About

Asim Ijaz Khwaja is the Sumitomo-FASID Professor of International Finance and Development at Harvard Kennedy School. His role involves research and teaching in the fields of international finance and development. The page indicates his involvement in various courses, research projects, and engagement activities related to economic development, social entrepreneurship, and social innovation. His work is associated with several research centers, including the Center for Economic Research in Pakistan (CERP) and the Entrepreneurial Finance Lab (EFL). His contact information is provided, including his office location at Rubenstein-434, Harvard Kennedy School, and his email address. The page emphasizes his academic and research contributions in the areas of economic development and finance, though specific details of his research focus or background are not included in the provided text.

Research topics

• Internal medicine
• Medicine
• Oncology
• Gastroenterology
• Immunology
• Intensive care medicine
• Biology
• Pediatrics

Selected publications

• Helping Schools Survive: Experimental Evidence on the Impact of Financial and Educational Support to Private Schools

  SSRN Electronic Journal · 2025-01-01

  articleOpen access
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• Helping Schools Survive: Experimental Evidence on the Impact of Financial and Educational Support to Private Schools

  National Bureau of Economic Research · 2025-07-01

  reportOpen access

  Low-cost private schools have increased educational access in low-income countries, but frequent school closures lead to costly disruptions in children's schooling.We provide experimental evidence from Pakistan that both school loans and educational products and services (EPS) are (a) commercially viable products and (b) substantially and similarly improve school survival rates.Moreover, loans decrease closure rates more for schools with larger initial enrollments and lower baseline test scores, while EPS show no such differential impact.These results demonstrate how financial and educational input constraints can significantly affect school survival while underscoring that the fungibility of entrepreneurial support matters.

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• Preclinical development of anti-CD21 chimeric antigen receptor T cells to treat T cell acute lymphoblastic leukemia

  Science Translational Medicine · 2025-04-16

  articleOpen access

  Patients with relapsed/refractory (r/r) T cell acute lymphoblastic leukemia (T-ALL) have a dismal prognosis, highlighting the urgent need for effective therapies. Chimeric antigen receptor (CAR)-T cell approaches targeting pan-T cell antigens may be limited by T cell aplasia and fratricide, necessitating "rescue" allogeneic hematopoietic stem cell transplantation. In this study, we identify CD21, a pan-B cell marker, as a promising target for T-ALL immunotherapy. CD21 is expressed in 50% of T-ALL cases at diagnosis but in fewer than 10% of mature T cells. We observed that CAR-T cells targeting membrane-distal CD21 epitopes were ineffective, likely because of the bulky, glycosylated nature of the antigen. However, when we engineered CAR-T cells to target membrane-proximal CD21 epitopes using an antigen-binding fragment (Fab)-CAR design, we demonstrated robust activity against T-ALL cell lines, primary tumors, and patient-derived xenografts in both in vitro and in vivo models. The enhanced efficacy of this Fab-CAR design was driven by its high stability and reduced surface expression, addressing limitations of traditional CAR constructs. In addition, pharmacological inhibition of the phosphatidylinositol 3-kinase axis up-regulated CD21 expression in T-ALL, further enhancing the potency of anti-CD21 CAR-T cells in vitro and in a patient-derived xenograft in vivo model. This study establishes CD21 as a viable CAR-T target and highlights advances in CAR design for bulky antigens, as well as the potential for pharmacological strategies to augment target expression. Anti-CD21 CAR-T cells represent a promising therapeutic option for improving outcomes for patients with T-ALL.

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• Molecular monitoring versus standard clinical care in younger adults with acute myeloid leukaemia: results from the UK NCRI AML17 and AML19 randomised, controlled, phase 3 trials

