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Hodgkin's lymphoma

From Wikipedia, the free encyclopedia

Hodgkin's lymphoma , previously known as Hodgkin's disease , is a type of lymphoma ,

which is a cancer originating from white blood cells called lymphocytes . It was named

after Thomas Hodgkin , who first described abnormalities in the lymph system in 1832. [1]

[2] Hodgkin's lymphoma is characterized by the orderly spread of disease from one lymph

node group to another and by the development of systemic symptoms with advanced

disease. When Hodgkins cells are examined microscopically, multinucleated Reed-Sternberg

cells (RS cells) are the characteristic histopathologic finding. Hodgkin's lymphoma may be

treated with radiation therapy or chemotherapy , the choice of treatment depending on the

age and sex of the patient and the stage, bulk and histological subtype of the disease.

The disease occurrence shows two peaks: the first in young adulthood (age 1535) and the

second in those over 55 years old. [3]

The 10-year overall survival rate is more than 90% for early stage (stage I or II) Hodgkin's

lymphoma. Since many patients are young, they often live 40 years or more after treatment.

However, few studies follow patients as long as 25 years, and those studies are of older

treatments with more life-threatening adverse effects, so it is impossible to predict long-

term outcomes of newer, less-harmful treatments. Radiation treatments, and some

chemotherapy drugs, cause potentially fatal secondary cancers, heart disease, and lung

disease 40 or more years later. Modern treatments minimize these late effects. [4]

Patients with a history of infectious mononucleosis due to Epstein-Barr virus may have an

increased risk of HL. [citation needed ]

[edit ]Classification

[edit ]Types

Classical Hodgkin's lymphoma (excluding nodular lymphocyte predominant Hodgkin's

lymphoma ) can be subclassified into 4 pathologic subtypes based upon Reed-Sternberg

cell morphology and the composition of the reactive cell infiltrate seen in the lymph

node biopsy specimen (the cell composition around the Reed-Stenberg cell(s)).

Name Description ICD-10 ICD-O

Nodularsclerosing CHL

Is the most common subtype and is composed of large tumor nodules showing scattered lacunar classical RS

C81. 1

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cells set in a background of reactive lymphocytes , eosinophils and plasma cells withvarying degress of collagen fibrosis/ sclerosis .

Mixed-cellularitysubtype

Is a common subtype and is composed of numerous classic RScells admixed with numerous inflammatory cells includinglymphocytes, histiocytes, eosinophils, and plasma cells.without sclerosis. This type is most often associatedwith EBV infection and may be confused with the early, so-called 'cellular' phase of nodular sclerosing CHL.

C81. 2

M9652/3.

Lymphocyte -rich orLymphocyticpredominance

Is a rare subtype, show many features which may causediagnostic confusion with nodular lymphocyte predominant B-cell Non-Hodgkin's Lymphoma (B-NHL). This form also has themost favorable prognosis.

C81. 0 M9651/3

Lymphocytedepleted

Is a rare subtype, composed of large numbers of oftenpleomorphic RS cells with only few reactive lymphocytes whichmay easily be confused with diffuse large cell lymphoma . Manycases previously classified within this category would now bereclassified under anaplastic large cell lymphoma . [5]

C81. 3 M9653/3

Unspecified C81. 9 M9650/3

Nodular lymphocyte predominant Hodgkin's lymphoma expresses CD20 , and is not currently

considered a form of classical Hodgkin's.

For the other forms, although the traditional B cell markers (such as CD20 ) are not

expressed on all cells, [5] Reed-Sternberg cells are usually of B cell origin. [6][ 7] Although

Hodgkin's is now frequently grouped with other B cell malignancies, some T cell markers

(such as CD2 and CD4 ) are occasionally expressed. [8] However, this may be an artifact of the

ambiguity inherent in the diagnosis.

Hodgkin's cells produce Interleukin-21 (IL-21), which was once thought to be exclusive to T

cells . This feature may explain the behavior of classical Hodgkin's lymphoma, including

clusters of other immune cells gathered around HL cells (infiltrate) in cultures. [9]

[edit ]Staging

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On the basis of this staging, the patient will be classified according to a staging classification

(the Ann Arbor staging classification scheme is a common one):

Stage I is involvement of a single lymph node region (I) (mostly the cervical region)

or single extralymphatic site (Ie);Stage II is involvement of two or more lymph node regions on the same side of

the diaphragm (II) or of one lymph node region and a contiguous extralymphatic site

(IIe);

Stage III is involvement of lymph node regions on both sides of the diaphragm, which

may include the spleen (IIIs) and/or limited contiguous extralymphatic organ or site (IIIe,

IIIes);

Stage IV is disseminated involvement of one or more extralymphatic organs.

The absence of systemic symptoms is signified by adding 'A' to the stage; the presence of

systemic symptoms is signified by adding 'B' to the stage. For localized extranodal extension

from mass of nodes that does not advance the stage, subscript 'E' is added.

[edit ]Signs and symptoms

Patients with Hodgkin's lymphoma may present with the following symptoms:

Night Sweats

Unexplained weight lossLymph nodes : the most common symptom of Hodgkin's is the painless enlargement

of one or more lymph nodes. The nodes may also feel rubbery and swollen when

examined. The nodes of the neck and shoulders ( cervical and supraclavicular ) are most

frequently involved (8090% of the time, on average). The lymph nodes of the chest are

often affected, and these may be noticed on a chest radiograph .

Splenomegaly : enlargement of the spleen occurs in about 30% of people with

Hodgkin's lymphoma. The enlargement, however, is seldom massive and the size of the

spleen may fluctuate during the course of treatment.

Hepatomegaly : enlargement of the liver , due to liver involvement, is present in about

5% of cases.

Hepatosplenomegaly : the enlargement of both the liver and spleen caused by the

same disease.

