Blood Cancer Treatment in Aurangabad — Expert Haematological Oncology at Karnawat Cancer Hospital
“Blood cancer” is not a single disease. It is an umbrella term covering a wide spectrum of cancers that originate in the blood, bone marrow, or lymphatic system — each with distinct biology, treatment, and prognosis. Some blood cancers, like Hodgkin lymphoma and Chronic Myeloid Leukaemia (CML), are now among the most effectively treated cancers in all of oncology — with cure rates exceeding 85% for Hodgkin lymphoma and long-term molecular remission achievable for the majority of CML patients on oral targeted therapy. Others, like Acute Myeloid Leukaemia (AML) and relapsed myeloma, remain challenging and require complex, expert management.
At Karnawat Cancer Hospital, Aurangabad, Dr. Khushboo Jain Karnawat (DM Medical Oncology — Gold Medalist, ESMO-certified) is the primary specialist for all haematological cancers. She manages diagnosis, molecular and immunophenotypic workup, chemotherapy and targeted therapy, immunotherapy, and bone marrow transplant coordination for patients requiring transplant at specialist centres.
- DM Medical Oncologist — Gold Medalist, ESMO Certified
- Leukaemia, Lymphoma & Myeloma — Full Spectrum Haematological Oncology
- CML Oral Targeted Therapy (BCR-ABL Inhibitors)
- Hodgkin Lymphoma — Curative Chemotherapy + Radiation Coordination
- Bone Marrow Transplant Coordination for Eligible Patients
Blood Cancer in India — Key Facts
| STATISTIC | FIGURE | CONTEXT |
|---|---|---|
| New blood cancer cases per year (India) | ~1,00,000+ | Combined leukaemia, lymphoma, and myeloma; significant underdiagnosis in rural India |
| Most common blood cancer in Indian adults | Non-Hodgkin Lymphoma (NHL) | DLBCL is the single most common subtype |
| Most common leukaemia in Indian adults | CML (Chronic Myeloid Leukaemia) | Higher proportion than in Western countries; BCR-ABL targeted therapy has transformed outcomes |
| Most common blood cancer in children | Acute Lymphoblastic Leukaemia (ALL) | ~80% of childhood leukaemia; >80% cure rate with modern chemotherapy |
| Hodgkin Lymphoma cure rate | ~85–90% | One of the most curable cancers in young adults; full cure is a realistic goal |
| CML — molecular remission rate | ~80–85% (on targeted therapy) | Most CML patients achieve deep molecular remission on oral BCR-ABL targeted therapy |
| Multiple Myeloma — median survival (modern treatment) | 5–7 years | Not yet curable but increasingly manageable as a chronic disease with novel agents + transplant |
WHAT IS BLOOD CANCER
What Is Blood Cancer? The Three Major Categories
| Category | Origin | Main Subtypes | Key Feature |
|---|---|---|---|
| Leukaemia | Bone marrow; abnormal white blood cells enter the bloodstream | ALL, AML, CLL, CML | Diagnosed by blood count + bone marrow biopsy; systemic from the outset |
| Lymphoma | Lymph nodes and lymphatic tissue; lymphocytes become malignant | Hodgkin Lymphoma, Non-Hodgkin Lymphoma (DLBCL, follicular, mantle cell, Burkitt, T-cell lymphomas) | Usually presents as painless lymph node swelling; staged by Ann Arbor system |
| Myeloma (Multiple Myeloma) | Plasma cells in the bone marrow; malignant plasma cells produce abnormal antibodies (M-protein) | Multiple myeloma, plasmacytoma | Causes bone destruction, anaemia, kidney failure, hypercalcaemia |
| Myelodysplastic Syndromes (MDS) | Bone marrow; defective blood cell production; pre-leukaemia | MDS with single lineage dysplasia, MDS with excess blasts | Causes cytopenias; risk of transformation to AML |
Types of Blood Cancer — Leukaemia, Lymphoma & Myeloma Explained
LEUKAEMIA
Acute Lymphoblastic Leukaemia (ALL)
ALL is the most common cancer in children — accounting for ~80% of childhood leukaemia. It can also occur in adults (adult ALL is more aggressive and has lower cure rates than childhood ALL). In ALL, immature lymphoid precursor cells (lymphoblasts) proliferate uncontrollably. ALL can involve the central nervous system — intrathecal (into the spinal fluid) chemotherapy is given for CNS prophylaxis and treatment. Cure rates for childhood ALL with modern chemotherapy exceed 80–85%. Philadelphia chromosome-positive ALL (BCR-ABL fusion, found in ~25–30% of adult ALL) requires targeted therapy added to chemotherapy.