  The Lancet Haematology · 2025-04-28 · 9 citations

  articleOpen access

  <h2>Summary</h2><h3>Background</h3> In patients with acute myeloid leukaemia treated with curative intent, the detection of measurable residual disease (MRD) generally confers a poor prognosis. This study aimed to identify whether altering treatment based on MRD results can improve survival. <h3>Methods</h3> In the UK NCRI AML17 and AML19 randomised, controlled, phase 3 trials, performed in the UK, Denmark, and New Zealand, we screened patients aged 16–60 years with newly diagnosed acute myeloid leukaemia for molecular markers suitable for disease monitoring, including <i>NPM1</i> mutations and fusion genes. Patients with a marker were randomly assigned (2:1) to either sequential molecular MRD monitoring during treatment and for 3 years after, or standard clinical care only with no molecular monitoring. In the monitoring group, treating physicians decided whether and how to incorporate the MRD results into the patient's therapy, including in cases of MRD relapse. The primary endpoint was overall survival. Prespecified subgroup analysis of the primary outcome included analysis by molecular group (<i>NPM1^mut</i> with <i>FLT3</i>-ITD, <i>NPM1^mut</i> without <i>FLT3</i>-ITD, and fusion gene transcripts). Both trials were registered with ISRCTN, ISRCTN55675535 and ISRCTN78449203, and are completed. <h3>Findings</h3> In the AML17 trial, 1836 patients were enrolled between June 1, 2012 and Dec 31, 2014. In the AML19 trial, 965 patients were enrolled between Nov 9, 2015, and Jan 23, 2018. 637 patients were randomly assigned across both trials (289 to MRD monitoring and 144 to no monitoring in AML17 and 136 to MRD monitoring and 68 to no monitoring in AML19). With a median follow-up time of 4·9 years (IQR 3·6–5·9), overall survival at 3 years was 70% (95% CI 66–75) in patients in the monitoring group and 73% (68–80) in patients in the no-monitoring group. Meta analysis of the two studies showed no difference in overall survival (hazard ratio [HR] 1·11, 95% CI 0·83–1·49; p=0·25). In the pre-specified subgroup analysis of the primary endpoint, overall survival at 3 years in patients with both <i>NPM1</i> and <i>FLT3</i> internal tandem duplication (ITD) mutations was 69% (95% CI 60–79) in the monitoring group and 58% (45–74) in the no-monitoring group (HR 0·53, 95% CI 0·31–0·91; p=0·021). However there was no difference in survival by randomisation in patients with <i>NPM1</i> mutations without <i>FLT3</i>-ITD (overall survial 69% [95% CI 62–77] in the monitoring group and 78% [70–87] in the no monitoring group; HR 1·56, 95% CI 0·96–2·52) or those with fusion gene transcripts (overall survial 72% [95% CI 65–79] in the monitoring group and 77% [68–87] in the no monitoring group; HR 1·28, 95% CI 0·80–2·18). <h3>Interpretation</h3> Sequential molecular MRD monitoring, coupled with MRD-guided treatment, did not improve overall survival in the entire study population; however, in the subgroup of patients with baseline <i>NPM1</i> and <i>FLT3</i> ITD mutations, we observed a survival benefit for MRD monitoring. <h3>Funding</h3> National Institute for Health Research, Blood Cancer UK, and Cancer Research UK.

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• Co-operation of MCL-1 and BCL-XL anti-apoptotic proteins in stromal protection of MM cells from carfilzomib mediated cytotoxicity

  Frontiers in Oncology · 2024-04-08 · 5 citations

  articleOpen access

  Introduction BCL-2 family proteins are important for tumour cell survival and drug resistance in multiple myeloma (MM). Although proteasome inhibitors are effective anti-myeloma drugs, some patients are resistant and almost all eventually relapse. We examined the function of BCL-2 family proteins in stromal-mediated resistance to carfilzomib-induced cytotoxicity in MM cells. Methods Co-cultures employing HS5 stromal cells were used to model the interaction with stroma. MM cells were exposed to CFZ in a 1-hour pulse method. The expression of BCL-2 family proteins was assessed by flow cytometry and WB. Pro-survival proteins: MCL-1, BCL-2 and BCL-X L were inhibited using S63845, ABT-199 and A-1331852 respectively. Changes in BIM binding partners were examined by immunoprecipitation and WB. Results CFZ induced dose-dependent cell death of MM cells, primarily mediated by apoptosis. Culture of MM cells on HS-5 stromal cells resulted in reduced cytotoxicity to CFZ in a cell contact-dependent manner, upregulated expression of MCL-1 and increased dependency on BCL-X L . Inhibiting BCL-X L or MCL-1 with BH-3 mimetics abrogated stromal-mediated protection only at high doses, which may not be achievable in vivo . However, combining BH-3 mimetics at sub-therapeutic doses, which alone were without effect, significantly enhanced CFZ-mediated cytotoxicity even in the presence of stroma. Furthermore, MCL-1 inhibition led to enhanced binding between BCL-X L and BIM, while blocking BCL-X L increased MCL-1/BIM complex formation, indicating the cooperative role of these proteins. Conclusion Stromal interactions alter the dependence on BCL-2 family members, providing a rationale for dual inhibition to abrogate the protective effect of stroma and restore sensitivity to CFZ.

