Ki-1 Lymphoma

Other names
Types
Causes
Common symptoms and signs
Diagnostic tests
Non-pharmacological treatments (therapies & others)
Drug treatments
Dietary molecular supplements
Immunity-booster / regenerative / stem-cell–related” drugs
Surgeries
Preventions
When to see a doctor
What to eat & what to avoid
FAQs

“Ki-1 lymphoma” is an older name for a cancer now called anaplastic large cell lymphoma (ALCL). The term “Ki-1” came from the Ki-1 antibody, which detects a protein on the tumor cell surface called CD30. In the 1980s, pathologists used the Ki-1 antibody to identify a group of large, “anaplastic” (very abnormal-looking) lymphoid cells. That discovery helped define ALCL as its own disease. Today, doctors use CD30 rather than “Ki-1” in everyday practice, but “Ki-1 lymphoma” still appears in older papers and some summaries. PMC+2PubMed+2

Ki-1 lymphoma is the older term for a group of aggressive lymphomas defined by strong expression of the CD30 (Ki-1) antigen on tumor cells; today they’re classified under anaplastic large cell lymphoma (ALCL), a mature T-cell neoplasm that can be ALK-positive, ALK-negative, primary cutaneous ALCL (pcALCL), or breast-implant–associated ALCL (BIA-ALCL). Synonyms/related labels you’ll see in the literature include CD30-positive large cell lymphoma, Ki-1–positive lymphoma, and CD30+ T-cell lymphoma. Modern WHO 5th-edition classification places ALCL within mature T-/NK-cell neoplasms and emphasizes CD30 positivity, ALK status, and special entities like BIA-ALCL. PMC+3NCBI+3Nature+3

The antibody that first highlighted these tumors was called Ki-1, which recognized CD30—initially found on Hodgkin/Reed–Sternberg cells and later in ALCL; as classification evolved, “Ki-1 lymphoma” was replaced by the more precise ALCL terminology. PMC+1

In simple words: Ki-1 lymphoma = a CD30-positive lymphoma of T-cell type called ALCL. The tumor cells are big, look very abnormal under the microscope, and strongly show CD30 on their surface. Medscape+1

Other names

Anaplastic large cell lymphoma (ALCL)
CD30-positive T-cell lymphoma
CD30 (Ki-1)–positive large cell lymphoma
ALK-positive ALCL (a subtype)
ALK-negative ALCL (a subtype)
Primary cutaneous ALCL (pcALCL) (mainly in skin)
Breast implant–associated ALCL (BIA-ALCL) (a special form linked to certain breast implants) PMC+2Cancer.gov+2

Ki-1 lymphoma is a non-Hodgkin lymphoma that usually comes from mature T-cells (a type of white blood cell). The sick cells are large and anaplastic (they don’t look like normal cells). Almost all of them show a strong CD30 signal. Some tumors also make a protein called ALK, caused by a gene change (rearrangement) in the ALK gene; those cases are called ALK-positive. Other cases are ALK-negative. Doctors split the disease into systemic (lymph nodes and organs), primary cutaneous (starts in the skin), and breast implant–associated types. The name “Ki-1” reflects the history of the test used to find CD30, not a separate disease. Medscape+2PMC+2

Types

Systemic ALK-positive ALCL
Happens when the tumor has an ALK gene rearrangement (most often NPM1-ALK from a t(2;5) swap). These tumors show ALK protein by immunostain, often affect younger people, and generally have better outcomes than ALK-negative cases. MDPI
Systemic ALK-negative ALCL
These lack ALK. A share of them carry DUSP22 or TP63 gene rearrangements, which may influence behavior and prognosis. The DUSP22-rearranged subgroup has distinct features; TP63-rearranged cases tend to behave more aggressively. Many cases are “triple-negative” (no ALK, DUSP22, TP63). ScienceDirect+3ASH Publications+3Haematologica+3
Primary cutaneous ALCL (pcALCL)
Starts in the skin. Often presents as one or a few nodules or plaques that may ulcerate. Usually ALK-negative and often behaves more indolently than systemic disease. PMC
Breast implant–associated ALCL (BIA-ALCL)
Arises in the breast implant capsule fluid or scar tissue, most often with textured implants. It is a CD30-positive, usually ALK-negative T-cell lymphoma. Risk is low but clearly increased with textured devices. PMC+1

Causes

There isn’t a single lifestyle cause. Instead, ALCL develops through genetic changes in lymphocytes and, in some settings, chronic immune stimulation. Below are 20 contributors/associations explained simply.