Pain

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Pain following alcohol consumption: classically, involved nodes are painful after

alcohol consumption, though this phenomenon is very uncommon. [10]

Back pain : nonspecific back pain (pain that cannot be localized or its cause

determined by examination or scanning techniques) has been reported in some cases of

Hodgkin's lymphoma. The lower back is most often affected. [citation needed ]

Red-coloured patches on the skin, easy bleeding and petechiae due to low platelet

count (as a result of bone marrow infiltration, increased trapping in the spleen etc. i.e.

decreased production, increased removal)

Systemic symptoms: about one-third of patients with Hodgkin's disease may also

present with systemic symptoms, including low-grade fever ; night sweats ; unexplained

weight loss of at least 10% of the patient's total body mass in six months or less, itchy

skin ( pruritus ) due to increased levels of eosinophils in the bloodstream;

or fatigue (lassitude). Systemic symptoms such as fever, night sweats, and weight lossare known as B symptoms ; thus, presence of fever, weight loss, and night sweats

indicate that the patient's stage is, for example, 2B instead of 2A. [11]

Cyclical fever: patients may also present with a cyclical high-grade fever known as

the Pel-Ebstein fever , [12] or more simply "P-E fever". However, there is debate as to

whether or not the P-E fever truly exists. [13]

[edit ]Cause

There are no guidelines for preventing Hodgkin's lymphoma because the cause is unknownor multifactorial. A risk factor is something that statistically increases your chance of getting

a disease or condition. Risk factors include:

Sex: male [14]

Ages: 1540 and over 55 [14]

Family history [14]

History of infectious mononucleosis or infection with Epstein-Barr virus , a causative

agent of mononucleosis [14]

Weakened immune system, including infection with HIV or the presence of AIDS [14]

Prolonged use of human growth hormone [14]

Exotoxins, such as Agent Orange

[edit ]Pathogenesis

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[edit ]Management

Patients with early stage disease (IA or IIA) are effectively treated with radiation therapy or

chemotherapy. The choice of treatment depends on the age, sex, bulk and the histological

subtype of the disease. Patients with later disease (III, IVA, or IVB) are treated with

combination chemotherapy alone. Patients of any stage with a large mass in the chest are

usually treated with combined chemotherapy and radiation therapy.

ABVD Stanford V BEACOPP

Currently, the ABVD chemotherapyregimen is the standard treatment of Hodgkin's disease in the US. Theabbreviation stands for the fourdrugs Adriamycin , bleomycin , vinblastine , and dacarbazine . Developed inItaly in the 1970s, the ABVDtreatment typically takes betweensix and eight months, althoughlonger treatments may be required.

The newer StanfordVregimen is typicallyonly half as long asthe ABVD but involvesa more intensivechemotherapyschedule andincorporates radiationtherapy. In arandomizedcontrolled study in

BEACOPP is a form of treatmentfor stages > II mainly used inEurope. The cure rate with theBEACOPP esc. regimen isapproximately 1015% higherthan with standard ABVD inadvanced stages. This wasshown in a paper in The NewEngland Journal of Medicine(Diehl et al.), but US physiciansstill favor ABVD, maybe because

http://en.wikipedia.org/w/index.php?title=Hodgkin%27s_lymphoma&action=edit&section=9http://en.wikipedia.org/wiki/Radiation_therapyhttp://en.wikipedia.org/wiki/ABVDhttp://en.wikipedia.org/wiki/Stanford_Vhttp://en.wikipedia.org/wiki/BEACOPPhttp://en.wikipedia.org/wiki/ABVDhttp://en.wikipedia.org/wiki/Chemotherapy_regimenhttp://en.wikipedia.org/wiki/Chemotherapy_regimenhttp://en.wikipedia.org/wiki/Chemotherapy_regimenhttp://en.wikipedia.org/wiki/Adriamycinhttp://en.wikipedia.org/wiki/Bleomycinhttp://en.wikipedia.org/wiki/Vinblastinehttp://en.wikipedia.org/wiki/Vinblastinehttp://en.wikipedia.org/wiki/Dacarbazinehttp://en.wikipedia.org/wiki/Dacarbazinehttp://en.wikipedia.org/wiki/Stanford_Vhttp://en.wikipedia.org/wiki/Stanford_Vhttp://en.wikipedia.org/wiki/BEACOPPhttp://en.wikipedia.org/wiki/File:Mind_map_3.jpghttp://en.wikipedia.org/w/index.php?title=Hodgkin%27s_lymphoma&action=edit&section=9http://en.wikipedia.org/wiki/Radiation_therapyhttp://en.wikipedia.org/wiki/ABVDhttp://en.wikipedia.org/wiki/Stanford_Vhttp://en.wikipedia.org/wiki/BEACOPPhttp://en.wikipedia.org/wiki/ABVDhttp://en.wikipedia.org/wiki/Chemotherapy_regimenhttp://en.wikipedia.org/wiki/Chemotherapy_regimenhttp://en.wikipedia.org/wiki/Adriamycinhttp://en.wikipedia.org/wiki/Bleomycinhttp://en.wikipedia.org/wiki/Vinblastinehttp://en.wikipedia.org/wiki/Vinblastinehttp://en.wikipedia.org/wiki/Dacarbazinehttp://en.wikipedia.org/wiki/Stanford_Vhttp://en.wikipedia.org/wiki/Stanford_Vhttp://en.wikipedia.org/wiki/BEACOPP

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Italy, Stanford V wasinferior to ABVD. [15]

some physicians think thatBEACOPP induces moresecondary leukemia. However,this seems negligible comparedto the higher cure rates.

BEACOPP is more expensivebecause of the requirement forconcurrent treatmentwith GCSF to increaseproduction of white blood cells.Currently, the German HodgkinStudy Group tests 8 cycles (8x)BEACOPP esc vs. 6x BEACOPPesc vs. 8x BEACOPP-14 baseline(HD15-trial). [16]

Doxorubicin Doxorubicin Doxorubicin

Bleomycin Bleomycin Bleomycin

Vinblastine Vinblastine , Vincristine Vincristine

Dacarbazine Mechlorethamine Cyclophosphamide , Procarbazine

Etoposide Etoposide

Prednisone Prednisone

It should be noted that the common non-Hodgkin's treatment, rituximab (which targets CD-

20) is not used to treat Hodgkin's due to the lack of CD-20 surface antigens in Hodgkin's.