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• Economic shocks and skill acquisition: Evidence from a national online learning platform at the onset of COVID-19

  Labour Economics · 2024-06-04 · 2 citations

  articleOpen access

  We study how large shocks impact individuals’ skilling decisions using data from a large, government-sponsored, online learning platform in Saudi Arabia. The onset of the COVID-19 pandemic brought about a massive increase in online skilling, and demand shifted towards courses that offered skills, such as telework, likely to be immediately valuable during the pandemic. Consistent with a model where individuals trade off reskilling costs with their expectations of future labor market conditions and their duration of work, we find that shifts into telework courses were largest for older workers. In contrast, younger workers increased enrollments in courses related to new skills, such as general, occupation-specific, and computer-related skills. Using national administrative employment data, we provide descriptive evidence that these investments in skills in early 2020 helped users maintain employment over the course of the pandemic.

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• P503: A RANDOMISED TRIAL OF MOLECULAR MONITORING VERSUS STANDARD CLINICAL CARE IN YOUNGER ADULTS WITH ACUTE MYELOID LEUKAEMIA: RESULTS FROM THE UK NCRI AML17 AND AML19 STUDIES

  HemaSphere · 2023-08-01 · 6 citations

  articleOpen access

  Topic: 3. Acute myeloid leukemia - Biology & Translational Research Background: Several studies have demonstrated the prognostic impact of measurable residual disease (MRD) evaluated by molecular methods in patients with AML with recurrent genetic abnormalities. It remains unclear whether intervention guided by MRD results improves outcome. Aims: We performed a randomised study to evaluate the effect of providing sequential MRD results to treating clinicians, compared to clinical monitoring only. The primary endpoint was overall survival. Secondary endpoints included health care resource use and quality of life, which will be reported separately. Methods: The UK NCRI AML17 and AML19 studies included patients generally aged 18-60y with newly diagnosed AML eligible for intensive chemotherapy. Cytogenetics, PCR and RNA sequencing were used to identify targets for molecular MRD monitoring (NPM1 mutation [mut] or any fusion gene). Patients with a molecular marker were randomised 2:1 to receive MRD monitoring after each cycle of chemotherapy and then every three months for two years, or no monitoring. For patients randomised to monitoring, results were provided to treating clinicians who made the decision to intervene or not in conjunction with a trial co-ordinator; there were no protocol specified interventions. Early repeat samples were requested when samples were inadequate or concerning for molecular relapse or progression. Treating clinicians answered a questionnaire about how the MRD results influenced treatment. Earlier results from AML17 indicated a high risk of relapse for NPM1mut patients testing MRD positive in the blood after two cycles of chemotherapy (PB PC2+). Therefore, in AML19 all NPM1mut patients received MRD monitoring after the first two cycles and PB PC2+ patients were excluded from the randomisation. Results: 638 patients entered the monitoring randomisation: 433 in AML17 (between 2012-2014) and 205 in AML19 (between 2015-2018). The MRD marker was NPM1mut in 398 (62%, of whom 140 had a FLT3 ITD), CBFB::MYH11 in 87 (14%) RUNX1::RUNX1T1 in 62 (10%) KMT2A::R in 52 (8%) DEK::NUP214 in 12 (2%) and other fusion gene in 27 (4%). In AML17, 3y overall survival (OS) was 64% in patients randomised to monitoring and 71% in patients randomised to no monitoring (HR 1.2 p=0.2). In AML19 3y OS was 84% and 78% respectively (HR 0.79, p=0.46). Meta analysis of the two studies showed no difference in overall survival (HR 1.11, 95CI 0.83-1.49, figure 1a). In a pre-specified subgroup analysis, we detected an overall survival benefit for monitoring in patients with NPM1mut and FLT3ITD+ (HR 0.53, 95CI 0.31-0.91, p=0.02) with significant heterogeneity between this subgroup and the remaining patients. When excluding PB PC2 MRD+ patients in AML17, the survival benefit was maintained (HR 0.41 95CI 0.23-0.74, p<0.01, figure 1b). We did not detect a survival benefit in any of the other subgroups, either when defined by molecular marker or ELN group. The most common MRD-guided treatment changes were reduction in the number of chemotherapy cycles given to MRD negative patients, pre-emptive treatment mainly with salvage chemotherapy at the time of molecular relapse while in haematological remission, allogeneic stem cell transplant, and modification of pre- and post- transplant care including immunosuppression and donor lymphocyte infusion. Few molecularly targeted interventions were deployed. Summary/Conclusion: In this large randomised study we observed a substantial survival benefit for MRD monitoring in patients with AML with NPM1mut and FLT3ITD+ mutations. This suggests a benefit from early salvage therapy prior to overt relapse specific to this group. This study was performed at a time when few MRD-guided molecularly targeted interventions were available.Keywords: Molecular markers, MRD, AML

