Overview
Acute Lymphoblastic Leukemia (ALL) is a rapidly progressing cancer of the bone
marrow and blood in which immature lymphoid cells (lymphoblasts) multiply
uncontrollably.
ALL is the most common childhood leukemia, but it also occurs in adults, particularly
in those over 50.
At Coimbatore Cancer Clinic, we combine precision diagnostics, targeted
therapies, and advanced supportive care to maximize cure rates and minimize
side-effects.
Causes & Risk Factors
● Genetic predisposition: Down syndrome, Fanconi anemia, Bloom
syndrome.
● Prior radiation or chemotherapy exposure.
● Chromosomal abnormalities: t(9;22) – Philadelphia chromosome
(BCR-ABL).
● Environmental: benzene, radiation.
● Family history: rare but relevant.
Symptoms & Warning Signs
● Fatigue, weakness, or pallor (anemia)
● Fever or recurrent infections (neutropenia)
● Easy bruising or bleeding (thrombocytopenia)
● Bone pain or limb aches
● Swollen lymph nodes, spleen, or liver
● Headache, vomiting, or blurred vision (CNS involvement)
Diagnosis & Investigations
1. CBC & Peripheral smear: blast cells in circulation.
2. Bone marrow aspiration & biopsy: > 20 % lymphoblasts confirm ALL.
3. Flow cytometry: immunophenotyping to classify (B-cell vs T-cell ALL).
4. Cytogenetics & molecular tests: BCR-ABL, IKZF1, KMT2A
rearrangements.
5. CSF analysis: CNS involvement.
6. Baseline echo, LFT, renal profile for treatment planning.
Stage-wise Treatment
Although leukemia doesn’t form solid “stages,” treatment proceeds through phases:
1️⃣ Induction Phase (4–6 weeks)
Goal – achieve complete remission.
● Combination chemo (Vincristine + Daunorubicin + Dexamethasone ±
Asparaginase).
● Tyrosine kinase inhibitor (Imatinib/Dasatinib) for Ph+ ALL.
● CNS prophylaxis (intrathecal methotrexate).
2️⃣ Consolidation Phase (2–3 months)
● High-dose Methotrexate, Cytarabine ± Asparaginase.
● Allogeneic stem cell transplant for high-risk cases.
3️⃣ Maintenance Phase (2–3 years)
● 6-Mercaptopurine + Methotrexate ± Vincristine & Prednisone.
● CNS monitoring & maintenance chemo.
Relapsed ALL → targeted therapy (Blinatumomab, Inotuzumab, CAR-T therapy).
Recent Advances
● Targeted TKIs (Imatinib, Dasatinib) in Ph+ ALL improve survival.
● Bispecific antibodies (Blinatumomab) and antibody-drug conjugates
(Inotuzumab ozogamicin).
● CAR-T cell therapy for refractory B-cell ALL (available at selected centres in
India).
● Minimal Residual Disease (MRD) monitoring for therapy response.
Our Expertise at Coimbatore Cancer Clinic
We offer comprehensive ALL care:
● Bone marrow diagnostics & molecular profiling.
● NCCN-aligned chemo protocols with supportive care.
● Access to CAR-T and transplant programs through partner centres.
● Dedicated infection control and nutrition monitoring units.
When to Consult / FAQs
Any persistent fatigue, bruising, fever, or unexplained pallor warrants immediate
evaluation.
FAQ: Is ALL curable? Yes — childhood ALL has > 85 % cure rate with modern
protocols; adult ALL outcomes are improving rapidly with targeted therapy.
Disclaimer
For educational use only; consult qualified oncologists for personalized
management.
Acute Myeloid Leukemia (AML)
Overview
Acute Myeloid Leukemia (AML) is a rapidly progressing cancer of the bone marrow
characterized by the accumulation of immature myeloid cells, known as myeloblasts.
These abnormal cells crowd out healthy blood-forming cells, causing anemia,
infection, and bleeding tendencies.
AML primarily affects adults but can occur at any age.
At Coimbatore Cancer Clinic, we integrate molecular diagnostics, targeted therapy,
and advanced chemotherapy regimens to personalize treatment based on the
biology of each patient’s disease.
Causes & Risk Factors
● Genetic predisposition: Down syndrome, Fanconi anemia.
● Prior chemotherapy or radiation exposure.
● Myelodysplastic syndromes or other marrow disorders.
● Environmental factors: benzene exposure, smoking.
● Specific chromosomal translocations: t(8;21), inv(16), t(15;17).
Symptoms & Warning Signs
● Fatigue, weakness, or pallor due to anemia.
● Fever or recurrent infections.
● Easy bruising or bleeding (petechiae, gums).
● Bone pain or tenderness.
● Swollen gums or enlarged spleen/liver.
AML often develops abruptly over days or weeks, so early recognition is vital.
Diagnosis & Investigations
1. CBC & peripheral smear: anemia, thrombocytopenia, circulating blasts.
2. Bone marrow aspiration & biopsy: ≥20% myeloblasts confirms diagnosis.
3. Flow cytometry: defines subtype (myelomonocytic, promyelocytic, etc.).
4. Cytogenetic & molecular analysis: FLT3, NPM1, IDH1/2, TP53, RUNX1
mutations guide prognosis and therapy.
5. Coagulation profile: especially for Acute Promyelocytic Leukemia (APL).
6. Echocardiogram & renal/liver function tests before chemotherapy.
Stage-Wise (Risk-Based) Treatment
AML is classified as favorable, intermediate, or adverse risk based on
cytogenetics/mutations.
1️⃣ Induction Therapy
Goal – achieve complete remission.
● Standard: “7+3” regimen (Cytarabine × 7 days + Anthracycline × 3 days).
● FLT3-mutated AML: Add Midostaurin.
● APL (t15;17): All-trans Retinoic Acid (ATRA) + Arsenic Trioxide; extremely
high cure rate.
2️⃣ Consolidation Therapy
● High-dose Cytarabine (HiDAC) for fit adults.
● Allogeneic stem cell transplant for intermediate/high-risk disease or
relapsed AML.
3️⃣ Elderly / Unfit Patients
● Venetoclax + Azacitidine or Decitabine (low-intensity targeted regimen).
● Supportive care with antibiotics, antifungals, transfusions, and growth factors.
Recent Advances
● Targeted therapies: FLT3 inhibitors (Midostaurin, Gilteritinib), IDH1/2
inhibitors (Ivosidenib, Enasidenib).
● Venetoclax combinations improving remission rates in older adults.
● Measurable Residual Disease (MRD) monitoring for personalized therapy.
● CAR-T and bispecific antibodies under investigation.
Our Expertise at Coimbatore Cancer Clinic
● Comprehensive molecular profiling for personalized AML therapy.
● NCCN-aligned chemotherapy protocols.
● Close coordination for stem cell transplantation at partner centers.
● Dedicated supportive care unit to manage infections and cytopenias.
When to Consult
Persistent fatigue, bleeding, or infections that don’t resolve warrant immediate
evaluation — AML can progress within days if untreated.
Disclaimer
For educational purposes only; patients should seek individualized consultation.
Hodgkin Lymphoma (HL)
Overview
Hodgkin lymphoma (HL) is a highly curable cancer of B lymphocytes, marked by the
presence of Reed–Sternberg cells.