CD30 pathway activation
CD30 is an activation marker on lymphocytes. In ALCL, tumor cells strongly express CD30, which drives signaling that helps cells grow and survive. This is a defining feature rather than a lifestyle cause. Medscape
ALK gene rearrangements (ALK-positive ALCL)
A DNA swap (often NPM1-ALK) turns on ALK signaling, pushing uncontrolled growth. This change defines ALK-positive disease. MDPI
DUSP22 rearrangement (ALK-negative subset)
Some ALK-negative tumors have DUSP22 rearrangements. They show distinctive lab patterns and biology compared with other ALK-negative cases. ASH Publications
TP63 rearrangement (ALK-negative subset)
A smaller group has TP63 rearrangements, which generally predict more aggressive behavior. ASH Publications
JAK/STAT pathway mutations
Mutations activating JAK1/STAT3 are found in BIA-ALCL and other ALK-negative cases, helping tumor cells grow and avoid normal controls. PMC
Immune stimulation around breast implants (BIA-ALCL)
Chronic inflammation near textured implants may promote tumor development in that local environment. Risk remains small, but higher than in people without textured devices. PMC
Male sex (systemic ALCL)
Systemic ALCL shows a male predominance, especially ALK-positive disease. Sex is a risk pattern, not a cause you can change. Medscape
Younger age for ALK-positive; older age for ALK-negative
ALK-positive cases tend to occur in younger patients; ALK-negative cases are more common in older adults. MDPI
Cutaneous immune environment (pcALCL)
In pcALCL, local immune signals in the skin may favor growth of CD30-positive T-cells, leading to skin-limited disease in many patients. PMC
Cytotoxic T-cell program
ALCL cells often express cytotoxic markers (e.g., TIA-1, granzyme B), reflecting their T-cell origin and function. This is a biological feature rather than a lifestyle trigger. Haematologica
Loss or aberrant expression of T-cell antigens
Tumor cells may lose typical T-cell markers or show them abnormally, indicating a disturbed T-cell identity. Medscape
MYC copy number changes (subset)
Some ALK-positive cases show MYC dysregulation, which can add to tumor growth signaling. Haematologica
PD-L1/STAT3 signaling
Upregulation of PD-L1 and STAT3 activation is described in systemic ALCL and may help the tumor escape immune attack. Haematologica
Rare genetic patterns beyond ALK/DUSP22/TP63
Research keeps finding additional, less common genetic changes (e.g., MSC E116K) that contribute to disease biology. Haematologica
General lymphoma risk conditions
Like other lymphomas, prior immunosuppression or altered immunity (from illness or medicines) may raise overall lymphoma risk, though this link to ALCL specifically is not strong. (General NHL context.) NCBI
Extranodal tissue microenvironments
ALCL often involves skin, soft tissue, bone, liver, spleen, and lung, suggesting certain tissues can provide signals that favor tumor growth. PMC
Possible microbial biofilm on textured implants (BIA-ALCL hypothesis)
Some studies propose bacterial biofilm on textured devices as a chronic antigen source—still an area of study rather than a proven cause. PMC
Prior cancer treatment/medical exposures
As with other lymphomas, prior radiation or chemotherapy may slightly change long-term risks, though this is not a classic driver for ALCL specifically. (General NHL risk context.) NCBI
Genetic background (host factors)
Emerging data suggest host genetics can influence who develops particular ALCL subtypes (e.g., age/sex patterns and immune genes), but no single inherited cause is known. MDPI
Unknown/idiopathic
In most patients we do not find a clear trigger. The disease reflects a mix of chance DNA errors and micro-environmental signals that let abnormal T-cells grow unchecked. (Consensus understanding across sources.) Medscape+1