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• Olutasidenib (FT-2102) induces durable complete remissions in patients with relapsed or refractory <i>IDH1</i>-mutated AML

  Blood Advances · 2023-02-01 · 120 citations

  articleOpen access

  Olutasidenib (FT-2102) is a potent, selective, oral, small-molecule inhibitor of mutant isocitrate dehydrogenase 1 (mIDH1). Overall, 153 IDH1 inhibitor-naive patients with mIDH1R132 relapsed/refractory (R/R) acute myeloid leukemia (AML) received olutasidenib monotherapy 150 mg twice daily in the pivotal cohort of this study. The median age of participants was 71 years (range, 32-87 years) and the median number of prior regimens received by patients was 2 (1-7). The rate of complete remission (CR) plus CR with partial hematologic recovery (CRh) was 35%, and the overall response rate was 48%. Response rates were similar in patients who had, and who had not, received prior venetoclax. With 55% of patients censored at the time of data cut-off, the median duration of CR/CRh was 25.9 months. The median duration of overall response was 11.7 months, and the median overall survival was 11.6 months. Of 86 patients who were transfusion dependent at baseline, a 56-day transfusion independence was achieved in 29 (34%), which included patients in all response groups. Grade 3 or 4 treatment-emergent adverse events (≥10%) were febrile neutropenia and anemia (n = 31; 20% each), thrombocytopenia (n = 25; 16%), and neutropenia (n = 20; 13%). Differentiation syndrome adverse events of special interest occurred in 22 (14%) patients, with 14 (9%) grade ≥3 and 1 fatal case reported. Overall, olutasidenib induced durable remissions and transfusion independence with a well-characterized and manageable side effect profile. The observed efficacy represents a therapeutic advance in this molecularly defined, poor-prognostic population of patients with mIDH1 R/R AML. This trial was registered at www.clinicaltrials.gov as #NCT02719574.

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• P1459: SAFETY AND EFFICACY FINDINGS OF AUTO1, A FAST-OFF RATE CD19 CAR, IN RELAPSED/REFRACTORY B-CELL NON-HODGKIN’S LYMPHOMA (B-NHL), AND CHRONIC LYMPHOCYTIC LEUKEMIA (CLL) / SMALL LYMPHOCYTIC LYMPHOMA (SLL)