It primarily affects young adults and presents with painless lymph node swelling,
often in the neck or chest.
At Coimbatore Cancer Clinic, our team follows evidence-based therapy combining
ABVD chemotherapy and modern imaging-guided radiation to achieve cure in
>90% of early-stage patients.
Causes & Risk Factors
● Epstein–Barr Virus (EBV) infection.
● Family history of lymphoma.
● Immunodeficiency (HIV).
● Male gender, age 15–35 or >55.
Symptoms
● Painless lymphadenopathy (neck, mediastinum).
● Fever, night sweats, weight loss (B symptoms).
● Fatigue, pruritus.
● Chest discomfort or cough from mediastinal mass.
Diagnosis & Investigations
1. Excisional lymph node biopsy – confirms Reed–Sternberg cells.
2. IHC panel: CD15+, CD30+, PAX5 weak.
3. PET-CT for staging (Lugano system).
4. Bone marrow biopsy in advanced cases.
Stage-Wise Treatment
Early Stage (I–II)
● ABVD × 2–4 cycles (Adriamycin, Bleomycin, Vinblastine, Dacarbazine) +
involved-site radiation.
Advanced Stage (III–IV)
● ABVD × 6 cycles or A+AVD (Adcetris + chemo).
● PET-adapted therapy to guide radiation need.
Relapsed / Refractory
● Salvage chemo (ICE, DHAP) + Autologous Stem Cell Transplant.
● Brentuximab vedotin or PD-1 inhibitors (Nivolumab, Pembrolizumab).
Recent Advances
● Brentuximab vedotin now frontline (A+AVD).
● Immunotherapy (PD-1 inhibitors) for relapsed HL.
● Proton therapy / IMRT for precise radiation
Our Expertise
● PET-guided therapy to minimize toxicity.
● Access to modern drugs (Brentuximab, PD-1).
● Supportive services for fertility, survivorship, and rehabilitation.
When to Consult
Any painless neck lump or unexplained fever/sweats should prompt evaluation —
early treatment yields near-100% cure.
Chronic Lymphocytic Leukemia / Small Lymphocytic Lymphoma (CLL /
SLL)
Overview
CLL is a slow-growing leukemia of mature B-cells, often discovered incidentally on
blood tests.
The same disease in lymph nodes is termed Small Lymphocytic Lymphoma (SLL).
It is the most common leukemia in adults and is often manageable for years.
At Coimbatore Cancer Clinic, we emphasize personalized, risk-adapted therapy —
integrating molecular diagnostics, targeted oral drugs, and watchful observation
when appropriate.
Causes & Risk Factors
● Genetic predisposition and family history.
● Chromosomal abnormalities: del(13q), del(17p), TP53 mutations.
● Male sex, age > 60 years.
● Exposure to pesticides or solvents
Symptoms
● Often asymptomatic; discovered incidentally.
● Fatigue or weight loss.
● Lymph node enlargement in neck, armpit, or groin.
● Recurrent infections due to low immunity.
● Bruising or bleeding (rare).
Diagnosis & Investigations
1. CBC: lymphocyte count > 5 × 10⁹/L.
2. Peripheral smear: mature lymphocytes with smudge cells.
3. Flow cytometry: CD5+, CD19+, CD23+.
4. FISH panel: del(17p), TP53, IGHV mutation status.
5. Imaging / PET-CT: bulky nodes or spleen.
Stage-Wise Treatment
Early Stage (Rai 0 / Binet A)
● Observation only (“watch and wait”).
● No therapy until disease progression.
Progressive / Symptomatic Disease
● Targeted oral therapy:
o BTK inhibitors (Ibrutinib, Acalabrutinib).
o BCL2 inhibitor Venetoclax + Obinutuzumab.
● Chemoimmunotherapy: FCR (Fludarabine, Cyclophosphamide, Rituximab)
only for fit, TP53-wild patients.
Relapsed / High-Risk (del17p / TP53)
● BTK inhibitor or Venetoclax-based therapy preferred
Recent Advances
● Oral targeted drugs replacing chemotherapy.
● Fixed-duration Venetoclax therapy achieving deep remission.
● MRD-guided discontinuation of therapy.
● CAR-T therapy for resistant cases (under trials).
Our Expertise
● Precision genetic testing (TP53, IGHV).
● Access to targeted oral drugs with ongoing monitoring.
● Focus on infection prophylaxis and vaccination guidance.
● Long-term survivorship and quality-of-life support.
When to Consult
Persistent high lymphocyte counts, recurrent infections, or enlarging lymph nodes
warrant hematologic evaluation.
T-Cell Lymphomas
Overview
T-cell lymphomas are uncommon, often aggressive malignancies arising from
mature T lymphocytes.
They account for 10–15% of non-Hodgkin lymphomas and include peripheral T-cell
lymphoma (PTCL), angioimmunoblastic T-cell lymphoma (AITL), and anaplastic
large cell lymphoma (ALCL).
At Coimbatore Cancer Clinic, we specialize in accurate subtyping and
evidence-based immunochemotherapy for these complex diseases.
Causes & Risk Factors
● Viral infections: HTLV-1 (adult T-cell leukemia/lymphoma), EBV.
● Autoimmune diseases.
● Immunodeficiency states.
● Environmental exposure: pesticides, solvents.
● Unknown genetic mutations: TET2, DNMT3A, RHOA.
Symptoms
● Painless lymphadenopathy.
● Fever, weight loss, night sweats.
● Skin rashes or pruritus (cutaneous T-cell lymphoma).
● Fatigue, hepatosplenomegaly.
Diagnosis & Investigations
1. Excisional biopsy – mandatory for diagnosis.
2. IHC panel: CD3+, CD4/CD8 typing, ALK testing (for ALCL).
3. PET-CT for staging.
4. Bone marrow biopsy.
5. Viral testing (HTLV-1, EBV).
Stage-Wise Treatment
Localized Disease
● CHOP / CHOEP chemotherapy ± involved-field radiation.
Advanced or Aggressive Subtypes
● CHOEP or EPOCH regimens.
● Brentuximab vedotin for CD30⁺ ALCL.
● Stem cell transplant consolidation in responders.
Relapsed Disease
● Romidepsin, Pralatrexate, Belinostat (epigenetic agents).
● Allogeneic stem cell transplant for fit patients.
Cutaneous T-Cell Lymphomas (CTCL)
● Phototherapy (NB-UVB or PUVA).
● Topical steroids or retinoids.
● Low-dose systemic therapy for progressive disease.
Recent Advances
● Brentuximab vedotin (anti-CD30) in frontline ALCL.
● Checkpoint inhibitors for selected relapsed cases.
● Epigenetic therapies (HDAC inhibitors) for PTCL.
Our Expertise
● Expert pathologic diagnosis and immunotyping.
● Multidisciplinary management for aggressive and cutaneous forms.
● Access to novel targeted drugs via collaborations.
● Focus on symptom relief and skin care in cutaneous T-cell lymphoma.
When to Consult
Unexplained generalized lymph node swelling or persistent skin lesions with itching
should prompt evaluation.
Diffuse Large B-Cell Lymphoma (DLBCL)
Overview
Diffuse Large B-Cell Lymphoma (DLBCL) is the most common non-Hodgkin
lymphoma worldwide, accounting for roughly one-third of all cases.
It is an aggressive but highly curable cancer of mature B-cells. Cure rates exceed
70 % when treated promptly.