Acute Myeloid Leukaemia (AML)
AML is the most common acute leukaemia in adults. Abnormal myeloid precursor cells (blasts) accumulate in the bone marrow. AML is a medical emergency — it can be fatal within weeks without treatment. Molecular testing — FLT3, NPM1, IDH1, IDH2, CEBPA mutations — is mandatory at diagnosis as these guide targeted treatment additions and risk stratification. Treatment involves intensive induction chemotherapy followed by consolidation (repeat chemotherapy cycles or allogeneic bone marrow transplant depending on risk category).
Chronic Myeloid Leukaemia (CML)
CML is characterised by the Philadelphia chromosome — a reciprocal translocation between chromosomes 9 and 22 [t(9;22)] — producing the BCR-ABL fusion gene, which generates a constitutively active tyrosine kinase that drives uncontrolled myeloid cell proliferation. CML is more common in India proportionally than in Western countries. The discovery of targeted therapy (BCR-ABL tyrosine kinase inhibitors — TKIs, given as oral tablets) transformed CML from a disease requiring bone marrow transplant in most patients to one that is managed as a chronic condition with oral medication in the majority. The goal of treatment is deep molecular remission (BCR-ABL transcript levels undetectable on PCR). Most CML patients on TKIs have a near-normal life expectancy.
Chronic Lymphocytic Leukaemia (CLL)
CLL is the most common leukaemia in adults in Western countries (less common in India and East Asia — India has a lower CLL incidence than the West). Mature-appearing but functionally incompetent B-lymphocytes accumulate in the blood, bone marrow, and lymph nodes. Many CLL patients require no treatment initially ("watch and wait") — treatment is started when the disease causes symptoms, rapid lymphocyte doubling, or significant cytopenia. Molecular markers (IGHV mutation status, TP53, del17p, del11q, del13q, NOTCH1) determine prognosis and guide treatment choice. Novel oral targeted agents (BTK inhibitors, BCL-2 inhibitors) have replaced chemoimmunotherapy as standard first-line therapy for most CLL patients.
LYMPHOMA
Hodgkin Lymphoma (HL) — Highly Curable
Hodgkin Lymphoma is defined by the presence of Reed-Sternberg cells — large, binucleate "owl-eye" cells visible on lymph node biopsy. HL primarily affects young adults (bimodal age peak: 15–35 years and >55 years). It is one of the most successfully treated cancers in all of oncology — overall cure rates exceed 85–90% with chemotherapy ± radiation therapy, even for advanced-stage disease. The primary challenge in HL management is now late effects of treatment — radiation-induced secondary cancers and cardiac disease — rather than the lymphoma itself. HL subtypes: Nodular Sclerosis (most common — ~70%), Mixed Cellularity, Lymphocyte-Rich, Lymphocyte-Depleted, Nodular Lymphocyte Predominant (NLPHL — distinct biology and treatment).
MULTIPLE MYELOMA
Multiple Myeloma (MM) is a cancer of plasma cells — the antibody-producing cells in the bone marrow. Malignant plasma cells proliferate in the bone marrow and produce a single abnormal immunoglobulin (M-protein or paraprotein) detectable in the blood or urine. Myeloma causes a characteristic constellation of end-organ damage known by the CRAB criteria:
- C — Hypercalcaemia (elevated blood calcium from bone destruction)
- R — Renal failure (from M-protein deposition in kidney tubules)
- A — Anaemia (bone marrow replacement by myeloma cells)
- B — Bone lesions (punched-out lytic lesions, vertebral fractures, pathological fractures from plasma cell infiltration of bone)
Multiple Myeloma is currently not curable, but has become increasingly manageable as a chronic disease with modern treatment — triple and quadruple drug combinations including proteasome inhibitors, immunomodulatory drugs, and anti-CD38 monoclonal antibodies, followed by autologous stem cell transplant (ASCT) for eligible patients. Median survival with modern treatment is 5–7 years and improving significantly with each treatment generation.