  HemaSphere · 2022-06-01 · 1 citations

  articleOpen access

  Background: We have previously described AUTO1, a CD19 CAR with a fast off-rate CD19 binding domain, designed to reduce CAR T-cell immune toxicity and improve engraftment. Its clinical activity has been tested in r/r paediatric and adult B-ALL (Ghorashian S et al., Nat Med 2019; Roddie C et al., JCO 2021). This data confirms the intended function of the receptor, with low levels of CRS/ICANS and long-term engraftment of CAR T-cells observed in both patient groups. Aims: We have initiated testing of AUTO1 in the setting of B-NHL and CLL/SLL (NCT02935257). Methods: Manufacturing: CAR T-cell products were generated using a semi-automated closed process from non-mobilised patient leukapheresate. Study design: Subjects ≥ 16y underwent lymphodepletion with fludarabine (30mg/m x3) and cyclophosphamide (60mg/kg x1) prior to AUTO1 infusion, with the exception of the DLBCL cohort who additionally received a single dose of pembrolizumab (200mg) on day -1 to potentiate CAR-T expansion. AUTO1 dose varies based on the indication. Split dosing of 230 x106 CD19 CAR T-cells at day 0 and day 9 is employed in the CLL cohort. A single dose of 200 x106 CD19 CAR T-cells is delivered to patients with B-NHL. Study endpoints include feasibility of manufacture, grade 3-5 toxicity and remission rates at 1 and 3 months. Results: As of 8th February 2022, we enrolled 23 patients: 11 low grade NHL (LG-NHL:7 with FL and 3 with MCL), 7 DLBCL and 5 CLL. Apheresis was successful in all 23 patients and product manufacture was successful in 22 (pending in the last). 19 patients were infused: 10 with LG-NHL, 6 with DLBCL and 3 with CLL. 1 CLL patient was pending infusion at time of data cut-off and 2 patients died pre-infusion: 1 MCL patient, from COVID-19 and 1 CLL patient, from intracerebral haemorrhage. Patients treated with AUTO1 had a median age of 60 years (range 39-79), had received a median of 3 prior lines of treatment (range 2-8). Grade 1 CRS was reported in 6/19 and Grade 2 CRS in 3/19. No ICANS was observed in the B-NHL and CLL cohorts. CAR engraftment was observed in 13/13 patients evaluated by qPCR with ongoing persistence in 12/13 patients at last follow-up. In the LG-NHL and DLBCL cohorts 10/10 and 4/5 evaluable patients respectively were in CMR by 18FDG PET-CT post-treatment. Responses were ongoing in 9/10 LG-NHL at 12 months and in 4/4 DLBCL at months 1, 3, 3 and 6. In the CLL cohort, 2/3 evaluable patients achieved MRD negative remission in the bone marrow with residual small volume lymph nodes by CT at 6 and 3 months of follow-up respectively. 1 CLL patient did not engraft and had SD at month 1. Summary/Conclusion: AUTO1 has a tolerable safety profile in patients with r/r B-NHL and CLL despite high disease burden. Early data shows excellent complete remission rates and excellent CAR engraftment/expansion. Additional patients, updated data and longer follow up will be presented.

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• Antibody responses to <scp>SARS‐CoV</scp> ‐2 vaccination in patients with acute myeloid leukaemia and high risk <scp>MDS</scp> on active anti‐cancer therapies