At Coimbatore Cancer Clinic, we use precise biopsy typing, PET-based staging,
and biologic-targeted therapy (e.g. rituximab + chemotherapy) to tailor treatment
for every patient.
Causes & Risk Factors
● Prior immunosuppression (HIV, organ transplant)
● Chronic viral infections (EBV, HCV)
● Autoimmune diseases (RA, Sjögren)
● Genetic mutations: BCL6, BCL2, MYC (“double-hit”)
● Increasing age and male sex
Symptoms & Warning Signs
● Rapidly enlarging, painless lymph-node mass
● Fever, drenching night sweats, unexplained weight loss (“B symptoms”)
● Fatigue, loss of appetite
● Abdominal fullness or pain (spleen/liver involvement)
Diagnosis & Investigations
1. Excisional lymph-node biopsy – essential; FNAC is inadequate.
2. Immunohistochemistry: CD20+, BCL6+, PAX5+ confirms B-cell origin.
3. Cell-of-origin typing: GCB vs ABC subtype (prognostic).
4. FISH testing: MYC/BCL2/BCL6 rearrangements → “double-hit.”
5. PET-CT for staging and response assessment.
6. Bone-marrow biopsy in advanced cases
Stage-Wise Treatment
Limited Stage (I–II Non-Bulky)
● R-CHOP × 3–4 cycles + involved-site radiation (30–36 Gy).
Advanced Stage (III–IV or Bulky)
● R-CHOP × 6 cycles.
● Interim PET after 2–4 cycles to guide escalation or de-escalation.
Relapsed / Refractory Disease
● Salvage chemotherapy (R-ICE, R-DHAP) → autologous stem-cell transplant if responsive.
● CAR-T cell therapy (axi-cel, liso-cel) for transplant-ineligible or chemo-refractory cases.
● Bispecific antibodies (epcoritamab, glofitamab) are promising emerging therapies.
Recent Advances
● Polatuzumab + R-CHP frontline regimen (POLARIX trial) improves PFS.
● CAR-T therapy providing durable remission in resistant disease.
● PET-adapted therapy minimizing toxicity
Our Expertise
● Precision molecular diagnosis (GCB vs ABC).
● Access to novel biologics and CAR-T referral programs.
● Comprehensive supportive-care – infection prevention, nutrition, rehab.
When to Consult
Rapidly enlarging nodes or B-symptoms should prompt evaluation; early diagnosis
ensures cure in most cases
Disclaimer
Information only; management should be individualized by oncologists.
Follicular Lymphoma (FL)
Overview
Follicular Lymphoma is a slow-growing (indolent) B-cell lymphoma arising from
germinal-centre B cells.
It often behaves as a chronic condition with long remissions and occasional
relapses.
At Coimbatore Cancer Clinic, therapy is customized between observation,
rituximab-based treatment, and maintenance depending on stage and symptoms.
Causes & Risk Factors
● Chromosomal translocation t(14;18) → BCL2 overexpression.
● Age > 50 years, slight female predominance.
● Immune suppression or autoimmune disease
Symptoms
● Gradually enlarging painless lymph nodes.
● Fatigue, weight loss, low-grade fever or sweats.
● Abdominal distension (spleen enlargement).
Diagnosis
1. Excisional biopsy: follicular growth pattern.
2. IHC: CD20+, CD10+, BCL2+.
3. PET-CT and Bone-marrow biopsy for staging.
Stage-Wise Treatment
Stage I–II (Localized)
● Involved-site radiation (24–30 Gy) is potentially curative in selected patients.
Stage III–IV or Symptomatic Disease
● Immunochemotherapy options: R-CHOP / R-CVP / R-Bendamustine.
● Rituximab maintenance every 2 months × 2 years to prolong remission.
Relapsed Disease
● Lenalidomide + Rituximab (R² regimen).
● Radioimmunotherapy (Y-90 ibritumomab tiuxetan).
● PI3K or EZH2 inhibitors for selected molecular profiles.
Recent Advances
● Fixed-duration rituximab achieving 10-year PFS > 80 %.
● CAR-T therapy (axi-cel for FL) now approved.
● MRD-guided discontinuation trials ongoing.
Our Expertise
● Accurate grading (1–3A vs 3B).
● Tailored therapy balancing control vs toxicity.
● Long-term survivorship care.
When to Consult
Any persistent lymph-node swelling > 6 weeks or relapse after remission needs
review
Mantle Cell Lymphoma (MCL)
Overview
Mantle Cell Lymphoma is a rare, typically aggressive lymphoma arising from the
mantle zone of lymphoid follicles.
It shows features of both indolent and high-grade disease.
At Coimbatore Cancer Clinic, we combine intensive immunochemotherapy and
maintenance rituximab to prolong survival.
Causes & Risk Factors
● t(11;14) translocation → Cyclin D1 overexpression.
● Male > female (3 : 1), age > 60 years.
● Genetic mutations: ATM, TP53.
Symptoms
● Generalized lymphadenopathy.
● Splenomegaly, abdominal discomfort.
● Fatigue, weight loss, fever.
● Bone-marrow and GI involvement common (polyposis).
Diagnosis
● Excisional biopsy: CD20+, CD5+, Cyclin D1+.
● Ki-67 index assesses proliferation.
● PET-CT & Bone-marrow biopsy for staging.
Stage-Wise Treatment
Fit / Younger Patients
● Cytarabine-containing induction regimens (e.g., Nordic MCL protocol, R-CHOP followed by HiDAC).
● Autologous stem-cell transplant followed by maintenance Rituximab.
Older or Comorbid Patients
● R-Bendamustine × 6 cycles.
● Maintenance Rituximab every 2 months for 2 years.
Relapsed / Refractory Disease
● BTK inhibitors: Ibrutinib, Acalabrutinib, Zanubrutinib.
● CAR-T cell therapy (brexu-cel) for multiply relapsed or refractory cases.
Recent Advances
● BTK inhibitors as frontline in older patients.
● MRD-guided therapy to minimize overtreatment.
● CAR-T therapy achieving long-term control.
Our Expertise
● Flow-cytometric and molecular confirmation of MCL.
● Early integration of targeted therapy.
● Long-term maintenance and infection prophylaxis.
Marginal Zone Lymphoma (MZL)
Overview
Marginal Zone Lymphoma is an indolent B-cell lymphoma derived from
post-germinal-centre B cells.
Subtypes include MALT, nodal, and splenic MZL.
It often arises from chronic antigenic stimulation.
At Coimbatore Cancer Clinic, we focus on treating the underlying cause (infection
or inflammation) along with targeted therapy.
Causes & Risk Factors
● H. pylori infection (gastric MALT).
● Chronic Hepatitis C (splenic MZL).
● Autoimmune diseases: Sjögren, Hashimoto.
Symptoms
● Localized mass (stomach, salivary gland, thyroid).
● Indigestion, abdominal pain (gastric MALT).
● Fatigue, cytopenias (splenic).
Stage-Wise Treatment
Localized Gastric MALT
● H. pylori eradication therapy → remission in >70% of cases.
● Involved-site radiation for persistent or H. pylori–negative disease.
Advanced or Extranodal MALT
● Rituximab ± Chlorambucil or Bendamustine.
Relapsed Disease
● BTK inhibitors (e.g., Ibrutinib).