Myelodysplastic Syndromes (MDS)
MDS are a group of clonal bone marrow disorders characterised by ineffective blood cell production (dysplasia) — causing anaemia, neutropenia, and thrombocytopenia — with risk of progression to AML. MDS is more common in older adults (median age at diagnosis: 70+ years). Risk stratification (IPSS-R score) determines prognosis and treatment intensity — ranging from supportive care (transfusions, growth factors) for lower-risk MDS to hypomethylating agent therapy for higher-risk MDS, and allogeneic bone marrow transplant for eligible younger patients with high-risk disease.
Non-Hodgkin Lymphoma (NHL)
NHL Subtype | Frequency | Behaviour | Key Feature |
Diffuse Large B-Cell Lymphoma (DLBCL) | ~30–35% of NHL | Aggressive; rapidly growing; potentially curable | Most common NHL; requires prompt treatment; can be cured with chemoimmunotherapy in ~60–70% of cases |
Follicular Lymphoma | ~20% of NHL (less common in India) | Indolent; slow-growing; not curable but very long natural history | Watch and wait appropriate for asymptomatic low-burden disease; transforms to aggressive lymphoma (~3%/year) |
Mantle Cell Lymphoma (MCL) | ~5–7% | Aggressive; typically presents at advanced stage | Generally not curable with standard chemotherapy; BTK inhibitors now standard |
Burkitt Lymphoma | ~3–5% (higher in children) | Extremely aggressive; fastest-growing human tumour; highly curable with intensive regimens | Medical emergency — treatment must start within 24–48 hours of diagnosis; very high cure rate with correct treatment |
Marginal Zone Lymphoma (MZL) | ~8–10% | Indolent; includes MALT lymphoma | Gastric MALT: H. pylori eradication can cure early-stage; splenic MZL: splenectomy or treatment |
T-Cell Lymphomas (PTCL) | ~10–15% of NHL | Generally aggressive | Heterogeneous group; PTCL-NOS most common; generally poorer outcomes than B-cell lymphomas; ALK-positive ALCL has good prognosis |
Symptoms of Blood Cancer — What to Watch For
Leukaemia Symptoms — From Bone Marrow Failure
Leukaemia symptoms result primarily from failure of normal blood cell production in the marrow — crowded out by leukaemia cells:
- Fatigue, weakness, pallor — from anaemia (low red blood cells)
- Easy bruising, excessive bleeding, prolonged bleeding from cuts, nosebleeds, gum bleeding, heavy menstrual periods — from thrombocytopenia (low platelets)
- Recurrent or persistent infections, fever — from neutropenia (low neutrophils); fever in a leukaemia patient is a medical emergency until proven otherwise
- Bone pain — from leukaemia cell infiltration of the bone marrow (particularly in ALL)
- Lymph node enlargement, splenomegaly (enlarged spleen causing left upper abdominal fullness), hepatomegaly
- Night sweats and unintentional weight loss
- Petechiae (pinpoint red spots from platelet-related bleeding) on the skin
- CNS symptoms in ALL — headache, visual changes, cranial nerve palsies from CNS involvement
Lymphoma Symptoms — From Lymph Node and Organ Involvement
- Painless, persistently enlarged lymph nodes — the most important sign of lymphoma; commonly in the neck, armpits, or groins; not tender; firm to hard on palpation; persisting for weeks to months
- B Symptoms (constitutional symptoms) — fever >38°C (unexplained), drenching night sweats, unexplained weight loss >10% of body weight in 6 months; these “B symptoms” indicate more advanced or aggressive disease and are prognostically important in staging
- Mediastinal mass — Hodgkin lymphoma often presents as a mediastinal (chest) mass causing chest discomfort, dry cough, breathlessness, or SVC syndrome (facial swelling, distended neck veins)
- Pruritus (generalised itching) — classic in Hodgkin Lymphoma; may precede lymph node enlargement
- Abdominal fullness or pain — from retroperitoneal node involvement or splenomegaly
- Extranodal lymphoma symptoms — depend on site: gastric MALT (dyspepsia), CNS lymphoma (headache, confusion, focal neurology), testicular lymphoma (testicular swelling), cutaneous lymphoma (skin rash or plaques)
Multiple Myeloma Symptoms — From CRAB Criteria
- Bone pain — the most common symptom; typically in the back (vertebral involvement), ribs, and pelvis; persistent and worsening; vertebral fractures may cause acute severe back pain
- Anaemia symptoms — fatigue, weakness, pallor — from bone marrow replacement
- Renal failure symptoms — reduced urine output, swelling of legs, nausea, confusion — from M-protein kidney damage
- Hypercalcaemia symptoms — increased thirst, frequent urination, constipation, nausea, confusion, depression
- Recurrent infections — from impaired antibody production (immunoparesis)
- Neuropathy — from amyloid deposition or direct nerve compression in some patients
BACK PAIN + FATIGUE + RECURRENT INFECTIONS in a patient over 50 years: this combination should prompt urgent investigation for multiple myeloma — serum protein electrophoresis (SPEP), serum immunoglobulins, serum free light chains, and urine protein electrophoresis. Myeloma is often missed for months by treating the back pain without investigating for an underlying cause.