  British Journal of Haematology · 2022-05-10 · 3 citations

  letterOpen access

  Encouraging seroconversion rates to SARS-CoV-2 vaccination in acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS) patients have been reported in large cohort studies1-4; however, the majority of these patients were not receiving active systemic anti-cancer therapy (SACT) and its impact on vaccine responses remains to be fully elucidated. Mori et al.5 report seroconversion rates of 94.7 and 100% respectively in Japanese patients with AML and MDS after two doses of mRNA SARS-CoV-2 vaccine, of which 39% received SACT. We report SARS-CoV-2 antibody responses following vaccination in a UK cohort of AML and HR-MDS patients all receiving, or having recently completed SACT, and stratified by prior SARS-CoV-2 infection. Demographics, SACT history and laboratory parameters were collected from the electronic health records of patients following two doses of SARS-CoV-2 vaccine (BNT162b2 or ChAdOx1nCoV-19) between December 2020 and July 2021. Serological testing was performed using Roche Elecsys anti-SARS-CoV-2 enzyme immunoassays. A total of 39 patients (85% AML, 15% HR-MDS, median age 63 [21–76]), underwent serological testing after receiving two doses of vaccine (Table 1). All were tested for anti-S antibodies after two doses (median 40 days post-dose) and 59% after the first dose (median 39 days). Thirty-three patients (85%) underwent testing for anti-N antibodies, and seven (21% of those tested) had previous SARS-CoV-2 infection. Eleven patients (28%) received intensive chemotherapy, 51% venetoclax-combination therapy (with azacitidine, low-dose cytarabine or gilteritinib) and 21% non-intensive azacitidine. Seropositivity rates and antibody titres increased with consecutive vaccine doses, from 74% in all patients (75% AML, 67% MDS) to 95% (94% AML, 100% MDS), with a median anti-S titre of 5.90 U/ml (IQR 0.58–56.7) after dose one, rising to 333 U/ml (IQR 86.8–1971) post dose two. Significantly higher titres were detected after dose two in AML patients, but not in MDS, though numbers are small (Figure 1B). We report similar seroconversion rates following two doses as seen by Mori et al. (Figure 1A, Table 1), despite all our patients receiving SACT compared to 39% of their cohort; however, we found no difference in anti-S titres between AML and HR-MDS patients receiving SACT after two vaccine doses (333 iu/ml [IQR 105.9–1896] vs. 495.9 iu/ml [IQR 82.15–2320], p = 0.99). These patterns persisted in patients with no prior SARS-CoV-2 infection and negative anti-N serology (Figures 1C,D and S1, Table 1), although seroconversion rates and median anti-S titres were somewhat reduced. Previous SARS-CoV-2 infection was associated with higher titres after two vaccinations (median 2500 U/ml [IQR 141–2500]), consistent with higher post-vaccination antibody titres in healthy individuals with prior natural infection.6, 7 This highlights the importance of measuring antibody titres, as opposed to seropositivity alone, and considering prior SARS-CoV-2 infection to delineate vaccine responses. Mori et al. reported lower antibody titres after two doses in those AML/MDS patients receiving active SACT as treatment or maintenance therapy (the majority received HMA) compared to those receiving non-chemotherapeutic treatments or completed treatment.5 We observed that no significant difference in seropositivity or anti-S titres was seen in AML patients receiving intensive (28%) compared to non-intensive chemotherapy (21%); however, anti-S titres were significantly reduced in venetoclax-based regimens (55% AML patients, 33% HR-MDS, median 158.5 U/ml [IQR 34.85–873], p = 0.04), independent of previous SARS-CoV-2 infection (Figure 1E,F). Reduced serological responses in patients receiving venetoclax have been previously reported in mature B cell neoplasms and myeloma, but not in AML or MDS.3, 8, 9 Further studies to define the impact of SACT regimens on the magnitude/duration of humoral and T cell responses to SARS-CoV-2 vaccination will have clear implications for this vulnerable group and should be priority questions for larger studies. All patients n = 39 AML n = 33 HR-MDS n = 6 Negative baseline n = 26 Positive baseline n = 7 Jenny O'Nions conceived of the study, performed data collection, data analysis, literature search, and manuscript writing and revision; Wei Yee Chan data collection, data analysis, manuscript writing, and revision; Catherine Zhu performed data collection, manuscript review and revision; Elspeth M. Payne conceived of study, manuscript review and revision; Emilie Sanchez data collection, manuscript review and revision; Adele K. Fielding, Asim Khwaja, Rajeev Gupta, manuscript review and revision. We are extremely grateful to all the patients who participated in this study and to the NHS staff that provided their clinical care. E. M. P. is supported by a CRUK Advanced Clinician Scientist Fellowship (grant no. A24873). RG acknowledges funding from Cure Cancer@ UCL. All authors declare no conflicts of interest. Figure S1 Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

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Frequent coauthors

• David C. Linch

  London Cancer

  71 shared

• Nigel H. Russell

  University of Nottingham

  46 shared

• Robert K. Hills

  University of Oxford

  46 shared

• Alan K. Burnett

  University Hospital of Wales

  45 shared

• Richard Dillon

  King's College London

  43 shared

• Marc R. Mansour

  University College London

  42 shared

• Adele K. Fielding

  Hull York Medical School

  42 shared

• Victoria Grandage

  University College London Hospitals NHS Foundation Trust

  42 shared

Awards & honors

• Carnegie Scholar (2009)