CBD Oil For Leukemia

CBDISTILLERY

Buy CBD Oil Online

Clinical effects of a single dose of cannabinoids to patients with chronic lymphocytic leukemia Christopher M. Melén a Department of Medicine at Huddinge, Division of Hematology, Karolinska Cannabis Extract Treatment for Terminal Acute Lymphoblastic Leukemia with a Philadelphia Chromosome Mutation This is an Open Access article licensed under the terms of the Creative Commons Leukemia Did you know that cannabis can alleviate some symptoms of cancer and the painful side effects of certain cancer treatments? Since cannabinoid treatments are growing in availability,

Clinical effects of a single dose of cannabinoids to patients with chronic lymphocytic leukemia

Christopher M. Melén a Department of Medicine at Huddinge, Division of Hematology, Karolinska Institutet, Stockholm, Sweden;b Medical Unit Hematology, Karolinska University Hospital, Stockholm, Sweden Correspondence [email protected]
View further author information

Magali Merrien c Department of Laboratory Medicine, Division of Pathology, Karolinska Institutet, Stockholm, SwedenView further author information

Agata M. Wasik c Department of Laboratory Medicine, Division of Pathology, Karolinska Institutet, Stockholm, SwedenView further author information

Georgios Panagiotidis d Department of Laboratory Medicine, Division of Pharmacology, Karolinska Institutet, Stockholm, Sweden;e Unit of Clinical Pharmacology, University Hospital, Stockholm, SwedenView further author information

Olof Beck d Department of Laboratory Medicine, Division of Pharmacology, Karolinska Institutet, Stockholm, Sweden;e Unit of Clinical Pharmacology, University Hospital, Stockholm, Sweden https://orcid.org/0000-0002-3546-8872View further author information

Kristina Sonnevi a Department of Medicine at Huddinge, Division of Hematology, Karolinska Institutet, Stockholm, Sweden;b Medical Unit Hematology, Karolinska University Hospital, Stockholm, SwedenView further author information

Henna-Riikka Junlén a Department of Medicine at Huddinge, Division of Hematology, Karolinska Institutet, Stockholm, Sweden;b Medical Unit Hematology, Karolinska University Hospital, Stockholm, Sweden https://orcid.org/0000-0003-4749-0601View further author information

Birger Christensson c Department of Laboratory Medicine, Division of Pathology, Karolinska Institutet, Stockholm, Sweden;f Department of Clinical Pathology and Cytology, Karolinska University Hospital, Stockholm, SwedenView further author information

Birgitta Sander c Department of Laboratory Medicine, Division of Pathology, Karolinska Institutet, Stockholm, Sweden;f Department of Clinical Pathology and Cytology, Karolinska University Hospital, Stockholm, SwedenView further author information

Björn Engelbrekt Wahlin a Department of Medicine at Huddinge, Division of Hematology, Karolinska Institutet, Stockholm, Sweden;b Medical Unit Hematology, Karolinska University Hospital, Stockholm, Sweden https://orcid.org/0000-0003-3566-8847View further author information

  • Download citation
  • https://doi.org/10.1080/10428194.2021.2020776
  • CrossMark

Original Articles

Clinical effects of a single dose of cannabinoids to patients with chronic lymphocytic leukemia

Abstract

This phase II clinical trial investigates a one-time oromucosal dose of tetrahydrocannabinol/cannabidiol (THC/CBD) in 23 patients with indolent leukemic B cell lymphomas. Primary endpoint was a significant reduction in leukemic B cells. Grade 1 − 2 adverse events were seen in 91% of the patients; most common were dry mouth (78%), vertigo (70%), and somnolence (43%). After THC/CBD a significant reduction in leukemic B cells (median, 11%) occurred within two hours (p = .014), and remained for 6 h without induction of apoptosis or proliferation. Normal B cells and T cells were also reduced. CXCR4 expression increased on leukemic cells and T cells. All effects were gone by 24 h. Our results show that a single dose of THC/CBD affects a wide variety of leukocytes and only transiently reduce malignant cells in blood. Based on this study, THC/CBD shows no therapeutic potential for indolent B cell lymphomas (EudraCT trial no. 2014-005553-39).