Common symptoms and signs

Painless swollen lymph nodes
Most people notice a painless lump in the neck, armpit, or groin. This is a classic lymphoma sign. Cureus
B-symptoms: fever
Unexplained fevers happen because tumor cells release inflammatory signals. NCBI
B-symptoms: night sweats
Heavy sweating at night may drench clothes and sheets. NCBI
B-symptoms: weight loss
Unplanned weight loss reflects the body’s response to constant inflammation. NCBI
Skin lumps or sores (pcALCL)
In skin-limited disease, people get red-to-violaceous nodules or plaques that may ulcerate; often one area, sometimes several. PMC
Itchy or tender skin lesions (pcALCL)
Lesions can be itchy, sore, or ooze if ulcerated. MDPI
Mediastinal pressure symptoms
A large chest mass can cause cough, chest discomfort, or shortness of breath. Rarely, facial swelling from superior vena cava (SVC) compression. Cancer Network
Abdominal pain or fullness
From enlarged abdominal nodes, liver, or spleen. NCBI
Fatigue and weakness
Common in lymphoma due to inflammation, anemia, or treatment effects. NCBI
Bone pain (extranodal disease)
When bone is involved, people may feel localized bone pain. ScienceDirect
Easy infections if blood counts drop
If bone marrow is affected, white cell counts can fall, raising infection risk. NCBI
Swollen liver or spleen
Doctors may feel hepatosplenomegaly during exam in systemic disease. PMC
Anemia symptoms
Shortness of breath with exertion, paleness, or dizziness if red cells are low. NCBI
Localized breast swelling or fluid in BIA-ALCL
People with implants may notice late-onset fluid collection (seroma), swelling, or a new mass near the implant years after surgery. Radiopaedia
Occasional severe or unusual presentations
Rarely, people present acutely ill with multi-organ problems; this is uncommon but reported. PMC

Diagnostic tests

A) Physical examination

Full lymph node exam
The clinician checks all node regions (neck, armpits, groin) and also looks for skin lesions, abdominal fullness, and signs of chest pressure to map out possible disease sites. Physical exam guides which area to biopsy first. UpToDate
Organ exam for liver and spleen
Feeling for an enlarged liver or spleen helps stage the disease and judge symptom causes (e.g., pain or early satiety). PMC
Performance status assessment
A simple rating (e.g., ECOG) of how active you are. It predicts how well someone may handle treatment and often correlates with stage and lab findings. (General NHL practice.) NCBI

B) “Manual” bedside/procedural checks

Targeted palpation and mapping of skin lesions (pcALCL)
Counting and measuring nodules/plaques and checking for ulceration help track response over time. PMC
Focused breast exam for BIA-ALCL
In people with implants and late swelling, the clinician looks for capsular fluid or a peri-implant mass and plans sampling. Radiopaedia
Excisional lymph node biopsy (preferred)
Taking out all or part of a whole node gives enough tissue to make the right diagnosis. Fine-needle aspiration is not enough by itself for ALCL. UpToDate
Core biopsy of mass/skin lesion
If a node can’t be excised, a core (thicker needle) or skin punch biopsy is done to get tissue architecture for ALCL vs other CD30-positive disorders. PMC

C) Laboratory & pathological tests

Complete blood count (CBC) and chemistry panel
Looks for anemia, low white cells or platelets, LDH elevation, and organ function—useful for staging and tracking. NCBI
Immunohistochemistry (IHC) on biopsy
Key markers: CD30 (strong, diffuse); ALK (positive in ALK+); often EMA; variable T-cell markers (CD3, CD4). Negative for PAX5 and CD15 helps separate from Hodgkin lymphoma. This panel defines ALCL and its subtype. Medscape
ALK protein testing
IHC for ALK confirms ALK-positive disease and supports specific genetic fusions (e.g., NPM1-ALK). MDPI
Flow cytometry (immunophenotyping)
Profiles cell surface proteins to confirm T-cell lineage and exclude mimics. Often combined with IHC. Medscape
Molecular tests for ALK, DUSP22, TP63
FISH or PCR/NGS looks for ALK rearrangements and, in ALK-negative cases, DUSP22 or TP63 changes that can aid classification and prognosis discussion. ASH Publications+1
T-cell receptor (TCR) gene rearrangement testing
Shows a clonal T-cell population, supporting the diagnosis when morphology and stains suggest ALCL. PMC
EBER in situ hybridization
Helps exclude EBV-positive T/NK lymphomas that can mimic ALCL; most ALCLs are EBV-negative. PMC
Cytogenetics/NGS panels
Broader sequencing can uncover JAK/STAT or other pathway mutations (more common in ALK-negative/BIA-ALCL) and may guide trials. PMC
Bone marrow biopsy
Checks if the marrow is involved—important for staging in systemic disease. Chinese Clinical Oncology

