these patterns. Given the retrospective nature and limited sample size, further multicenter studies with uniform laboratory testing and molecular profiling are required to clarify potential biological heterogeneity among LA-HLH presentations.

Individuals with cancer commonly rely on their informal caregivers (e.g., spouse/partner, family member, close friend) to help them manage the demands of the disease and its treatment. Caregiving, including helping with patient care, performing household chores, and providing emotional and practical support, can be particularly demanding for employed caregivers, who must juggle their work responsibilities while providing care. Although a burgeoning literature describes the toll that balancing these oft-competing demands can exact, few resources exist to support employed cancer caregivers. To address this gap, we conducted a narrative review of the impacts of cancer on employed caregivers. We found that employed caregivers experience significant financial impacts in terms of lost time and income. They also experience a variety of work-related (e.g., reduced productivity, absenteeism) and mental health (e.g., stress, burden) impacts. Going forward, prospective studies are needed to characterize changes in caregiver support needs and preferences at different time points along the cancer care continuum (e.g., at diagnosis, during treatment, end-of-life) so that appropriate workplace accommodations can be provided. More population-based studies are also needed to develop models for identifying caregivers who are at increased risk for poor employment or mental health outcomes so that more targeted support programs can be developed. Ultimately, a multipronged effort on behalf of employers, healthcare, and community-based organizations may be needed to support and empower this vulnerable subgroup.

Background: Myeloid sarcoma (MS), or chloroma, is a rare extramedullary malignant tumor that consists of undifferentiated granulocytic cells, and it is most commonly associated with acute myeloid leukemia (AML). Intracranial MS accounts for 0.4% of MS cases, and involvement of the skull base and visual dysfunction is rarely reported. However, the optimal treatment and response to treatment of skull base MS in the presence of visual symptoms is unknown. Case Description: A 30-year-old male with a history of AML presented with rapidly progressive vision loss and a sellar and parasellar mass with bilateral cavernous sinus and optic nerve encasement. The patient underwent endoscopic endonasal transsphenoidal biopsy revealing intracranial MS. He was treated postoperatively with high-dose intravenous and intrathecal cytarabine and had complete restoration of his vision by postoperative day 11. A systematic review of the literature identified six cases of skull base MS, five of whom presenting with visual symptoms. All patients underwent systemic chemotherapy with cytarabine and/or cyclophosphamide, with infrequent use of intrathecal chemotherapy or radiation. Those with reported visual outcomes were diagnosed 4 months or longer after symptom onset and demonstrated no visual improvement with treatment. Conclusion: Skull base MS is a rare disease entity with a high prevalence of visual dysfunction. Our patient’s complete disappearance of intracranial disease and resolution of visual symptoms with systemic and intrathecal chemotherapy highlight the importance of timely diagnosis and appropriate treatment without a need for direct surgical decompression.

Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus endemic in many areas around the world. HTLV-1 can induce the development of adult T-cell leukemia (ATL) or myelopathy/tropical spastic paraparesis (HAM/TSP). We report a patient who presented to our outpatient clinic with massive splenomegaly, weight loss, urinary retention, and lower extremity weakness for the previous 3 years. The patient was found to have positive HTLV-1 by ELISA and Western blot from peripheral blood. Evaluation of the spleen demonstrated T-cell large granular lymphocyte leukemia consistent with ATL. In addition to progressive lower extremity weakness, hyperreflexia and clonus, cerebral spinal fluid was positive for HTLV-1 by ELISA and had a reversed CD4-to-CD8 ratio consistent with HAM/TSP. These findings suggest HTLV-1 induced ATL and HAM/TSP presenting simultaneously in the same patient.

Background: Among men in the U.S., prostate cancer is the most common cancer and the second leading cause of cancer death. Despite its prevalence, there are few established risk factors for prostate cancer. Some studies have found that intake of certain foods/nutrients may be associated with prostate cancer risk, but few have accounted for how intake and metabolic factors may interact to influence bioavailable nutrient levels and subsequent disease risk. Presentation of the hypothesis: The composition of the gastrointestinal (GI) microbiome may influence metabolism of dietary compounds and nutrients (e.g., plant phenols, calcium, choline) that may be relevant to prostate cancer risk. We, therefore, propose the hypothesis that GI microbiota may have a markedly different composition among individuals with higher prostate cancer risk. These individuals could have microbial profiles that are conducive to intestinal inflammation and/or are less favorable for the metabolism and uptake of chemopreventive agents. Testing the hypothesis: Because very little preliminary data exist on this potential association, a case–control study may provide valuable information on this topic. Such a study could evaluate whether the GI microbial profile is markedly different between three groups of individuals: healthy men, those with latent prostate cancer, and those with invasive prostate cancer. Any findings could then be validated in a larger study, designed to collect a series of specimens over time. Implications of the hypothesis: Given the plethora of information emerging from the Human Microbiome Project, this is an opportune time to explore associations between the microbiome and complex human diseases. Identification of profiles that alter the host’s risk for disease may clarify inconsistencies in the literature on dietary factors and cancer risk, and could provide valuable targets for novel cancer prevention strategies.

Background: Thrombotic thrombocytopenic purpura (TTP) is a life‐threatening disease resulting in systemic microvascular thrombosis. The disease is caused by excessive platelet (PLT) adhesion to ultra‐large (UL) von Willebrand factor (VWF) multimers inadequately cleaved by the processing enzyme ADAMTS‐13. While many cases respond to plasma exchange performed with or without concurrent corticosteroids, treatment of the 10% to 20% of patients with refractory disease is difficult. Experimental studies demonstrating that N‐acetylcysteine (NAC) inhibits PLT binding to endothelial cell–secreted and anchored UL VWF multimers suggest that NAC may be useful in the treatment of TTP.Case Report: A 44‐year‐old woman presented with malaise, confusion, chest and abdominal pain, and transient visual loss. Laboratory results and peripheral blood smear were consistent with TTP. The patient was begun on plasma exchange and corticosteroid treatment, but after 10 days the PLT count was still less than 10.0 × 10⁹/L and she developed a fever. Rituximab was initiated, but the patient's condition worsened and she became comatose. Antibiotics were initiated, but cultures remained sterile. After 3 days of coma and further clinical deterioration, treatment with N AC was begun. The patient received a loading dose of 150 mg/kg N AC intravenously (IV) over 1 hour. Within 18 hours the patient awakened abruptly and began communicating with medical personnel. Plasma exchange, corticosteroids, rituximab, and N AC infusion (150 mg/kg IV over 17 hr daily × 10 days) were continued and by Day 17 the PLT count was more than 50 × 10⁹/L. The patient fully recovered and was discharged on Day 31.Conclusion: This is the first complete report of a TTP patient treated with NAC. NAC was a safe and effective supplementary treatment for refractory TTP in this patient.