Introduction

Indolent B cell leukemias are malignant diseases with several available treatment options [ 1 , 2 ]. However, some patients do not respond to or do not tolerate these interventions, particularly the elderly. For these patients, the treatment contributes to a reduced quality of life and survival. Therefore, novel treatments and identification of factors influencing outcome are needed. Previous experimental studies have indicated that cannabinoids may induce cell death in lymphoma [ 3–5 ].

Two G-protein coupled receptors (CB1 and CB2) mediate most of the effects seen by cannabinoids [ 6–9 ]. CB1 is highly expressed in synapses within the central nervous system and to a lesser degree in the peripheral nerves and the enteric nervous system of the gastro-intestinal tract. CB1 regulates synaptic signaling and it is through this receptor that delta-9-tetrahydrocannabinol (THC) produces the psychoactive effects associated with Cannabis sativa [ 8 , 10 ]. While THC is an agonist to CB1, the other major component of Cannabis sativa, cannabidiol (CBD), acts as a CB1 antagonist [ 11 ], counteracting the psychotropic effects of THC [ 12 ]. CB2 is expressed in the immune system including B cells, T cells, monocytes/macrophages, and dendritic cells [ 7 , 13 ]. In mice, CB2 signaling is important for retention of immature B cells in bone marrow sinusoids [ 14 ] and for the positioning and retention of marginal zone B cells in splenic marginal zones [ 15 , 16 ].

A key mechanism for lymphocyte migration and tissue localization is the chemokine receptor CXCR4 and its ligand CXCL12 [ 14 ]. Specifically, CXCR4 expression is high on lymphocytes in blood and these lymphocytes migrate toward CXCL12 which is produced by stroma cells in lymph nodes and bone marrow. CXCR4 is a G-protein coupled receptor, known to interact with other G-protein coupled receptors, such as CB2, to modulate the CXCL12-induced effects on cell migration and homing [ 17 , 18 ].

THC and CBD have shown various effects on the immune system, such as inhibition of mitogen-stimulated lymphocyte cell replication [ 19 ] and T-cell proliferation and cytokine production by signaling via CB2 [ 20 , 21 ].

Many B-cell lymphomas express CB1 and CB2. Extensive screening for CB1 mRNA expression across different B-cell leukemias/lymphomas demonstrated increased CB1 expression in most cases of mantle cell lymphoma, follicular lymphoma, and in approximately half of CLL cases compared to normal B cells [ 22 , 23 ]. Low CB1 expression levels have been associated with lymphocytosis in mantle cell lymphoma [ 24 ] and longer survival in CLL [ 25 ]. Micromolar concentrations of synthetic agonists to both CB1 and CB2 have been demonstrated to induce cell death of CB1- or CB2-expressing lymphoid cell-lines in vitro and in xenografts [ 3 , 5 , 26 ].

In view of these findings, we conducted a clinical trial to investigate the therapeutic potential of THC/CBD in indolent B cell leukemia/lymphoma. In this phase II clinical trial, patients received a single administration of an oromucosal spray approved for treating pain and spasticity in multiple sclerosis, Sativex ® (THC/CBD, in a molecular ratio 1/1) [ 27 ], to investigate 1) whether THC/CBD would reduce leukemia/lymphoma cells in blood and 2) how an elderly population would tolerate THC/CBD.