Although increased age is an adverse risk factor for Hodgkin's lymphoma, in general elderlypatients without major comorbidities are sufficiently fit to tolerate standard therapy, and

have a treatment outcome comparable to that of younger patients. However, the disease is

a different entity in older patients and different considerations enter into treatment

decisions . [17]

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For Hodgkin's lymphomas, radiation oncologists typically use external beam radiation

therapy (sometimes shortened to EBRT). Radiation oncologists deliver external beam

radiation therapy to the lymphoma from a machine called a linear accelerator. Patients

usually describe treatments as painless and similar to getting an X-ray. Treatments last less

than 30 minutes each, every day but Saturday and Sunday.

For lymphomas, there are a few different ways radiation oncologists target the cancer cells.

Involved field radiation is when the radiation oncologists give radiation only to the parts of

your body known to have the cancer. Very often, this is combined with chemotherapy.

Radiation therapy directed above the diaphragm to the neck, chest and/or underarms is

called mantle field radiation. Radiation to below the diaphragm to the abdomen, spleen

and/or pelvis is called inverted-Y field radiation. Total nodal irradiation is when your doctor

gives radiation to all the lymph nodes in the body to destroy cells that may have spread. [18]

The high cure rates and long survival of many patients with Hodgkin's lymphoma has led to

a high concern with late adverse effects of treatment, including cardiovascular disease and

second malignancies such as acute leukemias , lymphomas, and solid tumors within the

radiation therapy field. Most patients with early stage disease are now treated with

abbreviated chemotherapy and involved-field radiation therapy rather than with radiation

therapy alone. Clinical research strategies are exploring reduction of the duration of

chemotherapy and dose and volume of radiation therapy in an attempt to reduce late

morbidity and mortality of treatment while maintaining high cure rates. Hospitals are also

treating those who respond quickly to chemotherapy with no radiation.

Acute lymphoblastic leukemia

From Wikipedia, the free encyclopedia

Acute lymphoblastic leukemia (ALL ), is a form of leukemia , or cancer of the white blood

cells characterized by excess lymphoblasts .

Malignant , immature white blood cells continuously multiply and are overproduced in

the bone marrow . ALL causes damage and death by crowding out normal cells in the bone

marrow, and by spreading ( metastasizing ) to other organs. ALL is most common in childhood

with a peak incidence at 2-5 years of age, and another peak in old age. The overall cure rate

in children is about 80%, and about 45%-60% of adults have long-term disease-free survival.[1]

Acute refers to the relatively short time course of the disease (being fatal in as little as a few

weeks if left untreated) to differentiate it from the very different disease of Chronic

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ALL is associated with exposure to radiation and chemicals in animals and humans. The

association of radiation and leukemia in humans has been clearly established in studies of

victims of the Chernobyl nuclear reactor and atom bombs in Hiroshima and Nagasaki . In

animals, exposure to benzene and other chemicals can cause leukemia. Epidemiological

studies have associated leukemia with workplace exposure to chemicals, but these studies

are not as conclusive. Some evidence suggests that secondary leukemia can develop in

individuals who are treated for other cancers with radiation and chemotherapy as a result of

that treatment. [5]

[edit ]Classification

As ALL is not a solid tumour, the TNM notation as used in solid cancers is of little use.

[edit ]The FAB classification

Subtyping of the various forms of ALL used to be done according to the French-American-

British (FAB) classification , [18] which was used for all acute leukemias (including acute

myelogenous leukemia , AML).

ALL-L1: small uniform cells

ALL-L2: large varied cells

ALL-L3: large varied cells with vacuoles (bubble-like features)

Each subtype is then further classified by determining the surface markers of the abnormal

lymphocytes, called immunophenotyping. There are 2 main immunologic types: pre-B cell

and pre-T cell. The mature B-cell ALL (L3) is now classified as Burkitt's lymphoma /leukemia.

Subtyping helps determine the prognosis and most appropriate treatment in treating ALL.

[edit ]WHO proposed classification of acute lymphoblastic leukemia

The recent WHO International panel on ALL recommends that the FAB classification be

abandoned, since the morphological classification has no clinical or prognostic relevance. It

instead advocates the use of the immunophenotypic classification mentioned below.

1- Acute lymphoblastic leukemia/lymphoma Synonyms:Former Fab L1/L2

i. Precursor B acute lymphoblastic leukemia/lymphoma . Cytogenetic subtypes: [19]