D) Electrodiagnostic / treatment-planning tests

Electrocardiogram (ECG)
Not for diagnosing the lymphoma itself, but often done before therapy (e.g., anthracyclines) to screen for heart risks. (Standard NHL work-up practice.) NCBI
Echocardiogram
Similarly, a heart ultrasound may be done before certain chemotherapies to document baseline function. (Standard NHL practice.) NCBI

E) Imaging tests

PET-CT (FDG-PET/CT)
The preferred imaging to stage and assess response in most FDG-avid lymphomas, including ALCL, using Lugano 2014 criteria and a 5-point Deauville scale. Lymphoma+1
Contrast CT of neck/chest/abdomen/pelvis
Maps lymph nodes and organs when PET is not available and complements PET for anatomy. Chinese Clinical Oncology
Ultrasound (breast/axilla) for suspected BIA-ALCL
Helps detect peri-implant fluid or a mass; guides aspiration for cytology and CD30 testing. MRI can also be used. Radiopaedia
MRI (site-specific)
Useful for brain/spine symptoms or detailed soft-tissue mapping when needed. (General lymphoma imaging practice.) PMC
Chest imaging for mediastinal disease
Large chest masses or node clusters are common in some systemic ALCL cases and can be seen on CXR/CT; PET-CT refines the picture. Cancer Network
Staging system application (Lugano)
After imaging and marrow biopsy, clinicians assign stage using Lugano classification, which guides prognosis and treatment planning. bloodresearch.or.kr

Non-pharmacological treatments (therapies & others)

Excisional surgery for solitary pcALCL skin lesions: cures many single lesions; preserves tissue for diagnosis; avoids systemic toxicity. Mechanism is complete tumor removal with negative margins. Purpose is local disease control and symptom relief. Cutaneous Lymphoma Foundation+1
Involved-site radiotherapy (ISRT): highly effective for pcALCL and for palliative control in systemic ALCL; typical doses achieve high local control. Mechanism is DNA damage causing tumor cell death. Purpose: rapid control of bulky/painful sites. Cutaneous Lymphoma Foundation+1
Breast implant explantation + total capsulectomy (BIA-ALCL): cornerstone for disease confined to capsule/effusion; may be curative. Purpose: remove tumor source/niche. Mechanism: complete eradication of capsule-associated lymphoma. PMC
PET/CT-guided active surveillance after local therapy (pcALCL): many cutaneous cases are indolent; watchful waiting avoids overtreatment. Purpose: monitor for relapse/progression. Mechanism: treat only if clinically meaningful disease appears. PMC
Structured exercise during treatment: aerobic + resistance exercise reduces fatigue and improves function; recommended during curative-intent therapy. Mechanism: anti-inflammatory, preserves muscle and cardiorespiratory fitness. Purpose: symptom control and quality of life. ASCO Publications+1
Nutrition counseling: individualized energy/protein targets and symptom-directed strategies; avoid routine “neutropenic diets.” Purpose: maintain weight/lean mass. Mechanism: meets metabolic needs and reduces treatment interruptions. PubMed
Oral care bundle: soft brushing, saline/bicarbonate rinses, dental check before chemo to reduce mucositis/infections. Mechanism: lowers oral microbial load and trauma. PMC
Oral cryotherapy for selected chemo (e.g., bolus 5-FU, high-dose melphalan): 30-minute ice chips reduce mucositis risk. Purpose: prevent painful ulcers. Mechanism: vasoconstriction reduces mucosal exposure to drug. MASCC+1
Psychosocial counseling: addresses anxiety/depression, improves adherence and coping. Purpose: enhance well-being and decision quality. Mechanism: cognitive-behavioral and supportive therapy. ASCO Publications
Fertility preservation counseling: discuss sperm/egg preservation before chemo. Purpose: protect future fertility. Mechanism: cryopreservation prior to gonadotoxic therapy. Medscape
Vaccination planning: inactivated influenza/COVID per oncology guidance before chemo; live vaccines avoided during immunosuppression. Purpose: reduce severe infections. Mechanism: adaptive immunity. PubMed
Smoking cessation support: improves treatment tolerance and wound healing. Mechanism: reduced oxidative and vascular stress. ASCO Publications
Sleep hygiene & fatigue management: structured routines, brief daytime naps, light exposure. Purpose: reduce cancer-related fatigue. ASCO Publications
Physical therapy for neuropathy/balance: targeted exercises and safety strategies when vincristine-related neuropathy occurs. Purpose: reduce falls and disability. Cancer Care Ontario
Dermatologic wound care (pcALCL lesions): gentle cleansers, non-adherent dressings, infection prevention. Purpose: comfort and healing. PMC
Sun protection for skin disease: reduces irritation of cutaneous lesions and post-RT sites. PMC
Palliative care integration: early symptom-focused care for pain, pruritus, fatigue, and mood improves outcomes. Purpose: quality of life. ASCO Publications
Financial/toxicity navigation: helps adherence and reduces distress. Mechanism: coordinated supportive services. ASCO Publications
Infection-prevention education: hand hygiene, food safety, sick-contact avoidance during neutropenia. Purpose: fewer infections/hospitalizations. PubMed
Return-to-work and activity planning: phased schedules maintain function and morale. Purpose: survivorship quality. ASCO Publications