Methods

Study design

Asymptomatic patients with CLL or leukemic (lymphocytes > 5 × 10 9 /L) mantle, follicular or marginal zone lymphomas received a single dose of THC/CBD. The primary endpoint was a reduction of malignant (clonal) B cells in blood. Blood samples were collected at four timepoints (9 am, 11 am, 1 pm, and 3 pm) on a day prior to THC/CBD and at the same timepoints on a day with THC/CBD (administered at 9 am) and 24 and 168 h after THC/CBD. The maximum tolerated dose was established by stepwise increasing the dose of THC/CBD in every third patient until two adverse events grade 2 were seen in two or more consecutive patients (using common terminology criteria for adverse events, version 4.0), starting from 2.7 mg THC and 2.5 mg CBD (one actuation of Sativex) to 18.9 mg THC and 17.5 mg CBD (seven actuations). At the scheduled interim analysis when the seven actuation-dose was identified, 10 patients had been treated and we saw an early decrease of leukemic and normal lymphocytes already 2 h (11 am) after THC/CBD, which continued to 1 pm (4 h) and started to resolve by 3 pm. To ascertain that the changes were not due to a hitherto unknown diurnal rhythm of normal lymphocytes or leukemic cells, we sampled all subsequent 13 patients (12 with CLL) also on a date prior to THC/CBD (median 6 d before [range, 1–26]), and we included an additional measurement at 10 am on the THC/CBD day (Supplementary Figure S1).

The study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee in Stockholm (2015/281-31/2 with amendments 2016/210-32 and 2017/556-32) and by the Swedish Medical Products agency and registered as EudraCT trial no. 2014-005553-39. Patients were included, after providing informed consent, between April 2016 and February 2019. The date of last follow-up was 25 June 2020.

Adverse events and peak plasma concentrations of THC and CBD will also be reported in a parallel pharmacologic manuscript describing the evaluation of measuring THC and CBD in other fluids than plasma (Melén et al., manuscript submitted).

Chemistry, pharmacology assays, and flow cytometry

Complete blood counts and other routine chemistry analyses were conducted using the facilities of the Karolinska University Laboratory. Assays of THC and CBD concentration measurement were conducted at the Department of Pharmacology using liquid chromatography–mass spectrometry method as described previously [ 28 ]. Multiparameter flow cytometry on peripheral blood samples for characterizing lymphoid and myeloid cell populations, as well as for assessing caspase-3 activation (by cleavage of active caspase substrate – PhiPhiLux) for apoptosis in CD19 + CD5+ cells, was done in the routine flow cytometry unit at the Dept. of Clinical Pathology and Cytology (Supplementary Tables S1 and S2; Supplementary Methods). Surface expression of the homing chemokine receptor CXCR4 was analyzed using flow cytometry (Supplementary Figure S2) and CXCR4high/CXCR4low ratios were calculated.

Enrichment of malignant B cells and analysis of cell proliferation

Blood samples were enriched for B cells by negative selection using RosetteSep ™ , collected using Ficoll-Paque PLUS (GE Healthcare Life Science, Marlborough, MA). The flow cytometer BD FACSCanto II (BD Biosciences, San Diego, CA) was used to determine the purity of B cells (Supplementary Methods) and data analysis was performed using the FlowJo software version 10 (Ashland, USA). Cell proliferation of enriched malignant B cells was assessed by incorporation of 3 H-Thymidine (Supplementary Methods).

RNA isolation and real-time PCR

mRNA expression levels of genes encoding for CB1 (CNR1) and CB2 (CNR2) were assessed by real-time PCR [ 24 ] after RNA isolation and complementary DNA synthesis from enriched B cells (Supplementary Methods). Custom-made primers were purchased from Invitrogen, sequences for respective genes are provided in Supplementary Methods.

Statistics

Comparisons between repeated measurements in the same individuals were done, using the Wilcoxon matched-pairs signed-ranks test. The 9 am results from the day prior to, and the day of, THC/CBD were used as separate baselines. Survival was analyzed with Kaplan–Meier curves. Assessments of other associations were conducted using Spearman, Fisher’s exact, or Mann–Whitney–Wilcoxon tests, according to the nature of the variables. p values are two-tailed and calculated using Stata version 14.2 (StataCorp LLC, College Station, TX). Apoptosis and proliferation data were analyzed using GraphPad Prism version 8 (GraphPad software Inc., La Jolla, CA). p .05 was considered significant.

Results

Twenty-three (20 with CLL) elderly patients with indolent B cell malignancy received a one-time administration of THC/CBD. The patients are described in Table 1 .