Recent Advances
● Molecular subtyping (API2-MALT1 fusion) for prognosis.
● Oral BTK and PI3K inhibitors expanding options.
Our Expertise
● Combined infection-eradication and immunotherapy approach.
● Endoscopic surveillance for gastric MALT.
● Long-term follow-up protocols.
Burkitt Lymphoma (BL)
Overview
Burkitt Lymphoma is a highly aggressive B-cell lymphoma characterized by the
t(8;14) MYC translocation.
It progresses rapidly but is curable in > 80 % with timely intensive therapy.
At Coimbatore Cancer Clinic, rapid diagnosis and protocol-driven chemotherapy
are emphasized to prevent life-threatening complications.
Causes & Risk Factors
● Epstein–Barr Virus (EBV) – endemic variant.
● HIV infection.
● Immunodeficiency.
● MYC gene activation.
Symptoms
● Rapidly enlarging jaw or abdominal mass.
● B symptoms (fever, sweats, weight loss).
● Abdominal pain, bowel obstruction, or kidney involvement.
Diagnosis
● Excisional biopsy: “starry-sky” pattern.
● IHC: CD10+, BCL6+, Ki-67 ≈ 100 %.
● FISH: MYC rearrangement.
● CSF cytology / Bone marrow for staging
Stage-Wise Treatment
● Intensive short-course chemotherapy (CODOX-M/IVAC or DA-EPOCH-R).
● Rituximab improves outcomes.
● CNS prophylaxis (intrathecal MTX/Cytarabine) mandatory.
● Supportive care for tumour-lysis syndrome (hydration, rasburicase).
Recent Advances
● DA-EPOCH-R protocol: high cure with less toxicity.
● Risk-adapted regimens reducing overtreatment.
Our Expertise
● Rapid diagnostic turnaround.
● ICU-grade supportive infrastructure.
● NCCN-aligned chemotherapy delivery.
● Nutritional and infection-control support
When to Consult
Any rapidly enlarging jaw, neck, or abdominal mass, especially in young patients,
needs urgent oncology referral.
Peripheral T-Cell Lymphoma (PTCL-NOS)
Overview
Peripheral T-Cell Lymphoma, Not Otherwise Specified (PTCL-NOS) represents a
heterogeneous group of aggressive lymphomas arising from mature T-cells.
It accounts for about 25–30 % of all T-cell lymphomas and is characterized by rapid
progression, frequent extranodal involvement, and variable responses to therapy.
At Coimbatore Cancer Clinic, we emphasize early molecular diagnosis,
PET-guided staging, and evidence-based multi-drug regimens tailored to disease
biology.
Causes & Risk Factors
● Viral links: Epstein–Barr virus (EBV) or Human T-lymphotropic virus (HTLV-1)
infection.
● Autoimmune conditions (RA, celiac disease).
● Long-term immunosuppression or organ transplant.
● Genetic mutations: TET2, DNMT3A, RHOA found in many cases.
● Male gender and age > 60 years.
Symptoms
● Painless, progressive lymph-node swelling in neck, armpit, or groin.
● Fever, night sweats, weight loss.
● Skin rashes or itching.
● Fatigue, loss of appetite.
Diagnosis & Investigations
1. Excisional biopsy – essential for definitive diagnosis.
2. Immunohistochemistry (IHC): CD3+, CD4+, CD8 variable, CD30 negative
(unless ALCL).
3. PET-CT scan for staging (Ann Arbor system).
4. Bone-marrow biopsy.
5. Viral testing (EBV, HTLV-1).
6. Molecular profiling for prognostic markers (e.g. GATA3 vs TBX21 subtype).
Treatment Approach
First-Line Therapy
● CHOP or CHOEP (± Etoposide) × 6 cycles.
● Brentuximab Vedotin + CHP for CD30-positive disease.
● Radiation therapy to residual or bulky sites.
Consolidation
● Autologous stem-cell transplant recommended for fit patients achieving first remission.
Relapsed / Refractory Disease
● Romidepsin, Pralatrexate, Belinostat (HDAC inhibitors).
● Allogeneic stem-cell transplant for eligible patients.
Recent Advances
● Incorporation of Brentuximab Vedotin into front-line therapy.
● Checkpoint inhibitors and epigenetic drugs under evaluation.
● Gene-expression profiling guiding risk-adapted therapy.
Our Expertise
● Accurate histopathologic typing with IHC and molecular support.
● NCCN-aligned multi-agent chemotherapy.
● Early referral for stem-cell transplant in eligible cases.
● Comprehensive support – nutrition, infection prevention, psychological care.
When to Consult
Any progressive lymph-node enlargement with fever or weight loss should prompt
urgent evaluation.
Anaplastic Large Cell Lymphoma (ALCL)
Overview
Anaplastic Large Cell Lymphoma is a distinct T-cell lymphoma characterized by large
anaplastic cells expressing CD30.
It is classified as ALK-positive (more common in younger patients) or ALK-negative
(older patients, worse prognosis).
It often involves lymph nodes and skin and is highly responsive to modern
CD30-directed therapy.
Causes & Risk Factors
● Chromosomal translocation t(2;5) → NPM-ALK fusion gene.
● Immune dysregulation or HIV.
● Age: ALK+ younger; ALK− elderly
Symptoms
● Enlarged nodes or mass in neck or chest.
● Fever, night sweats, weight loss.
● Skin lesions or nodules.
Diagnosis
1. Excisional biopsy – Reed–Sternberg-like cells.
2. IHC: CD30+, ALK +/–, EMA+, CD3−.
3. PET-CT for extent and response.
Stage-Wise Treatment
ALK-Positive ALCL
● CHOP or Brentuximab Vedotin + CHP × 6 cycles.
● Excellent prognosis (5-yr OS > 80%).
ALK-Negative ALCL
● Brentuximab Vedotin + CHP is front-line standard per ECHELON-2 trial.
● Consider autologous stem-cell transplant in first remission for high-risk patients.
Relapsed Disease
● Brentuximab Vedotin monotherapy (ORR > 75%).
● Allogeneic stem-cell transplant for eligible, fit patients.
Recent Advances
● BV + CHP has replaced CHOP as standard of care.
● ALK inhibitors (e.g. Crizotinib) effective in relapsed ALK+ disease.
● CAR-T and checkpoint blockade under research.
Our Expertise
● Rapid ALK testing to guide therapy.
● CD30-targeted therapy integration.
● Expert management of skin and systemic ALCL variants.
When to Consult
Newly appearing pain-free lumps or persistent skin nodules need early biopsy and
review.
Angioimmunoblastic T-Cell Lymphoma (AITL)
Overview
AITL is an aggressive peripheral T-cell lymphoma arising from follicular helper T
cells.
It often presents with systemic symptoms, generalized lymphadenopathy, and
autoimmune features.
At Coimbatore Cancer Clinic, we approach AITL with precision diagnosis,
immunochemotherapy, and novel epigenetic agents.
Causes & Risk Factors
● EBV reactivation within tumour microenvironment.
● Mutations in TET2, RHOA, DNMT3A, IDH2.
● Age > 60 years, male predominance.
Symptoms
● Fever, weight loss, night sweats.
● Skin rash or itching.
● Generalized lymphadenopathy, hepatosplenomegaly.
● Autoimmune haemolytic anemia or polyclonal hypergammaglobulinemia.