Drug treatments

Brentuximab vedotin (anti-CD30 ADC) • 1.8 mg/kg IV q3w (with CHP for 6–8 cycles in frontline; solo in relapse/pcALCL per label) • Purpose: core CD30-targeted therapy • Mechanism: anti-CD30 antibody delivering MMAE • SE: neuropathy, neutropenia. Frontline A+CHP improved 5-yr PFS/OS vs CHOP (ECHELON-2). PubMed+1
Cyclophosphamide (chemo; in CHOP/CHP) • ~750 mg/m² IV day 1 q21d • Purpose: cytotoxic backbone • Alkylates DNA • SE: myelosuppression, cystitis. PMC
Doxorubicin (anthracycline) • 50 mg/m² IV day 1 q21d • Purpose: cytotoxic backbone • Intercalates DNA/topo-II inhibition • SE: cardiomyopathy—baseline cardiac assessment advised. PMC
Prednisone/Prednisolone • 100 mg PO daily days 1–5 q21d • Purpose: lympholytic, antiemetic • Mechanism: glucocorticoid-induced apoptosis • SE: hyperglycemia, insomnia, infection risk. PubMed
Vincristine (often omitted in A+CHP) • 1.4 mg/m² (cap 2 mg) IV day 1 q21d in CHOP • Purpose: mitotic inhibitor • Tubulin binding • SE: neuropathy/constipation. PMC
Methotrexate (low-dose, pcALCL) • e.g., 7.5–25 mg weekly regimens used • Purpose: control multifocal skin disease • Mechanism: antifolate • SE: mucositis, hepatotoxicity (monitor). E-ACFS
Pralatrexate (antifolate) • 30 mg/m² IV weekly (6 of 7 weeks) • Purpose: relapsed PTCL including ALCL • Mechanism: high-affinity uptake via RFC-1; DHFR inhibition • SE: mucositis—folate/B12 supplementation used. DailyMed+1
Belinostat (HDAC inhibitor) • 1000 mg/m² IV days 1–5 q21d • Purpose: relapsed PTCL • Mechanism: epigenetic modulation • SE: cytopenias, fatigue. PubMed+1
Romidepsin (HDAC inhibitor) • (Note: PTCL indication withdrawn in the U.S.; still used for CTCL/pcALCL per guidelines) • Purpose: second-line in cutaneous T-cell lymphoma; historical PTCL use varies by region • SE: cytopenias, ECG changes—check local label. Bristol Myers Squibb News+1
Gemcitabine • e.g., 1000 mg/m² d1,8,15 q28d • Purpose: active in T-cell lymphomas (salvage) • Mechanism: antimetabolite • SE: myelosuppression. Medscape
Etoposide (CHOEP regimens) • adds to CHOP in some younger PTCLs • Purpose: intensify cytotoxicity • Mechanism: topo-II inhibitor • SE: myelosuppression. MDPI
Crizotinib (ALK inhibitor) • oral; dosing per label • Purpose: relapsed/refractory ALK-positive ALCL (not frontline) • Mechanism: ALK kinase inhibition • SE: GI upset, transaminitis, visual changes. Aspen Journals
Alectinib/Lorlatinib (ALK inhibitors) • used off-label/case series in ALK+ ALCL relapse • Purpose: targeted salvage • SE: agent-specific. PubMed
Mogamulizumab (anti-CCR4) • used mainly in CTCL; occasional ALCL use depending on CCR4 • Mechanism: ADCC against CCR4+ cells • SE: rash/infusion reactions. Medscape
Lenalidomide • immunomodulator with activity in some T-cell lymphomas • SE: cytopenias, thrombosis (prophylaxis). MDPI
Pembrolizumab/Nivolumab (PD-1 inhibitors) • case-based in CTCL/pcALCL; consider after standard options • Immune activation • SE: immune-related AEs. Medscape
Ifosfamide-based salvage (e.g., ICE) • bridge to transplant in fit relapsed patients • Cytotoxic combination • SE: myelosuppression, encephalopathy (ifosfamide). MDPI
Brentuximab vedotin retreatment at relapse • objective responses seen even after prior A+CHP • Mechanism as above • SE: neuropathy/neutropenia. PubMed
Supportive antiemetics per ASCO • 5-HT3 + NK1 + dexamethasone based on chemo emetogenicity • Purpose: prevent CINV • SE: agent-specific. PubMed
Growth-factor prophylaxis (G-CSF) with A+CHP per label if high risk of neutropenia • Purpose: reduce febrile neutropenia • SE: bone pain. FDA Access Data