DIAGNOSIS & STAGING
How Is Blood Cancer Diagnosed and Staged?
Step 1: Complete Blood Count (CBC) + Peripheral Blood Smear
Step 2: Bone Marrow Biopsy + Aspirate — The Definitive Diagnostic Test
Immunophenotyping — Flow Cytometry
Cytogenetics (Karyotype + FISH)
| CYTOGENETIC FINDING | ASSOCIATED CANCER | CLINICAL SIGNIFICANCE |
|---|---|---|
| Philadelphia chromosome t(9;22) BCR-ABL | CML; Ph+ ALL | Most important in CML — defines the disease; dictates targeted therapy; also found in 25–30% of adult ALL (poor prognosis → needs targeted therapy addition) |
| t(15;17) PML-RARA | APL (Acute Promyelocytic Leukaemia) | Medical emergency; very responsive to targeted therapy (ATRA + arsenic) — >90% cure rate; must be diagnosed and treated emergently |
| t(8;14) c-MYC rearrangement | Burkitt lymphoma | Diagnostic of Burkitt; requires urgent treatment |
| t(14;18) BCL-2 | Follicular lymphoma; DLBCL (subset) | Diagnostic of follicular; BCL-2 inhibitors available for relapsed disease |
| del(17p) / TP53 mutation | CLL; AML; MDS | High-risk marker; chemotherapy resistance; requires novel targeted agents |
| del(13q) | CLL (most common) | Favourable prognosis in CLL |
| t(11;14) Cyclin D1 | Mantle Cell Lymphoma | Diagnostic of MCL; BTK inhibitors now standard |
Step 4: Cytogenetics (Karyotype + FISH)
| MOLECULAR TEST | CANCER TYPE | SIGNIFICANCE |
|---|---|---|
| BCR-ABL PCR (quantitative) | CML; Ph+ ALL | Monitors treatment response; defines deep molecular remission; guides treatment discontinuation attempts in CML |
| FLT3 mutation (ITD and TKD) | AML | FLT3-ITD — poor prognosis; FLT3 inhibitors now standard addition to induction chemotherapy |
| NPM1 mutation | AML | Favourable prognosis (in absence of FLT3-ITD); guides consolidation strategy |
| IDH1 / IDH2 mutation | AML; MDS | Targetable with specific IDH inhibitors |
| CEBPA mutation (biallelic) | AML | Favourable prognosis |
| IGHV mutation status | CLL | Mutated IGHV: favourable; unmutated: less favourable response to chemoimmunotherapy |
| TP53 / del(17p) | CLL; AML; Lymphoma | High-risk; resistance to standard chemotherapy; requires targeted approach |
| JAK2 V617F | Myeloproliferative neoplasms (PV, ET, MF) | Diagnostic; JAK inhibitors available for myelofibrosis |
| FISH for IGH rearrangements | Myeloma | del(17p), t(4;14), t(14;16) — high-risk cytogenetics in myeloma; t(11;14) — standard risk |
Step 6: Lymphoma Staging — Ann Arbor System
| STAGE | DEFINITION | CLINICAL MEANING |
|---|---|---|
| Stage I | Single lymph node region OR single extranodal site | Limited, localised disease |
| Stage II | Two or more lymph node regions on the same side of the diaphragm | Regional disease, same side of body |
| Stage III | Lymph node regions on both sides of the diaphragm involved | Widely distributed nodal disease |
| Stage IV | Diffuse extranodal involvement (bone marrow, liver, lung, etc.) | Disseminated disease — still potentially curable in Hodgkin lymphoma |
Suffix A: No B symptoms. Suffix B: Fever, night sweats, or weight loss present. Stage IIIB and IVB indicate more advanced symptomatic disease.