t(12;21)(p12,q22) TEL/AML-1

t(1;19)(q23;p13) PBX/E2A

t(9;22)(q34;q11) ABL/BCR

http://en.wikipedia.org/wiki/Ionizing_radiationhttp://en.wikipedia.org/wiki/Chernobylhttp://en.wikipedia.org/wiki/Atom_bombshttp://en.wikipedia.org/wiki/Hiroshimahttp://en.wikipedia.org/wiki/Nagasaki,_Nagasakihttp://en.wikipedia.org/wiki/Nagasaki,_Nagasakihttp://en.wikipedia.org/wiki/Benzenehttp://en.wikipedia.org/wiki/Acute_lymphoblastic_leukemia#cite_note-smith-4http://en.wikipedia.org/w/index.php?title=Acute_lymphoblastic_leukemia&action=edit&section=6http://en.wikipedia.org/wiki/TNM_staging_systemhttp://en.wikipedia.org/w/index.php?title=Acute_lymphoblastic_leukemia&action=edit&section=7http://en.wikipedia.org/wiki/French-American-British_classificationhttp://en.wikipedia.org/wiki/French-American-British_classificationhttp://en.wikipedia.org/wiki/French-American-British_classificationhttp://en.wikipedia.org/wiki/Acute_lymphoblastic_leukemia#cite_note-urlACS_::_How_Is_Acute_Lymphocytic_Leukemia_Classified.3F-17http://en.wikipedia.org/wiki/Acute_myelogenous_leukemiahttp://en.wikipedia.org/wiki/Acute_myelogenous_leukemiahttp://en.wikipedia.org/wiki/Acute_myelogenous_leukemiahttp://en.wikipedia.org/wiki/Vacuolehttp://en.wikipedia.org/wiki/Burkitt's_lymphomahttp://en.wikipedia.org/w/index.php?title=Acute_lymphoblastic_leukemia&action=edit&section=8http://en.wikipedia.org/wiki/Precursor_B_acute_lymphoblastic_leukemia/lymphomahttp://en.wikipedia.org/wiki/Acute_lymphoblastic_leukemia#cite_note-urlAdvances_in_Acute_Lymphoblastic_Leukemia_.7C_Clinical_Laboratory_Science_.7C_Find_Articles_at_BNET.com-18http://en.wikipedia.org/wiki/Ionizing_radiationhttp://en.wikipedia.org/wiki/Chernobylhttp://en.wikipedia.org/wiki/Atom_bombshttp://en.wikipedia.org/wiki/Hiroshimahttp://en.wikipedia.org/wiki/Nagasaki,_Nagasakihttp://en.wikipedia.org/wiki/Benzenehttp://en.wikipedia.org/wiki/Acute_lymphoblastic_leukemia#cite_note-smith-4http://en.wikipedia.org/w/index.php?title=Acute_lymphoblastic_leukemia&action=edit&section=6http://en.wikipedia.org/wiki/TNM_staging_systemhttp://en.wikipedia.org/w/index.php?title=Acute_lymphoblastic_leukemia&action=edit&section=7http://en.wikipedia.org/wiki/French-American-British_classificationhttp://en.wikipedia.org/wiki/French-American-British_classificationhttp://en.wikipedia.org/wiki/Acute_lymphoblastic_leukemia#cite_note-urlACS_::_How_Is_Acute_Lymphocytic_Leukemia_Classified.3F-17http://en.wikipedia.org/wiki/Acute_myelogenous_leukemiahttp://en.wikipedia.org/wiki/Acute_myelogenous_leukemiahttp://en.wikipedia.org/wiki/Vacuolehttp://en.wikipedia.org/wiki/Burkitt's_lymphomahttp://en.wikipedia.org/w/index.php?title=Acute_lymphoblastic_leukemia&action=edit&section=8http://en.wikipedia.org/wiki/Precursor_B_acute_lymphoblastic_leukemia/lymphomahttp://en.wikipedia.org/wiki/Acute_lymphoblastic_leukemia#cite_note-urlAdvances_in_Acute_Lymphoblastic_Leukemia_.7C_Clinical_Laboratory_Science_.7C_Find_Articles_at_BNET.com-18

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T(V,11)(V;q23) V/MLL

ii. Precursor T acute lymphoblastic leukemia/lymphoma

2- Burkitt's leukemia /lymphoma Synonyms:Former FAB L33- Biphenotypic acute leukemia

[edit ]Variant Features of ALL

1- Acute lymphoblastic leukemia with cytoplasmic granules

2- Aplastic presentation of ALL

3- Acute lymphoblastic leukemia with eosinophilia

4- Relapse of lymphoblastic leukemia

5- Secondary ALL

[edit ]Immunophenotyping in the diagnosis and classification of ALL

The use of a TdT assay and a panel of monoclonal antibodies (MoAbs) to T cell and B cell

associated antigens will identify almost all cases of ALL.

Immunophenotypic categories of acute lymphoblastic leukemia (ALL)

Types FABClassTdt

T cell associateantigen

B cell associateantigen

cIg

sIg

Precursor B L1,L2 + - + -/+ -

Precursor T L1,L2 + + - - -

B-cell L3 - - + - +

[edit ]Treatment

The earlier acute lymphocytic leukemia is detected, the more effective the treatment. The

aim is to induce a lasting remission , defined as the absence of detectable cancer cells in the

body (usually less than 5% blast cells on the bone marrow).

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Treatment for acute leukemia can include chemotherapy , steroids , radiation therapy ,

intensive combined treatments (including bone marrow or stem cell transplants), and

growth factors. [20]

[edit ]Chemotherapy

Chemotherapy is the initial treatment of choice. Most ALL patients will receive a combination

of different treatments. There are no surgical options, due to the body-wide distribution of

the malignant cells . In general, cytotoxic chemotherapy for ALL combines multiple

antileukemic drugs in various combinations. Chemotherapy for ALL consists of three phases:

remission induction, intensification, and maintenance therapy.

Phase Description Agents

Remission induction

The aim of remissioninduction is torapidly kill mosttumor cells and getthe patient intoremission. This isdefined as thepresence of less than5% leukemic blastsin the bone marrow,normal blood cellsand absence of

tumor cells fromblood, and absenceof other signs andsymptoms of thedisease. CNSprophylaxis shouldbegin during thisphase of treatmentand continue duringtheconsolidation/intensif ication period. Therationale is based onthe presence of CNSinvolvement in 10%-40% of adult patientsat diagnosis.

Combinationof Prednisolone or dexamethasone , vincristine , asparaginase (better tolerance in pediatric patients),and daunorubicin (used in Adult ALL) is used toinduce remission.