Dietary molecular supplements

Important: supplements don’t treat ALCL; use to relieve symptoms/support nutrition. Avoid high-dose antioxidant cocktails during chemo unless your oncology team approves. PubMed

Vitamin D (to replete deficiency): typical repletion per labs; supports bone/muscle and immune function; no proof it treats lymphoma. PubMed
Omega-3 (fish oil): trials suggest help with cancer cachexia/weight maintenance in some settings; doses ~2 g/day EPA+DHA studied; watch bleeding with anticoagulants. Taylor & Francis Online
Oral glutamine: may reduce mucositis/severity in selected regimens; dosing varies (e.g., 10 g TID in studies); discuss with team. PMC
Ginger (nausea): RCTs/meta-analyses suggest modest CINV benefit; ~0.5–1 g/day divided; watch anticoagulant effects. PMC
Probiotics: avoid during profound neutropenia due to bacteremia risk; consider only with clinician advice. PMC
Protein supplements (whey/pea): to hit protein targets when intake is poor; dose individualized (e.g., 20–30 g between meals). PubMed
Zinc (short-term for taste changes): brief use may help dysgeusia; excess can cause copper deficiency—limit duration. PubMed
Vitamin B12 & folate: indicated if deficient; folate/B12 are part of pralatrexate protocols to cut mucositis risk. DailyMed
Melatonin (sleep): may assist sleep; oncology outcome data are inconsistent; typical 1–5 mg HS. PubMed
Electrolyte solutions: for dehydration from vomiting/diarrhea; follow clinician guidance. PubMed

Immunity-booster / regenerative / stem-cell–related” drugs

Filgrastim (G-CSF): daily SC after chemo to shorten neutropenia; function: stimulates neutrophil recovery; mechanism: G-CSF receptor signaling. FDA Access Data
Pegfilgrastim (long-acting G-CSF): single SC dose per cycle; same function/mechanism; convenient. FDA Access Data
Epoetin alfa / Darbepoetin: treat chemo-induced anemia in select cases; function: stimulate erythropoiesis; risks and hemoglobin targets apply. PubMed
Eltrombopag / Romiplostim: for refractory thrombocytopenia; function: TPO-receptor agonism to raise platelets. PubMed
IVIG: for severe hypogammaglobulinemia with recurrent infections; function: passive immunity. PubMed
Plerixafor (stem-cell mobilizer): used with G-CSF to collect peripheral stem cells for autologous transplant; mechanism: CXCR4 inhibition. PubMed