Step 7: PET-CT for Lymphoma — Standard of Care
PET-CT is mandatory for initial staging of Hodgkin lymphoma and aggressive NHL (DLBCL, Burkitt). It detects metabolically active nodal and extranodal disease with superior sensitivity to CT alone. PET-CT at mid-treatment and after treatment completion is used for response assessment (Deauville score 1–5) — determining whether further treatment is needed.
Myeloma Workup — SPEP, Bone Marrow, Imaging
Multiple myeloma diagnosis requires: serum protein electrophoresis (SPEP) + immunofixation (to identify and characterise M-protein), serum immunoglobulins (IgG, IgA, IgM), serum free light chains (kappa/lambda ratio), 24-hour urine protein electrophoresis + immunofixation (Bence Jones protein), bone marrow biopsy (plasma cell percentage + FISH for myeloma cytogenetics), and imaging — whole-body low-dose CT or PET-CT for bone lesion detection (replacing skeletal X-ray survey).
TREATMENT OF BLOOD CANCER
Treatment of Blood Cancer — By Disease Category
Treatment of Leukaemia
Acute leukaemias (ALL and AML) require urgent, intensive treatment — they can be fatal within weeks without therapy. Treatment follows the phases: Induction (intensive initial chemotherapy to achieve remission — aim: <5% blasts in marrow), Consolidation (further chemotherapy to eliminate residual disease and prevent relapse), and Maintenance (prolonged lower-intensity therapy to sustain remission — primarily in ALL).
- ALL: Intensive multi-agent chemotherapy + CNS-directed therapy (intrathecal chemotherapy ± cranial radiation). Philadelphia chromosome-positive ALL requires oral BCR-ABL targeted therapy added to chemotherapy — significantly improving outcomes. Children achieve >80% cure; adults have lower cure rates but improving with modern regimens. Allogeneic bone marrow transplant in first remission for high-risk patients.
- AML: Intensive induction chemotherapy followed by consolidation. Molecular markers guide risk stratification — standard-risk patients may receive consolidation chemotherapy alone; high-risk and intermediate-risk patients benefit from allogeneic bone marrow transplant in first remission. FLT3-mutant AML now routinely receives FLT3-targeted therapy added to induction. IDH1/IDH2-mutant AML has specific targeted therapy options. Acute Promyelocytic Leukaemia (APL, t(15;17)) is treated with targeted therapy (ATRA + arsenic) — NOT standard chemotherapy — achieving cure rates >90%.
- CML: Oral BCR-ABL targeted therapy (tyrosine kinase inhibitor) daily is the standard treatment for chronic phase CML. Deep molecular remission is the treatment goal, monitored by quantitative BCR-ABL PCR every 3 months. Most patients can expect a near-normal life expectancy on TKI therapy. In selected patients who achieve sustained deep molecular remission, treatment discontinuation is attempted under close monitoring. Allogeneic BMT is reserved for accelerated/blast phase CML or TKI-resistant disease.
- CLL: Many patients require only active surveillance (“watch and wait”) initially. When treatment is needed, novel oral targeted agents (BTK inhibitors, BCL-2 inhibitors) have replaced chemoimmunotherapy as standard first-line therapy — achieving deeper and more durable responses with better tolerance. TP53 deletion/mutation must be tested before treatment — it predicts resistance to standard chemoimmunotherapy and guides targeted agent selection.
Treatment of Lymphoma
- Hodgkin Lymphoma: Chemotherapy (multi-agent combination regimen) is the backbone of treatment — with or without involved-field radiation depending on stage, response, and risk factors. Early-stage HL: chemotherapy + consolidation radiation achieves ~95% cure. Advanced-stage HL: full-course chemotherapy; PET-adapted treatment (adjusting therapy based on interim PET-CT response) reduces toxicity without compromising cure rate. Relapsed HL: salvage chemotherapy + autologous stem cell transplant for chemosensitive relapse achieves ~50–60% long-term remission. Immunotherapy (anti-PD-1) is highly active in relapsed/refractory HL.
- DLBCL: Chemoimmunotherapy (anti-CD20 antibody + combination chemotherapy) is the standard first-line treatment — achieving cure in ~60–70% of patients. High-risk DLBCL features (high IPI score, MYC + BCL-2 or BCL-6 double-expressor) require intensified regimens. CNS prophylaxis is given for high-risk patients. Relapsed/refractory DLBCL: salvage chemoimmunotherapy + autologous SCT for transplant-eligible patients; CAR-T cell therapy for relapsed disease.