Diagnosis
● Excisional lymph-node biopsy – effaced architecture with high vascularity.
● IHC: CD3+, CD4+, CXCL13+, PD-1+.
● PET-CT and bone-marrow biopsy.
● Molecular testing: TET2, RHOA mutations.
Treatment
Front-Line Therapy
● CHOEP × 6 cycles.
● Autologous stem-cell transplant recommended for eligible patients achieving remission.
Relapsed / Refractory Disease
● Epigenetic therapies: Romidepsin, Belinostat, or Azacitidine + Romidepsin combinations.
● Allogeneic stem-cell transplant offers the best chance for durable long-term control.
Recent Advances
● Combined hypomethylating agents + HDAC inhibitors show promising
responses.
● Next-generation sequencing guiding targeted approaches.
Our Expertise
● Advanced pathology and molecular diagnostics.
● Integration of epigenetic and immune-based therapies.
● Focus on managing autoimmune complications.
When to Consult
Systemic symptoms with widespread nodes or autoimmune-like features require
evaluation for AITL.
Cutaneous T-Cell Lymphoma (CTCL)
Overview
CTCL is a group of T-cell lymphomas that primarily affect the skin.
The most common forms are Mycosis Fungoides (MF) and Sézary Syndrome
(SS).
It typically presents with itchy, red, scaly patches that progress to plaques or tumour
nodules.
Though chronic, most cases are controllable for years with skin-directed and
targeted therapy.
Causes & Risk Factors
● Unknown; chronic antigenic stimulation and HTLV-1 suspected.
● Middle-aged to elderly patients most affected.
Symptoms
● Persistent itchy rash or patches unresponsive to steroids.
● Skin thickening or nodules.
● Enlarged lymph nodes in advanced stages.
● Red skin (erythroderma) in Sézary Syndrome.
Diagnosis
● Skin biopsy: epidermotropism of atypical T cells.
● IHC: CD3+, CD4+, CD7 loss.
● Flow cytometry / Sézary cell count.
● PET-CT for staging.
Stage-Wise Treatment
Early Stage (IA–IIA)
● Skin-directed therapy: topical steroids, phototherapy (NB-UVB / PUVA),
bexarotene, localized radiation.
Advanced Stage (IIB–IV)
● Systemic therapy: Interferon-α, Bexarotene, Romidepsin, Brentuximab
Vedotin (for CD30+).
● Extracorporeal photopheresis (ECP) for Sézary Syndrome.
● Allogeneic transplant in selected fit patients.
Recent Advances
● Brentuximab Vedotin and Mogamulizumab (CCR4 antibody) extend
survival.
● New immunomodulators and checkpoint inhibitors under trials.
● Topical HDAC inhibitors show early promise.
Our Expertise
● Combined care by oncologists and dermatologists.
● State-of-the-art phototherapy and radiation facilities.
● Focus on skin care and infection control to enhance quality of life.
When to Consult
Any persistent itchy rash or non-healing skin lesion should be evaluated for possible
CTCL.
Chronic Myeloid Leukemia (CML)
Overview
Chronic Myeloid Leukemia (CML) is a slowly progressing cancer of the bone marrow
characterized by the uncontrolled production of mature myeloid cells.
It is defined by the Philadelphia chromosome, resulting from a genetic
translocation between chromosomes 9 and 22 — forming the BCR-ABL fusion
gene, which drives abnormal cell growth.
CML accounts for about 15–20% of adult leukemias and typically affects individuals
between 40 and 70 years of age.
With the advent of Tyrosine Kinase Inhibitors (TKIs), CML has transformed from a
once-fatal disease into a chronic, controllable condition with near-normal life
expectancy.
At Coimbatore Cancer Clinic, we follow global NCCN and ESMO guidelines to
provide precise molecular monitoring and personalized TKI-based therapy for every
patient.
Causes & Risk Factors
● Genetic driver: Philadelphia chromosome (t9;22, BCR-ABL1).
● Radiation exposure: rare, linked to atomic or therapeutic radiation.
● No hereditary risk: CML is not inherited.
Symptoms & Warning Signs
● Often asymptomatic, detected on routine blood test.
● Fatigue, weakness, or unexplained weight loss.
● Fullness or discomfort in the left upper abdomen due to splenomegaly.
● Night sweats or low-grade fever.
● Bone pain or easy bruising in advanced stages.
Diagnosis & Investigations
1. Complete Blood Count (CBC): very high WBC count with all maturation
stages.
2. Peripheral smear: myeloid cell proliferation with basophilia and eosinophilia.
3. Bone marrow biopsy: hypercellular marrow with granulocytic hyperplasia.
4. Cytogenetic testing: detection of Philadelphia chromosome.
5. Molecular testing (RT-PCR): BCR-ABL1 transcript quantification —
diagnostic and for treatment monitoring.
6. Sokal / Hasford risk scoring to predict response.
Treatment Phases
CML is classified into three phases:
● Chronic phase (CP) – stable disease, >90% diagnosed here.
● Accelerated phase (AP) – rising blast count, resistance developing.
● Blast crisis (BC) – behaves like acute leukemia.
Stage-Wise Treatment
Chronic Phase (CP)
● Tyrosine Kinase Inhibitors (TKIs):
o Imatinib 400 mg daily – first-line option with excellent long-term outcomes.
o Dasatinib / Nilotinib – preferred for high-risk disease or resistance to imatinib.
o Bosutinib / Ponatinib – used in multi-resistant cases or T315I mutation.
● Response Monitoring:
o CBC monthly for the first 3 months.
o BCR-ABL PCR every 3 months until major molecular response is stable.
Accelerated Phase (AP)
● Escalate TKI dose or switch to a second-generation agent.
● Evaluate for allogeneic stem-cell transplant in suitable candidates.
Blast Crisis (BC)
● Combination chemotherapy + TKI to induce remission.
● Proceed to allogeneic stem-cell transplant once remission is achieved.
Treatment Goals
● Complete Hematologic Response (CHR) – normal blood counts.
● Complete Cytogenetic Response (CCyR) – no Philadelphia chromosome.
● Major Molecular Response (MMR) – BCR-ABL ≤ 0.1%.
● Deep Molecular Response (DMR) – undetectable disease.
Some patients achieve Treatment-Free Remission (TFR) after sustained
DMR.
Recent Advances
● Asciminib, a STAMP inhibitor, offers targeted control even in resistant
disease.
● Treatment-free remission (TFR) studies show 40–50% of patients can stop
therapy safely.
● Digital PCR now allows ultra-sensitive disease monitoring.
Our Expertise at Coimbatore Cancer Clinic
● Regular molecular testing (BCR-ABL monitoring).
● Personalized TKI therapy selection.
● Side-effect management — cardiovascular, metabolic, or hepatic.
● Support for long-term survivorship, fertility, and pregnancy during CML.
When to Consult
Persistent high WBC count, fatigue, or abdominal fullness should prompt immediate
hematologic evaluation.
Disclaimer
For educational purposes only. Always consult an oncologist before starting or
adjusting therapy.
Multiple Myeloma (MM)
Overview
Multiple Myeloma is a cancer of plasma cells — specialized immune cells that
produce antibodies.
In myeloma, these cells multiply uncontrollably within the bone marrow and secrete
abnormal immunoglobulins (“M-protein”), leading to bone destruction, anemia,
kidney dysfunction, and immune suppression.