Consolidation/Intensification

Intensification useshigh doses of intravenous

Typical intensification protocols usevincristine, cyclophosphamide ,cytarabine ,daunorubicin, etoposide , thioguanine or mercapto

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multidrugchemotherapy tofurther reduce tumorburden. Since ALLcells sometimes

penetrate theCentral NervousSystem ( CNS ), mostprotocols includedelivery of chemotherapy intothe CNS fluid(termed intrathecalchemotherapy ).Some centers deliverthe drugthrough Ommayareservoir (a device

surgically placedunder the scalp andused to deliver drugsto the CNS fluid andto extract CNS fluidfor various tests).Other centers wouldperform multiplelumbar punctures asneeded for testingand treatmentdelivery.

purine given as blocks in different combinations.For CNS protection, intrathecal methotrexate orcytarabine is usually used combined with orwithout cranio-spinal irradiation (the use of radiation therapy to the head and spine). Centralnervous system relapse is treated withintrathecal administration of hydrocortisone ,

methotrexate, and cytarabine.

Maintenancetherapy

The aim of maintenance therapyis to kill any residualcell that was notkilled by remissioninduction, andintensificationregimens. Althoughsuch cells are few,they will causerelapse if noteradicated.

For this purpose, daily oral mercaptopurine , onceweekly oral methotrexate , once monthly 5-daycourse of intravenous vincristine and oralcorticosteroids are usually used. The length of maintenance therapy is 3 years for boys, 2 yearsfor girls and adults. [21]

As the chemotherapy regimens can be intensive and protracted (often about 2 years in case

of the GMALL UKALL, HyperCVAD or CALGB protocols; for ALL about 3 years, 2 months for

males on COG protocols; 2 years, 2 months for females- longer for males as testicles are a

potential reservoir), many patients have an intravenous catheter inserted into a large vein

(termed a central venous catheter or a Hickman line ), or a Portacath , a cone-shaped port

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with a silicone nose that is surgically planted under the skin, usually near the collar bone,

and the most effective product available, due to low infection risks and the long-term

viability of a portacath.

[edit ]Radiation therapy

Radiation therapy (or radiotherapy) is used on painful bony areas, in high disease burdens,

or as part of the preparations for a bone marrow transplant (total body irradiation).

Radiation in the form of whole brain radiation is also used for central nervous system

prophylaxis, to prevent recurrence of leukemia in the brain. Whole brain prophylaxis

radiation used to be a common method in treatment of childrens ALL. Recent studies

showed that CNS chemotherapy provided results as favorable but with less developmental

side effects. As a result, the use of whole brain radiation has been more limited. Most

specialists in adult leukemia have abandoned the use of radiation therapy for CNS

prophylaxis.

Acute lymphocytic leukemia (ALL)

Acute lymphocytic leukemia (ALL) is a fast-growing cancer in which the body produces a

large number of immature white blood cells (lymphocytes). These cells are found in the

blood, bone marrow, lymph nodes, spleen, and other organs.

Causes

ALL makes up 80% of childhood acute leukemias. Most cases occur in children ages 3 - 7. The disease may also occur in adults.

In acute leukemia, cancerous cells multiply quickly and replace normal cells. Cancerous cells

take over normal parts of the bone marrow, often causing low blood counts .

Most cases of ALL have no obvious cause. However, the following may play a role in the

development of leukemia:

Certain chromosome problems Radiation exposure or being exposed to x-rays before birth Past treatment with chemotherapy drugs Receiving a bone marrow transplant Toxins such as benzene

Persons with Down syndrome or other genetic disorders, or who have a brother or sister with

leukemia are at increased risk for ALL.

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Symptoms

A person with ALL is more likely to bleed and have infections because there are fewer

normal blood cells and platelets. Life-threatening symptoms may develop.

Bone and joint pain or tenderness Easy bruising and bleeding (bleeding gums, skin bleeding,

nosebleeds, menstrual irregularities ) Feeling weak or tired Fever Loss of appetite and weight loss Paleness Pain or feeling of fullness below the ribs Pinpoint red spots on the skin (petechiae) Swollen glands ( lymphadenopathy ) in the neck, under arms, and groin Night sweats

Note: These symptoms can occur with other conditions. Talk to your doctor about the

meaning of your specific symptoms.

Exams and Tests

A physical exam may reveal the following:

Bruising Enlarged liver , lymph nodes, and spleen Signs of bleeding ( petechiae , purpura )

Blood tests may show the following:

Abnormal white blood cell (WBC) count Low red blood cell count ( anemia ) Low platelet count ( thrombocytopenia )

A bone marrow aspiration will show abnormal levels of certain cells. The bone marrow is

usually taken from the back of one of the hip bones, but can be taken from other bones.

Tests are done on the bone marrow cells to identify the type of leukemia.

A lumbar puncture or spinal tap is usually done to both detect if leukemia cells are in the

spinal fluid and to give chemotherapy to prevent spread to the spinal fluid.

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Doctors look for chromosome changes in the cells of some leukemias. This helps aid in

diagnosis and prognosis. Leukemias with certain types of chromosome changes have a poor

outlook, while those with other types of genes can have a very good outlook. This may

determine what kind of therapy is used to treat the ALL.

Treatment

The goal of treatment is to get the blood counts and the bone marrow back to normal. If this

occurs and the bone marrow looks healthy under the microscope, the cancer is said to be in

remission.

If you have ALL, you will need chemotherapy. For the first round of chemotherapy (called

induction), you may need to stay in the hospital for 3 - 6 weeks.

Later you may get chemotherapy on an outpatient basis (living at home and going to a clinic

to receive your treatments). If you have a low white blood cell count, you may need to be

placed in a room by yourself so you do not catch an infection.

Many chemotherapy drugs given into the veins do not reach the brain and spinal cord tissue.

Therefore, many patients will also receive radiation therapy to the brain or chemotherapy

drugs injected into the space around the brain and spinal column to prevent later spread to

these sites.

If you go into remission, you may receive additional chemotherapy or radiation therapy to

kill any cancer cells that are in the spinal fluid. You may also receive chemotherapy from

time to time to prevent relapse. A bone marrow or stem cell transplant may also be

recommended, especially if one of your siblings is proven to be a full match.

If your leukemia returns or does not respond to other treatments, a bone marrow or stem

cell transplant is usually recommended.