- Follicular Lymphoma: Indolent — “watch and wait” is appropriate for asymptomatic low-bulk disease. When treatment is needed, anti-CD20 antibody + chemotherapy, followed by anti-CD20 maintenance, is standard. Not curable with standard therapy but has a very long natural history. BCL-2 inhibitors and PI3K inhibitors are options for relapsed disease.
- Burkitt Lymphoma: Highly aggressive but highly curable with correct treatment — requires URGENT initiation of specific intensive chemotherapy within 24–48 hours of diagnosis. Standard chemotherapy is NOT adequate; Burkitt requires a specific intensive regimen. Cure rates exceed 90% in children and 60–80% in adults with correct treatment.
Treatment of Multiple Myeloma
Multiple myeloma treatment aims for deep response — ideally complete remission with MRD (minimal residual disease) negativity — which correlates with longer remission duration and survival. Treatment is stratified by transplant eligibility:
- Transplant-eligible patients (typically <65–70 years, good performance status): Induction therapy (triple or quadruple drug regimen) × 4–6 cycles → Autologous Stem Cell Transplant (ASCT — patient’s own stem cells harvested before high-dose chemotherapy, then reinfused) → Maintenance therapy. ASCT deepens response and prolongs remission duration.
- Transplant-ineligible patients (older age, frailty, comorbidities): Full-dose or dose-attenuated combination regimens without ASCT, followed by maintenance. Novel agents (proteasome inhibitors, anti-CD38 antibodies, IMiDs) are incorporated based on fitness and comorbidities.
- Bone disease management: Bisphosphonates (or denosumab) for all patients with bone involvement — reduces skeletal events and fracture risk. Radiation therapy for painful bone lesions or pathological fractures. Vertebroplasty/kyphoplasty for vertebral fractures causing pain.
- Renal failure in myeloma: Rapid treatment initiation — some myeloma regimens are safe even with severe renal impairment; renal function may recover substantially with effective myeloma treatment.
BURKITT LYMPHOMA IS A MEDICAL EMERGENCY. It has the fastest tumour doubling time of any human cancer. Treatment must begin within 24–48 hours of diagnosis. Ensure the oncologist is aware of the urgency and that the correct Burkitt-specific regimen is used — not a standard lymphoma regimen.
Bone Marrow Transplant (BMT / Stem Cell Transplant — SCT)
Transplant Type | Stem Cell Source | Used For | Key Points |
Autologous SCT (auto-SCT) | Patient’s own stem cells — collected from blood before high-dose chemotherapy | Multiple myeloma (standard); relapsed Hodgkin and DLBCL (chemosensitive relapse) | No graft-versus-host disease; no graft-versus-leukaemia effect; suitable for older patients; lower risk of transplant-related mortality |
Allogeneic SCT (allo-SCT) | Matched sibling donor (best); matched unrelated donor (MUD); haploidentical (half-matched, usually parent/sibling/child) | AML and ALL in remission (high-risk patients); MDS (high-risk); relapsed CML; CLL (high-risk relapse) | Graft-versus-leukaemia (GVL) effect can cure leukaemia; higher risk including graft-versus-host disease (GVHD); sibling donor preferred |
FERTILITY PRESERVATION BEFORE BLOOD CANCER TREATMENT
Fertility Preservation — For Young Patients Starting Blood Cancer Treatment
Options for Fertility Preservation
- Sperm cryopreservation (semen freezing): For males — should be performed before starting any chemotherapy. Rapid, affordable, and highly effective. Can be arranged within 24–48 hours in most cases.
- Oocyte cryopreservation (egg freezing) or embryo freezing: For females — requires an IVF stimulation cycle (10–14 days). May delay chemotherapy start slightly but is often feasible, particularly for non-emergency cases (Hodgkin lymphoma, CML, CLL). Embryo freezing requires a partner or donor sperm.
- Ovarian tissue cryopreservation: For pre-pubertal girls or patients who cannot delay treatment — ovarian cortical tissue is frozen for future reimplantation. Increasingly available at specialist centres.