At Coimbatore Cancer Clinic, we provide comprehensive care — from early
diagnosis to transplant and advanced immunotherapy — using NCCN-aligned
protocols.
Causes & Risk Factors
● Age > 60 years is the most significant risk factor.
● Monoclonal Gammopathy of Undetermined Significance (MGUS) can
precede myeloma.
● Radiation or chemical exposure.
● Family history (rare)
Symptoms & Warning Signs
● Bone pain, especially back or ribs.
● Fatigue and weakness (anemia).
● Recurrent infections.
● Thirst, confusion, or constipation (due to hypercalcemia).
● Kidney dysfunction (foamy urine).
Remember: C.R.A.B. → Calcium ↑, Renal failure, Anemia, Bone lesions.
Diagnosis
1. Serum Protein Electrophoresis (SPEP) – M spike.
2. Immunofixation electrophoresis.
3. Free light-chain assay (κ/λ ratio).
4. Bone marrow biopsy: ≥10% clonal plasma cells.
5. PET-CT / MRI: detects lytic bone lesions.
6. Cytogenetics / FISH: t(4;14), del(17p), 1q gain → poor prognosis.
Stage-Wise Treatment
Smoldering (Asymptomatic) Myeloma
● No immediate treatment; close observation every 3–6 months.
Symptomatic Myeloma
Transplant-Eligible
● Induction: Bortezomib + Lenalidomide + Dexamethasone (VRd).
● Autologous Stem Cell Transplant (ASCT).
● Maintenance: Lenalidomide 10–15 mg daily.
Non-Transplant Eligible
● Daratumumab + Lenalidomide + Dexamethasone (DRd) or VRd-Lite.
Relapsed / Refractory Myeloma
● Carfilzomib, Pomalidomide, Elotuzumab, or Daratumumab-based combinations.
● BCMA-targeted therapies: CAR-T therapy or bispecific antibodies (e.g., Teclistamab) for resistant disease.
Recent Advances
● Triplet & quadruplet combinations improving deep remission rates.
● MRD negativity now correlates with long-term survival.
● CAR-T therapy achieving 70–80% response in refractory disease.
Our Expertise
● In-house diagnostic and response monitoring facilities.
● Coordination with transplant and immunotherapy centers.
● Pain management, bone-strengthening (zoledronic acid, denosumab).
● Holistic care: renal protection, nutrition, infection prophylaxis.
When to Consult
Any persistent bone pain, fatigue, or unexplained anemia in adults over 50 should
prompt evaluation for myeloma.
Myelodysplastic Syndromes (MDS)
Overview
MDS are a group of bone marrow disorders in which blood stem cells produce
abnormal, ineffective, or immature blood cells.
They can evolve into acute myeloid leukemia if untreated.
At Coimbatore Cancer Clinic, our approach emphasizes accurate molecular
profiling, risk-based therapy, and patient-centered care to balance control and quality
of life.
Symptoms
● Fatigue, breathlessness, pallor (anemia).
● Frequent infections (low WBC).
● Bruising or bleeding (low platelets).
Diagnosis
1. CBC: cytopenias in one or more lineages.
2. Peripheral smear: dysplastic changes.
3. Bone marrow biopsy: dysplasia, blasts < 20%.
4. Cytogenetics: del(5q), del(7q), monosomy 7, complex karyotype.
5. Molecular profiling: TP53, SF3B1, TET2, ASXL1, DNMT3A.
6. Risk classification: IPSS-R and IPSS-M scores.
Treatment
Low-Risk MDS
● Erythropoiesis-stimulating agents (EPO).
● Lenalidomide for isolated del(5q).
● Luspatercept for anemia in SF3B1-mutated disease.
High-Risk MDS
● Azacitidine or Decitabine (hypomethylating agents) – disease-modifying and standard first-line.
● Allogeneic stem-cell transplant – the only curative therapy.
Supportive Care
● Red cell and platelet transfusions as needed.
● Antibiotics for infections.
● Iron chelation for transfusion-dependent patients.
Recent Advances
● Venetoclax + Azacitidine showing strong synergy in higher-risk MDS.
● Molecular risk-based therapy (IPSS-M) allows tailored management.
Our Expertise
● Advanced diagnostics for MDS subtype and mutation analysis.
● Integration of HMA therapy and supportive care.
● Transplant coordination for eligible patients.
Myeloproliferative Neoplasms (MPN)
Overview
Myeloproliferative neoplasms are long-term disorders in which the bone marrow
makes too many mature blood cells—red cells, white cells or platelets.
The three main types are:
● Polycythemia Vera (PV) – overproduction of red cells
● Essential Thrombocythemia (ET) – excessive platelets
● Primary Myelofibrosis (PMF) – scarring of the marrow with
progressive
failure
These diseases often develop slowly. Many people live well for years when
treatment keeps blood counts balanced and prevents clotting or bleeding problems.
At Coimbatore Cancer Clinic, our hematology team provides accurate molecular
diagnosis (JAK2, CALR, MPL mutations), evidence-based therapy and long-term
monitoring so that patients can live active, full lives.
Causes and Risk Factors
● Acquired gene mutations (JAK2 V617F in >90 % of PV, ~60 % of ET and MF)
● Less often CALR or MPL gene changes
● Usually not inherited; develops spontaneously with age >50 years
● Radiation or chemical exposure (rare)
Common Symptoms
● Headache, dizziness or blurred vision
● Red or flushed face (PV)
● Itching after a warm bath
● Fullness or pain under left ribs (spleen enlargement)
● Tiredness, night sweats or bone pain
● Unusual bleeding or clots (stroke, DVT)
Diagnosis and Tests
1. Complete blood count (CBC): elevated red cells, white cells or platelets
2. Erythropoietin level: low in PV
3. Mutation testing: JAK2, CALR, MPL
4. Bone marrow biopsy: cellularity or fibrosis
5. Ultrasound spleen for enlargement
6. Risk assessment for clotting (age, history of thrombosis)
Treatment Approach
Polycythemia Vera (PV)
● Low-risk: Phlebotomy (venesection) to maintain hematocrit < 45% + low-dose Aspirin.
● High-risk: Hydroxyurea or Peg-interferon-α; Ruxolitinib for hydroxyurea-resistant or intolerant cases.
Essential Thrombocythemia (ET)
● Low-risk: Aspirin only (if no contraindications).
● High-risk: Hydroxyurea or Anagrelide to reduce platelet count.
Primary Myelofibrosis (PMF)
● JAK inhibitors (Ruxolitinib, Fedratinib, Momelotinib) for spleen reduction and symptom control.
● Allogeneic stem-cell transplant – the only curative treatment, suitable for selected younger/fit patients.
● Supportive care: blood transfusions, erythropoietin, management of pruritus and fatigue.
Recent Advances
● New JAK inhibitors (Momelotinib approved 2024) that improve anemia and
symptoms.
● Interferon-α for PV/ET in younger patients with fewer side effects.
● Combination therapy studies (Ruxolitinib + Venetoclax).
Our Expertise
● In-house molecular diagnostics for JAK2/CALR/MPL.
● Personalized therapy to balance control and quality of life.
● Prevention of clotting and bleeding complications.
● Coordination for stem-cell transplant at partner centres.