Surgeries

Excisional lymph node biopsy: definitive diagnosis/typing (essential for ALCL). Medscape
Primary lesion excision (pcALCL): curative for solitary/few skin tumors; preferred with or without adjuvant RT. Cutaneous Lymphoma Foundation
Breast implant explantation + total capsulectomy (BIA-ALCL): first-line for localized peri-implant disease. PMC
Central venous catheter/port placement: reliable access for multi-cycle chemotherapy. Cancer Care Ontario
Splenectomy (selected cases): rarely for hypersplenism/symptom control when medical options fail. Medscape

Preventions

Avoid textured breast implants (BIA-ALCL risk is linked to textured surfaces).
Vaccinate (inactivated flu/COVID) before immunosuppression when possible.
Hand/food hygiene during neutropenia.
Dental check + oral care before chemo.
Exercise during and after treatment.
Sun protection for skin disease/RT sites.
Smoking cessation.
Fertility preservation discussions early.
Medication interaction checks (e.g., azoles with vincristine).
No routine neutropenic diet—use safe food handling instead. PMC+2PubMed+2

When to see a doctor

See your cancer team promptly for fever ≥38 °C, chills, new rapidly enlarging nodes or skin lesions, uncontrolled pain, dyspnea or chest swelling (especially with implants), persistent vomiting/diarrhea, new numbness/weakness (possible neuropathy), bleeding/bruising, or night sweats/weight loss. These can signal infection, progression, or treatment toxicity and need quick evaluation. PMC+1

What to eat & what to avoid

Eat: (1) small, frequent high-protein meals; (2) lean proteins (eggs, fish, pulses); (3) whole grains & fruits/veg you can tolerate; (4) oral nutrition shakes if needed; (5) hydration with ORS when nauseated. Avoid/limit: (6) raw/undercooked meats/eggs during neutropenia; (7) unpasteurized products; (8) high-dose antioxidant/herbal cocktails without oncologist approval; (9) excessive alcohol; (10) grapefruit if your meds have interactions. PubMed

FAQs

1) Is Ki-1 lymphoma the same as ALCL? Yes—Ki-1 refers to CD30, and “Ki-1 lymphoma” evolved into ALCL in modern classifications. NCBI
2) What does CD30 mean? It’s a cell-surface protein (formerly “Ki-1”) that ALCL cells strongly express; it’s also the target for brentuximab vedotin. Nature
3) How is ALK status used? ALK-positive ALCL generally has a better prognosis and may respond to ALK inhibitors at relapse; ALK-negative is more heterogeneous. ScienceDirect+1
4) What’s the current frontline standard for systemic CD30+ ALCL? A+CHP (brentuximab vedotin + CHP), which improved survival over CHOP in ECHELON-2. PubMed
5) Can radiation cure skin-only disease? Many single-site pcALCL lesions are cured with surgery or localized radiotherapy. Cutaneous Lymphoma Foundation
6) What is BIA-ALCL? A rare T-cell lymphoma linked to textured implants; first treatment is implant removal and total capsulectomy. PMC
7) Do I always need chemo for pcALCL? Not necessarily—some cases are managed with local therapy or low-dose methotrexate if multifocal. PMC
8) How is response measured? PET/CT using Lugano criteria (Deauville scale). PMC+1
9) Are supplements helpful? They don’t treat lymphoma; dietitians may suggest selected supplements for symptoms/deficits—avoid high-dose regimens during chemo unless approved. PubMed
10) Does exercise help? Yes—ASCO recommends regular aerobic and resistance exercise during treatment to reduce fatigue and improve function. ASCO Publications
11) What about neuropathy from treatment? Vincristine and brentuximab can cause neuropathy; dose changes, PT, and symptom care often help. FDA Access Data
12) Is transplant used? Some relapsed/systemic cases proceed to autologous (or allogeneic) transplant after salvage chemo; decisions are individualized. MDPI
13) Are PD-1 inhibitors used? Occasionally in refractory cutaneous T-cell lymphomas; evidence is evolving and not standard first-line for ALCL. Medscape
14) What’s the prognosis? It varies by subtype; ALK-positive tends to do better; A+CHP has improved outcomes for systemic CD30+ disease at 5 years. PubMed+1
15) Are textured implants still recommended? Many regulators and experts caution about risks; discuss implant surface choices with surgeons; routine removal isn’t advised if asymptomatic, but vigilance is key. Health

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