Myths vs Facts About Blood Cancer Follow-Up
Fact: Some blood cancers are among the most curable in all of oncology. Hodgkin lymphoma has >85% cure rates. Childhood ALL is cured in >80% of cases with modern chemotherapy. APL (a specific AML subtype) is cured in >90% of cases with targeted therapy. CML is managed as a chronic condition with oral targeted therapy in most patients — with near-normal life expectancy. Even for incurable blood cancers like myeloma, median survival has more than doubled in the last decade with modern treatment.
Fact: Blood cancer can affect people of all ages. While ALL (Acute Lymphoblastic Leukaemia) is the most common childhood cancer, the majority of blood cancer cases occur in adults. AML, CLL, myeloma, DLBCL, follicular lymphoma, and MDS are predominantly adult diseases, with incidence rising with age. Hodgkin lymphoma has a young adult peak (15–35 years) but also occurs in older adults. Any age group can develop blood cancer.
Fact: “Blood cancer” encompasses over 70 distinct diseases — leukaemias, lymphomas, myeloma, MDS, myeloproliferative neoplasms, and more. Leukaemia is just one category. Each subtype has different biology, treatment, and prognosis. A patient with Hodgkin lymphoma is treated completely differently from a patient with AML or myeloma. The specific diagnosis — confirmed by bone marrow biopsy, immunophenotyping, cytogenetics, and molecular testing — is essential before any treatment decision is made.
Fact: Bone marrow biopsy is performed under local anaesthesia at the posterior iliac crest (back of hip bone) and takes approximately 10–15 minutes. There is discomfort during the procedure — particularly during the aspiration — but it is tolerable and brief. Serious complications are very rare. Bone marrow biopsy is the essential diagnostic test for blood cancers and cannot be replaced by blood tests or imaging alone. The brief discomfort of the procedure is far outweighed by the critical information it provides.
Fact: Before the introduction of BCR-ABL targeted therapy (tyrosine kinase inhibitors), most CML patients required allogeneic bone marrow transplant to achieve long-term survival. This has completely changed. The vast majority of CML patients today achieve deep molecular remission on daily oral targeted therapy (a tablet) and have a near-normal life expectancy. Bone marrow transplant is now reserved for the minority of CML patients who fail targeted therapy or present in accelerated/blast phase. CML in the chronic phase is one of the most successfully managed haematological cancers.
Fact: Hodgkin lymphoma with widespread lymph node involvement — even stage IV disease — is still potentially curable with chemotherapy. The number of lymph node sites involved does not determine curability in Hodgkin lymphoma — the biology and treatment response do. DLBCL can also be cured even with stage III–IV disease in a significant proportion of patients. Lymphoma staging (Ann Arbor I–IV) guides treatment intensity, not whether cure is achievable.
Why Choose Karnawat Cancer Hospital for Blood Cancer Treatment in Aurangabad?
1. DM Medical Oncology Expertise — Full-Spectrum Haematological Oncology
Dr. Khushboo Jain Karnawat's DM Medical Oncology training includes haematological oncology — leukaemia, lymphoma, myeloma, and MDS. ESMO certification and gold medal training ensures that evidence-based, internationally current treatment protocols are applied at Karnawat Cancer Hospital, Aurangabad.
2. Complete Molecular Workup — BCR-ABL, FLT3, NPM1, TP53, IGHV
All blood cancer patients have comprehensive molecular and cytogenetic testing to guide precise treatment — identifying targetable mutations (BCR-ABL in CML, FLT3 in AML, IDH1/IDH2 in AML), risk stratifiers (TP53 in CLL and AML, cytogenetics in myeloma), and markers that determine transplant need.
3. CML Targeted Therapy — Oral Treatment Close to Home
CML patients in Marathwada no longer need to travel to Pune or Mumbai for BCR-ABL targeted therapy management. Dr. Khushboo Jain Karnawat initiates and monitors CML targeted therapy at Karnawat Cancer Hospital, with regular BCR-ABL PCR monitoring to ensure deep molecular remission is achieved and maintained.
4. Hodgkin Lymphoma — Curative Treatment for Young Adults
Hodgkin lymphoma in young adults is a curable disease when treated with full-course chemotherapy and appropriate radiation coordination. Karnawat Cancer Hospital manages Hodgkin lymphoma with PET-adapted treatment planning, fertility preservation counselling before chemotherapy, and coordination of radiation oncology with partner centres.