When to Seek Help
If routine blood tests show persistently high hemoglobin or platelets, or you
experience frequent headaches, clots, or unexplained itching, a hematology consult
is recommended.
Disclaimer
Educational content only; individual care plans must be decided by qualified
oncologists.
Systemic Mastocytosis
Overview
Systemic Mastocytosis (SM) is a rare condition in which mast cells—the immune
cells responsible for allergic responses—grow and accumulate abnormally in the
bone marrow, skin, liver and other organs.
It ranges from a mild, indolent form to an aggressive, life-threatening variant.
Many patients live well for years when their symptoms are controlled and triggers
avoided.
At Coimbatore Cancer Clinic, we combine accurate KIT mutation testing with
comprehensive symptom management and access to targeted drugs available in
India.
Causes and Mechanism
● KIT D816V mutation is present in >90 % of cases and causes continuous
mast-cell growth.
● Usually acquired later in life (not inherited).
● Sometimes associated with other bone-marrow diseases such as MDS or
CML.
Common Symptoms
● Flushing, itching, and episodes of hives
● Stomach pain, diarrhea, or nausea
● Dizziness or fainting due to low blood pressure (anaphylaxis)
● Bone pain, headache, or fatigue
● Swelling of liver or spleen in advanced cases
Diagnosis and Tests
1. Serum tryptase > 20 ng/mL
2. Bone-marrow biopsy: dense mast-cell clusters with aberrant CD25/CD2
markers
3. KIT D816V mutation testing (by PCR or NGS)
4. Liver and bone imaging to check organ involvement
Treatment Approach
Indolent Systemic Mastocytosis
● Antihistamines (H1 and H2 blockers) for flushing and itching.
● Leukotriene inhibitors for abdominal pain.
● Epinephrine auto-injector for anaphylaxis risk.
● Avoid triggers: alcohol, heat, opiates, NSAIDs, insect stings.
Advanced Systemic Mastocytosis
● Cytoreductive therapy: Cladribine or Interferon-α.
● Targeted therapy:
• Midostaurin (available in India) for KIT-mutated disease.
• Avapritinib (latest KIT inhibitor) offering deep, durable responses.
● Corticosteroids for symptom control.
Supportive Care
● Nutritional support for malabsorption
● Bone strength maintenance (Vit D and bisphosphonates)
● Counseling for lifestyle modifications
Recent Advances
● Avapritinib has become first-choice therapy for advanced SM.
● Combination KIT inhibitor + anti-IgE therapy is being explored globally.
● Greater use of molecular testing for early diagnosis in India.
Our Expertise
● On-site molecular confirmation of KIT mutation
● Multidisciplinary care (allergy + hematology specialists)
● Availability of Midostaurin through patient-support programs
● Continuous monitoring to prevent life-threatening reactions
When to Seek Help
Anyone with recurrent allergy-like episodes, flushing without obvious cause, or
unexplained bone pain should undergo evaluation for mast-cell disorders.
Disclaimer
Information for awareness only; management should be supervised by qualified
oncologists.
Amyloidosis (Systemic Light-Chain – AL Type)
Overview
Systemic Light-Chain Amyloidosis (AL Amyloidosis) is a rare condition in which
abnormal plasma cells in the bone marrow produce defective light chains.
These mis-folded proteins accumulate as “amyloid” deposits in vital organs such as
the heart, kidneys, liver and nerves.
Early recognition and treatment are critical because organ damage can be reversible
if therapy starts soon.
At Coimbatore Cancer Clinic, we use rapid diagnostic tools and modern
plasma-cell–directed therapies to halt disease progression and preserve organ
function.
Causes and Risk Factors
● Caused by a clone of plasma cells (similar to myeloma) producing unstable
light chains
● Can develop from MGUS (Monoclonal Gammopathy of Undetermined
Significance)
● More common after age 55 and slightly more frequent in men
Symptoms and Warning Signs
● Kidneys: swelling of feet, foamy urine (protein loss)
● Heart: shortness of breath, low blood pressure, palpitations
● Nerves: tingling, numbness in feet or hands
● Liver/Gut: bloating, weight loss, poor appetite
● Skin/Tongue: bruising around eyes and enlarged tongue (macroglossia)
Diagnosis and Tests
1. Serum and urine immunofixation to detect monoclonal protein
2. Serum free light-chain assay (κ/λ ratio)
3. Tissue biopsy (fat-pad or organ) with Congo red staining showing
apple-green birefringence
4. Cardiac evaluation: NT-proBNP, Troponin, Echocardiography or Cardiac MRI
5. Staging: Mayo criteria based on cardiac and renal markers
Treatment Strategy
First-Line Therapy
● Daratumumab + CyBorD (Cyclophosphamide + Bortezomib + Dexamethasone) is the current standard of care.
● Rapidly suppresses light-chain production and improves organ function.
Eligible Patients
● Autologous stem-cell transplant offers long-term remission in selected fit individuals.
Relapsed / Refractory Disease
● Pomalidomide- or Lenalidomide-based combinations.
● Clinical trials or targeted antibody therapies.
Supportive and Organ-Specific Care
● Cardiac: diuretics, salt restriction, avoid beta-blockers.
● Renal: ACE inhibitors, careful fluid balance, avoid NSAIDs.
● Neuropathy: vitamin support and pain control.
● Nutritional and physiotherapy support.
Recent Advances
● CAEL-101 (anti-amyloid antibody) in late-phase trials for clearing existing
deposits.
● Oral proteasome inhibitors and sub-cutaneous Daratumumab simplifying
therapy.
● India-based access programs for bortezomib and Daratumumab now
available.
Our Expertise
● Rapid diagnosis through Congo-red staining and light-chain quantification.
● NCCN-aligned plasma-cell therapy protocols.
● Cardiology, nephrology and hematology collaboration for integrated care.
● Long-term monitoring of light-chain levels and organ recovery.
When to Seek Help
If you have unexplained swelling, breathlessness, neuropathy or protein in urine, ask
for an evaluation for amyloidosis. Early treatment can prevent organ failure.
Waldenström Macroglobulinemia (WM)
Overview
Waldenström Macroglobulinemia is a rare, slow-growing blood cancer that arises
from lymphoplasmacytic cells—immune cells that behave like both lymphocytes and
plasma cells.
These cells secrete large quantities of a single antibody known as IgM, which
thickens the blood and interferes with normal circulation.
Although WM cannot yet be cured, modern targeted medicines allow most people to
live active lives for many years.
At Coimbatore Cancer Clinic, we focus on early diagnosis using advanced
molecular testing (MYD88 and CXCR4 mutations) and tailor therapy to symptoms,
organ function, and patient goals.
Causes & Risk Factors
● Gene changes: MYD88 L265P mutation (>90 % cases); CXCR4 mutation
(~30 %).
● Age > 60 years; slightly more common in men.
● Family history of lymphoma or monoclonal gammopathy.
● Chronic immune stimulation or infections (hepatitis C, H. pylori).
Symptoms & Warning Signs
● Fatigue or breathlessness (anemia).
● Blurred vision, headaches, or dizziness from thickened blood
(hyperviscosity).
● Numbness or tingling in hands/feet (peripheral neuropathy).
● Bleeding, easy bruising, or nosebleeds.
● Swollen lymph nodes or enlarged spleen.