Additional treatments depend on other symptoms. They may include:

Transfusion of blood products, such as platelets or red blood cells, to fight

thrombocytopenia and anemia Antibiotics to fight infection, especially if a fever occurs

Support Groups

Patients can ease the stress of their illness by joining a support group where members share

common experiences and problems.

See also: Cancer - support group

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Outlook (Prognosis)

Children usually have a better outcome than adults. Almost all children go into complete

remission. Without treatment, a person with ALL can expect to live for only about 3 months.

The following patients tend to do better:

Younger adults (especially those younger than age 50) Children between the ages of 1 and 9 Those who have a WBC count below 50,000 when first diagnosed Those who do not have a Philadelphia chromosome-positive ALL (a specific

genetic change) Those who achieve complete remission (disappearance of signs and

symptoms of cancer) within 4 - 5 weeks of starting treatment

Patients whose leukemia spreads to the brain or spinal cord tend to have a worse outcome.

Possible Complications

Bleeding Damage to different organs from chemotherapy Disseminated intravascular coagulation ( DIC) Relapse of ALL Severe infection Spread of the cancer to other parts of the body

When to Contact a Medical Professional

Call your health care provider if:

You develop ALL-like symptoms You have ALL and you have a persistent fever or other signs of infection

Prevention

Because the cause is usually unknown, it is not possible to prevent most cases. You may

reduce your risk of ALL by avoiding exposure to toxins, radiation, and chemicals.

Alternative Names

ALL; Acute childhood leukemia; Cancer - acute childhood leukemia (ALL); Leukemia - acute

childhood (ALL)

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Chronic myelogenous leukemia

From Wikipedia, the free encyclopedia

Chronic myelogenous (or myeloid) leukemia (CML ), also known as chronicgranulocytic leukemia (CGL) , is a cancer of the white blood cells . It is a form

of leukemia characterized by the increased and unregulated growth of

predominantly myeloid cells in the bone marrow and the accumulation of these cells in the

blood. CML is a clonal bone marrow stem cell disorder in which proliferation of

mature granulocytes (neutrophils , eosinophils , and basophils ) and their precursors is the

main finding. It is a type of myeloproliferative disease associated with a

characteristic chromosomal translocation called the Philadelphia chromosome . It is now

treated with imatinib and other targeted therapies , which have dramatically improved

survival.

[ edit ]Signs and symptoms

Patients are often asymptomatic at diagnosis, presenting incidentally with an elevated white

blood cell count on a routine laboratory test. In this setting, CML must be distinguished from

a leukemoid reaction , which can have a similar appearance on a blood smear . Symptoms of

CML may include: enlarged spleen, malaise , low-grade fever , gout , increased susceptibility

to infections , anemia , and thrombocytopenia with easy bruising (although

an increased platelet count ( thrombocytosis ) may also occur in CML). Splenomegaly may alsobe seen. [1] [2]

[ edit ]Diagnosis

Peripheral blood (MGG stain): marked leucocytosis with granulocyte left shift

CML is often suspected on the basis on the complete blood count , which shows

increased granulocytes of all types, typically including mature myeloid

cells .Basophils and eosinophils are almost universally increased; this feature may help

differentiate CML from a leukemoid reaction . A bone marrow biopsy is often performed aspart of the evaluation for CML, but bone marrow morphology alone is insufficient to diagnose

CML. [2][ 3]

Ultimately, CML is diagnosed by detecting the Philadelphia chromosome . This

characteristic chromosomal abnormality can be detected by routine cytogenetics ,

by fluorescent in situ hybridization , or by PCR for the bcr-abl fusion gene. [2]

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Controversy exists over so-called Ph-negative CML, or cases of suspected CML in which the

Philadelphia chromosome cannot be detected. Many such patients in fact have complex

chromosomal abnormalities which mask the (9;22) translocation, or have evidence of the

translocation by FISH or RT-PCR in spite of normal routine karyotyping. [4] The small subset of

patients without detectable molecular evidence of bcr-abl fusion may be better classified as

having an undifferentiated myelodysplastic/myeloproliferative disorder , as their clinical

course tends to be different from patients with CML. [5]

[ edit ]Pathophysiology

CML was the first malignancy to be linked to a clear genetic abnormality, the chromosomal

translocation known as the Philadelphia chromosome . This chromosomal abnormality is so

named because it was first discovered and described in 1960 by two scientists

from Philadelphia, Pennsylvania , USA: Peter Nowell of the University of Pennsylvania and

David Hungerford of the Fox Chase Cancer Center at Temple University . [6]

In this translocation, parts of two chromosomes (the 9th and 22nd by

conventional karyotypic numbering) switch places. As a result, part of the BCR ("breakpoint

cluster region") gene from chromosome 22 is fused with the ABL gene on chromosome 9.

This abnormal "fusion" gene generates a protein of p210 or sometimes p185 weight (p is a

weight measure of cellular proteins in kDa ). Because abl carries a domain that can

add phosphate groups to tyrosine residues (a tyrosine kinase ), the bcr-abl fusion gene

product is also a tyrosine kinase. [1][ 3]

The fused BCR-ABL protein interacts with the interleukin 3beta(c) receptor subunit. The BCR-

ABL transcript is continuously active and does not require activation by other cellular

messaging proteins. In turn, BCR-ABL activates a cascade of proteins which control the cell

cycle , speeding up cell division. Moreover, the BCR-ABL protein inhibits DNA repair , causing

genomic instability and making the cell more susceptible to developing further genetic

abnormalities. The action of the BCR-ABL protein is the pathophysiologic cause of chronic

myelogenous leukemia. With improved understanding of the nature of the BCR-ABLprotein

and its action as a tyrosine kinase, targeted therapies have been developed (the first of

which was imatinib mesylate ) which specifically inhibit the activity of the BCR-ABL protein.