5. Bone Marrow Transplant Coordination
Dr. Khushboo Jain Karnawat assesses all blood cancer patients for transplant eligibility, orders HLA typing for allogeneic SCT candidates, coordinates sibling HLA testing, and manages referral and transfer to accredited BMT centres in Mumbai, Pune, and Hyderabad — ensuring patients access the appropriate centre without delay.
6. Fertility Preservation Counselling Before Chemotherapy
Every young blood cancer patient at Karnawat Cancer Hospital receives fertility preservation counselling before starting chemotherapy — ensuring sperm cryopreservation or egg/embryo freezing is arranged before treatment begins for those who wish to preserve future fertility.
Meet the Blood Cancer Specialists in Aurangabad
Dr. Anand Vinay Karnawat — Surgical Oncologist
Qualifications: MBBS | MS (General Surgery) | MCh (Surgical Oncology) | FMAS | FICRS | Fellowship in Microvascular Surgery Performs surgical biopsy of lymph nodes (excisional lymph node biopsy for lymphoma diagnosis when core needle biopsy is non-diagnostic), splenectomy for splenic marginal zone lymphoma or hypersplenism, and port/central line placement for long-term chemotherapy access in blood cancer patients. Profile: /best-oncologist-in-aurangabad-dr-anand-karnawat/
Dr. Khushboo Jain Karnawat — Medical Oncologist (Primary Blood Cancer Specialist)
Qualifications: MBBS | MD (Radiation Oncology) | DM (Medical Oncology) — Gold Medalist | DrNB | ECMO (ESMO Certified) Primary specialist for all haematological malignancies at Karnawat Cancer Hospital. Manages diagnosis and molecular workup for leukaemia, lymphoma, myeloma, and MDS; initiates and monitors chemotherapy, targeted therapy (CML TKIs, FLT3 inhibitors, BCL-2 inhibitors), and immunotherapy; coordinates PET-CT staging and response assessment for lymphoma; assesses bone marrow transplant eligibility and coordinates referral to BMT centres; manages fertility preservation counselling before treatment. Profile: /cancer-specialist-in-aurangabad-dr-khushboo-jain-karnawat/
Frequently Asked Questions About Blood Cancer Treatment
No. "Blood cancer" is an umbrella term covering three major categories: leukaemia (cancer of blood-forming cells in bone marrow — ALL, AML, CML, CLL), lymphoma (cancer of lymphocytes in lymph nodes and lymphatic tissue — Hodgkin lymphoma, Non-Hodgkin lymphoma including DLBCL, follicular, mantle cell, Burkitt, and many others), and multiple myeloma (cancer of plasma cells — producing M-protein, causing bone disease, kidney failure, and anaemia). Each category has distinct biology, treatment, and prognosis. The specific subtype must be identified by bone marrow biopsy, immunophenotyping, and molecular testing before treatment begins.
No. Low blood counts (anaemia, low white cells, or low platelets) are caused by many conditions — most of which are not blood cancer. Common causes include iron deficiency anaemia, vitamin B12/folate deficiency, chronic disease, infections (particularly viral), thyroid disorders, autoimmune conditions, and medication side effects. However, blood counts that are severely low, involve multiple cell lines, or are not explained by common causes require bone marrow evaluation to exclude leukaemia or MDS. A haematologist or medical oncologist should evaluate unexplained cytopenias.
Persistent, painless lymph node swelling that does not resolve over 4–6 weeks must be investigated for lymphoma. However, lymph node enlargement is much more commonly caused by infections (including tuberculosis, which is very prevalent in India), reactive conditions, and other non-cancerous causes. The investigation typically includes: blood tests (CBC, LDH, ESR, CRP, LFT), chest X-ray or CT scan, and if a definitive diagnosis is needed — lymph node biopsy (excisional or core needle biopsy). A swollen lymph node that increases in size, is firm and non-tender, or is associated with fever, night sweats, and weight loss requires urgent evaluation.
Most CML patients in chronic phase do NOT need a bone marrow transplant today. The introduction of BCR-ABL targeted therapy (tyrosine kinase inhibitors — oral daily tablets) has transformed CML management. The majority of chronic phase CML patients achieve deep molecular remission on targeted therapy and have a near-normal life expectancy. Bone marrow transplant is now reserved for CML patients who fail targeted therapy, those who present in accelerated or blast phase, or selected young patients with specific risk features. Discuss your BCR-ABL PCR response to targeted therapy with Dr. Khushboo Jain Karnawat to understand your individual situation.