Because WM progresses slowly, many people have no symptoms at first and are
diagnosed on a routine blood test showing high protein levels.
Diagnosis & Investigations
1. Serum protein electrophoresis (SPEP) and immunofixation to detect IgM
M-spike.
2. Quantitative IgM level and viscosity measurement.
3. Bone-marrow biopsy showing lymphoplasmacytic infiltration (CD20+,
CD138+, CD5-).
4. Molecular testing for MYD88 and CXCR4 mutations.
5. Fundoscopy for retinal changes from hyperviscosity.
6. CT or PET-CT to check lymph-node or spleen enlargement.
Treatment Approach
Observation (Asymptomatic Stage)
If there is no anemia, organ involvement, or hyperviscosity, a “watch-and-wait”
approach is safe.
Follow-up every 3–6 months includes blood counts, IgM levels, and clinical review.
Active Disease / Symptomatic Stage
Treatment begins when patients have anemia, thickened blood, bulky nodes,
neuropathy, or systemic symptoms.
Common regimens
● Rituximab + Bendamustine or Rituximab + Cyclophosphamide +
Dexamethasone (R-CD).
● BTK inhibitors: Ibrutinib, Zanubrutinib, Acalabrutinib – oral, targeted drugs
that block B-cell signalling.
● Plasmapheresis (plasma exchange) for acute hyperviscosity—relieves
headache and vision issues within hours.
Relapsed Disease
● Re-use BTK inhibitors or switch between Zanubrutinib and Ibrutinib.
● Venetoclax (BCL-2 inhibitor) or PI3K inhibitors for resistant cases.
● Autologous stem-cell transplant in young, fit patients after multiple
relapses.
Recent Advances
● BTK inhibitors are now first-line options; Zanubrutinib offers better heart
safety than Ibrutinib.
● Venetoclax + Rituximab combinations achieving deep, time-limited
remissions.
● Research on next-generation antibodies and bispecific T-cell engagers is
promising.
● Access to BTK inhibitors is expanding in India through patient-assistance
programmes
Our Expertise at Coimbatore Cancer Clinic
● Molecular testing for MYD88 and CXCR4 mutations on site.
● Comprehensive care plan: targeted therapy, plasmapheresis, neuropathy
management.
● Close monitoring for heart rhythm, blood-pressure, and infection risk during
BTK therapy.
● Holistic support: nutrition, physiotherapy, and emotional well-being.
When to Consult
Persistent tiredness, blurred vision, unexplained bleeding, or a thick-blood report
(high IgM) should prompt hematology evaluation.
FAQ
Is WM curable?
Not yet, but most patients achieve long-term control with modern oral medicines.
Can BTK inhibitors be taken lifelong?
Yes, many tolerate them well; treatment can be paused if deep remission is
achieved.
Disclaimer
Educational information only; individual treatment decisions must be made with
qualified oncologists.
Pediatric Leukemias & Lymphomas
Overview
Cancers of the blood and lymph system are the most common childhood cancers,
yet they are also among the most curable.
The major types include:
● Acute Lymphoblastic Leukemia (ALL) – ≈ 75 % of childhood leukemias
● Acute Myeloid Leukemia (AML)
● Non-Hodgkin Lymphomas (especially Burkitt and Lymphoblastic types)
● Hodgkin Lymphoma
Modern protocols cure > 85 % of children with ALL and > 70 % with AML in
developed programmes.
At Coimbatore Cancer Clinic, pediatric-focused care combines global standards
with family-centered support—covering treatment, nutrition, mental health, and
long-term follow-up.
Why Children Develop Blood Cancers
In most cases, no clear external cause is found.
Occasional contributors include:
● Genetic predisposition (Down syndrome, Fanconi anemia)
● Prior radiation or chemotherapy exposure
● Certain viral infections or immune defects
These conditions are not contagious and almost never inherited directly.
Common Symptoms
● Persistent fever or frequent infections
● Unexplained tiredness, pallor, or breathlessness
● Bone pain, limp, or refusal to walk
● Painless swellings of neck, underarm, or groin nodes
● Easy bruising or bleeding gums
● Weight loss or night sweats
Because early symptoms mimic common illnesses, parents should seek medical
review if these persist beyond 2 weeks.
Diagnosis & Tests
1. Blood tests (CBC): anemia, low platelets, or circulating blasts.
2. Bone-marrow aspiration & biopsy: confirms leukemia type.
3. Flow cytometry & genetic testing: detects markers such as BCR-ABL,
TEL-AML1, FLT3.
4. Lumbar puncture: checks for cancer cells in spinal fluid.
5. Imaging (PET/CT/MRI): for lymphoma staging.
Treatment Overview
Acute Lymphoblastic Leukemia (ALL)
Therapy occurs in phases over 2–3 years:
1. Induction: multi-drug chemotherapy to achieve remission.
2. Consolidation/Intensification: higher doses to eliminate residual cells.
3. Maintenance: low-dose oral therapy and periodic IV drugs.
4. CNS prophylaxis: intrathecal therapy prevents brain relapse.
Targeted drugs such as Imatinib (for Philadelphia-positive ALL) and Blinatumomab (bispecific antibody) are increasingly used.
For relapsed disease, CAR-T cell therapy offers cure potential.
Acute Myeloid Leukemia (AML)
● Short, intensive chemotherapy (2–4 cycles) using Cytarabine and Anthracyclines.
● Stem-cell transplant for high-risk or relapsed cases.
● Supportive care for infection prevention is crucial.
Non-Hodgkin and Hodgkin Lymphomas
● Burkitt Lymphoma: high-intensity CODOX-M/IVAC protocol; cure rate >90%.
● Lymphoblastic Lymphoma: treated like ALL.
● Hodgkin Lymphoma: ABVD chemotherapy ± limited-field radiation for localized disease.
Supportive & Rehabilitation Care
● Dedicated pediatric oncology nurses for chemo administration.
● Antibiotic prophylaxis and strict infection control.
● Nutrition and dietitian support to maintain weight and immunity
● Psychological counselling for child and family.
● Fertility preservation and growth monitoring for long-term survivors.
Recent Advances
● MRD (Minimal Residual Disease) testing to personalize intensity.
● Targeted agents and immunotherapies (Blinatumomab, Inotuzumab, CAR-T).
● Supportive innovations: oral antibiotics, infection-free rooms,
tele-follow-ups.
● Indian centres, including Coimbatore Cancer Clinic, now offer access to
CAR-T and stem-cell transplant through partner institutions.
Our Expertise at Coimbatore Cancer Clinic
● Specialized pediatric hematology-oncology unit following BFM and COG
protocols.
● Comprehensive infection-controlled chemotherapy wards.
● Integrated rehabilitation and education support so children can continue
schooling.
● Long-term follow-up for growth, cognitive function, and second-cancer
screening.
When to Consult
Any child with persistent fever, bruising, unexplained pallor, or bone pain should see
a pediatric oncologist for blood evaluation.
FAQ
Are childhood leukemias curable?
Yes. Most children with ALL and many with AML can be cured completely.
Will my child need radiation?
Rarely. Most protocols avoid radiation to prevent long-term side effects.
Can children return to normal school life?
Yes. With proper rehabilitation and follow-up, they can resume school and sports
activities.
Disclaimer
This content is for general education and should not replace individual medical
advice.
Always consult qualified pediatric oncologists for diagnosis and treatment.