These tyrosine kinase inhibitors can induce complete remissions in CML, confirming the

central importance of bcr-abl as the cause of CML. [3]

[ edit ]Classification

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CML is often divided into three phases based on clinical characteristics and laboratory

findings. In the absence of intervention, CML typically begins in the chronic phase, and over

the course of several years progresses to an accelerated phase and ultimately to a blast

crisis . Blast crisis is the terminal phase of CML and clinically behaves like an acute leukemia .

One of the drivers of the progression from chronic phase through acceleration and blast

crisis is the acquisition of new chromosomal abnormalities (in addition to the Philadelphia

chromosome). [1] Some patients may already be in the accelerated phase or blast crisis by

the time they are diagnosed. [2]

[edit ]Chronic phase

Approximately 85% of patients with CML are in the chronic phase at the time of diagnosis.

During this phase, patients are usually asymptomatic or have only mild symptoms of fatigue

or abdominal fullness. The duration of chronic phase is variable and depends on how early

the disease was diagnosed as well as the therapies used. Ultimately, in the absence of

curative treatment, the disease progresses to an accelerated phase. [2]

[edit ]Accelerated phase

Criteria for diagnosing transition into the accelerated phase are somewhat variable; the

most widely used criteria are those put forward by investigators at M.D. Anderson Cancer

Center , [7] by Sokal et al. , [8] and the World Health Organization . [5][ 9] The WHO criteria are

perhaps most widely used, and define the accelerated phase by any of the following:

1019% myeloblasts in the blood or bone marrow

>20% basophils in the blood or bone marrow

Platelet count 1,000,000, unresponsive to therapy

Cytogenetic evolution with new abnormalities in addition to the Philadelphia

chromosome

Increasing splenomegaly or white blood cell count, unresponsive to therapy

The patient is considered to be in the accelerated phase if any of the above are present. Theaccelerated phase is significant because it signals that the disease is progressing and

transformation to blast crisis is imminent. [5]

[edit ]Blast crisis

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Blast crisis is the final phase in the evolution of CML, and behaves like an acute leukemia ,

with rapid progression and short survival. [2] Blast crisis is diagnosed if any of the following

are present in a patient with CML: [10]

>20% myeloblasts or lymphoblasts in the blood or bone marrowLarge clusters of blasts in the bone marrow on biopsy

Development of a chloroma (solid focus of leukemia outside the bone marrow)

[edit ]Treatment

[edit ]Chronic phase

Chronic phase CML is treated with inhibitors of tyrosine kinase , the first of which

was imatinib mesylate (marketed as Gleevec or Glivec; previously known as STI-571). In the

past, antimetabolites (e.g. cytarabine , hydroxyurea ), alkylating agents , interferon alfa 2b ,

and steroids were used, but these drugs have been replaced by imatinib . Imatinib was

approved by the United States FDA in 2001 and specifically targets BCR/abl, the

constitutively activated tyrosine kinase fusion protein caused by the Philadelphia

chromosome translocation. It is better tolerated and more effective than previous therapies.

The IRIS study is an international study that compared interferon/cytarabine combination

with imatinib. Long term follow up demonstrating the superiority of imatinib regimens is

clear cut. However, the data of this study which allowed cross-over to Glivec has never been

presented in an intent to treat analysis. It is not yet known whether Glivec treatmentfollowing cytarabine/interferon is better than Glivec alone in the long term. Bone marrow

transplantation was also used as initial treatment for CML in younger patients before the

advent of imatinib and; while it can often be curative, there was a high rate of transplant-

related mortality. The transplant-related mortality rate as of 2010 is less than 5%. [3]

As described below, a number of newer drugs are being used to treat the minority of

patients who develop imatinib resistance. Trials such as SPIRIT II are being carried out, to

evaluate these newer drugs as 'upfront' therapy for patients with newly diagnosed chronic

phase CML.

To overcome imatinib resistance and to increase responsiveness of TK inhibitors, two novel

agents have been developed. The first, dasatinib , is a TK inhibitor that blocks several

oncogenic proteins and was approved by the US FDA in 2007 to treat CML patients who are

either resistant to or intolerant of imatinib. Another TK inhibitor, nilotinib , has also been

approved by the US FDA for the same indication. Nilotinib is designed to bind more tightly

http://en.wikipedia.org/wiki/Acute_leukemiahttp://en.wikipedia.org/wiki/Acute_leukemiahttp://en.wikipedia.org/wiki/Chronic_myelogenous_leukemia#cite_note-Tefferi-1http://en.wikipedia.org/wiki/Chronic_myelogenous_leukemia#cite_note-9http://en.wikipedia.org/wiki/Myeloblasthttp://en.wikipedia.org/wiki/Lymphoblasthttp://en.wikipedia.org/wiki/Bone_marrow_biopsyhttp://en.wikipedia.org/wiki/Chloromahttp://en.wikipedia.org/w/index.php?title=Chronic_myelogenous_leukemia&action=edit&section=8http://en.wikipedia.org/w/index.php?title=Chronic_myelogenous_leukemia&action=edit&section=9http://en.wikipedia.org/wiki/Tyrosine_kinasehttp://en.wikipedia.org/wiki/Imatinibhttp://en.wikipedia.org/wiki/Cytarabinehttp://en.wikipedia.org/wiki/Hydroxyureahttp://en.wikipedia.org/wiki/Alkylating_antineoplastic_agenthttp://en.wikipedia.org/wiki/Interferonhttp://en.wikipedia.org/wiki/Steroidhttp://en.wikipedia.org/wiki/Imatinibhttp://en.wikipedia.org/wiki/Imatinibhttp://en.wikipedia.org/wiki/Food_and_Drug_Administrationhttp://en.wikipedia.org/wiki/Food_and_Drug_Administrationhttp://en.wikipedia.org/wiki/Philadelphia_chromosomehttp://en.wikipedia.org/wiki/Philadelphia_chromosomehttp://en.wikipedia.org/wiki/Bone_marrow_transplanthttp://en.wikipedia.org/wiki/Bone_marrow_transplanthttp://en.wikipedia.org/wiki/Chronic_myelogenous_leukemia#cite_note-Hehlmann-2http://en.wikipedia.org/wiki/Dasatinibhttp://en.wikipedia.org/wiki/Nilotinibhttp://en.wikipedia.org/wiki/Acute_leukemiahttp://en.wikipedia.org/wiki/Chronic_myelogenous_leukemia#cite_note-Tefferi-1http://en.wikipedia.org/wiki/Chronic_myelogenous_leukemia#cite_note-9http://en.wikipedia.org/wiki/Myeloblasthttp://en.wikipedia.org/wiki/Lymphoblasthttp://en.wikipedia.org/wiki/Bone_marrow_biopsyhttp://en.wikipedia.org/wiki/Chloromahttp://en.wikipedia.org/w/index.php?title=Chronic_myelogenous_leukemia&action=edit&section=8http://en.wikipedia.org/w/index.php?title=Chronic_myelogenous_leukemia&action=edit&section=9http://en.wikipedia.org/wiki/Tyrosine_kinasehttp://en.wikipedia.org/wiki/Imatinibhttp://en.wikipedia.org/wiki/Cytarabinehttp://en.wikipedia.org/wiki/Hydroxyureahttp://en.wikipedia.org/wiki/Alkylating_antineoplastic_agenthttp://en.wikipedia.org/wiki/Interferonhttp://en.wikipedia.org/wiki/Steroidhttp://en.wikipedia.org/wiki/Imatinibhttp://en.wikipedia.org/wiki/Food_and_Drug_Administrationhttp://en.wikipedia.org/wiki/Philadelphia_chromosomehttp://en.wikipedia.org/wiki/Philadelphia_chromosomehttp://en.wikipedia.org/wiki/Bone_marrow_transplanthttp://en.wikipedia.org/wiki/Bone_marrow_transplanthttp://en.wikipedia.org/wiki/Chronic_myelogenous_leukemia#cite_note-Hehlmann-2http://en.wikipedia.org/wiki/Dasatinibhttp://en.wikipedia.org/wiki/Nilotinib

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than imatinib to the Bcr-Abl abnormal fusion protein responsible for chronic myeloid

leukemia. Dasatanib is being compared with Imatinib for first-line therapy in the SPIRIT II

trial being undertaken in the United Kingdom. Study on the combination of alpha Interferon

with Imatanib is currently recruiting in higher risk patients in chronic phase CML.

Dasatanib and nilotinib failed to overcome the imatinib resistance caused by the T315I

mutation. All current treatments for this mutation are experimental. Recently Chemgenex

released results of their open-label Phase 2/3 study (CGX-635-CML-202) which investigated

the use of omacetaxine , administered subcutaneously in CML patients who had failed

imatinib and who have the highly drug-resistant T315I kinase domain mutation.

Stem cell transplantation is an option for patients who developed T315I mutation. [11] [12]

In 2005 favourable results of vaccination were reported with the BCR/abl p210 fusion protein

in patients with stable disease, with GM-CSF as an adjuvant.[13]

Acute Myelogenous Leukemia (AML)

Acute myelogenous leukemia (AML) is a fast-growing cancer of the blood and bone marrow.In AML, the bone marrow makes many unformed cells called blasts. Blasts normally developinto white blood cells that fight infection. However, the blasts are abnormal in AML. They donot develop and cannot fight infections. The bone marrow may also make abnormal redblood cells and platelets. The number of abnormal cells (or leukemia cells) grows quickly.

They crowd out the normal red blood cells, white blood cells and platelets the body needs.

Acute myelogenous leukemia symptoms and diagnosisAML is the most common type of acute leukemia. More than 11,900 new cases occur in theUnited States each year, mostly in older adults. The average age of a person with AML is 65years. Fewer than 10% of people with AML are children. Acute myelogenous leukemia is alsocalled acute myeloblastic leukemia, acute myeloid leukemia, acute granulocytic leukemia oracute nonlymphocytic leukemia.

Symptoms The symptoms of AML are caused by low numbers of healthy blood cells and high numbersof leukemia cells.

White blood cells fight infection. Low numbers can lead to fever and frequentinfections.

Red blood cells carry oxygen throughout the body. Low numbers can lead to anemia feeling tired or weak, being short of breath and looking pale.

Platelets control bleeding. Low numbers can lead to easy bleeding or bruising andtiny red spots under the skin (petechiae).

High numbers of leukemia cells may cause pain in the bones or joints.

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A person with AML may feel generally unwell and run-down. He or she may also have other,

less common symptoms.

DiagnosisAML is diagnosed when blood and bone marrow samples show a large number of leukemia

cells. AML has eight subtypes, labeled M0 through M7. The subtypes are based on the typeof blood cells affected. To find out the sub type and how well the leukemia might respond totreatment, the samples are looked at to find:

The number of healthy blood cells. The size and number of leukemia cells. The changes that appear in the chromosomes of the leukemia cells. This is called

cytogenetics. Other genetic abnormalities, e.g., FLT3 mutation, N-RAS.

Doctors also examine the patient to find out if leukemia cells have spread outside the blood

and bone marrow. Doctors may use a chest X-ray and an ultrasound of the abdomen to look

at the organs and tissues inside. They may also use a test called a lumbar puncture (spinal

tap) to find out whether there are leukemia cells in the fluid around the brain and spinal

cord.

Treatment options for acute myelogenous leukemiaAML can get worse quickly, so doctors usually begin treatment right away. To plantreatment, doctors look at a patient's risk factors (also called prognostic factors). Riskfactors are patient and disease traits that clinical studies have linked to better or worseoutcomes from treatment. Examples of risk factors are a patient's age and subtype of AML.

To learn more about AML risk factors as well as how treatment options may differ forchildren or for adults older than age 60, see Risk Factors for Planning Treatment of AML .

For a patient with AML, the treatment plan may include: Chemotherapy drugs that destroy cancer cells or stop them from growing

(described below). A bone marrow or cord blood transplant (described below