Published online:

Table 1. Clinical characteristics at inclusion.

Adverse events

The maximum tolerated dose was seven actuations (18.9 mg THC/17.5 mg CBD); this dose was given to 15 patients. Transient adverse events were seen in 21/23 patients, all grade 1 or 2; most common were dry mouth (78%), vertigo (70%), and somnolence (43%; Table 2 ). The adverse events occurred within the first 6 h, did not require hospitalization and all patients returned home at 4 pm.

Published online:

Table 2. Adverse events.

THC/CBD concentrations in plasma

The peak plasma concentrations of THC and CBD were reached at different time points for different patients. For THC, the peak concentration in plasma (median 8.8 ng/mL) was seen at 1 h (n = 5), 2 h (n = 12), and 4 h (n = 6) and ranged from 0.7 to 24.7 ng/mL. The peaks of CBD (median 4.9 ng/mL) were at 1 h (n = 7), 2 h (n = 8), 4 h (n = 7), and 6 h (n = 1), with a range of 0.2–17.3 ng/mL. The relation between the plasma concentrations of THC and CBD was linear (R 2 = 0.90; p < .00005; Figure 1 (A)). THC and CBD levels correlated with the number of actuations (p < .00005) and with the severity of adverse events (p = .043; Figure 1(B)).

Published online:

Figure 1. Peak plasma levels of THC and CBD, number of actuations and adverse events. (A) Peak plasma levels of delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), each dot representing a patient. (B) Peak plasma levels of THC and the number of actuations of THC/CBD and the worst adverse event per patient (gray dot, no adverse event; dark gray triangle, adverse event grade 1; black diamond, adverse event grade 2).

Figure 1. Peak plasma levels of THC and CBD, number of actuations and adverse events. (A) Peak plasma levels of delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), each dot representing a patient. (B) Peak plasma levels of THC and the number of actuations of THC/CBD and the worst adverse event per patient (gray dot, no adverse event; dark gray triangle, adverse event grade 1; black diamond, adverse event grade 2).

Effects of THC/CBD on blood cells

Baseline cell counts and relevant fold changes are presented in Table 3 , and representative graphs of the median values are shown in Figure 2. As expected, there was an increase of neutrophils, 4 h after THC/CBD, climaxing at 126% by 6 h (Figure 2; Table 3 ). Serum cortisol levels also increased 4 h after THC/CBD (Figure 2, Table 3 ). After THC/CBD, leukemic B cells decreased already by 10 am, reaching equal nadir at 11 am and 1 pm (11% decrease), and remained reduced at 3PM (8%; Figure 2(A); Table 3 ). There was a similar but larger reduction in normal B cells after THC/CBD, from 10 am with a nadir at 3 pm (37%; Figure 2(B); Table 3 ). There was also a decrease in CD3+ cells (nadir 35% at 3 pm; Figure 2(C); Table 3 ) but there was no change in CD4/CD8 ratio (Figure 2(D)). Decreases in CD56+ cells and in platelets were also observed (Figure 2(E,F)). Twenty-four hours after THC/CBD, no effects remained on any leukocyte subset ( Table 3 ).

Published online:

Figure 2. Changes in median levels of blood leukocyte subsets and serum cortisol levels during the days without and with THC/CBD. For simplicity, only median values are shown here, detailed data are represented in Table 3 . (A) Leukemic B cells. (B) Normal B cells. (C) CD3+ T cells. (D) CD4/CD8 ratio. (E) CD56+ NK cells. (F) Platelets. (G) Neutrophils. (H) Serum cortisol. Dashed black lines are from the day without treatment (n = 13) and solid gray lines are from the day with treatment (n = 23). All results are presented in relation to sampling at baseline (9 am) for each day. All cell-subset analyses were calculated from absolute blood counts, except CD4/CD8 (ratio). One circumflex (^) indicates significant changes at the day without treatment, with respect to baseline with p < .05. One asterisk (*) and two asterisks (**) indicate significant changes at the day with treatment, with respect to baseline with p < .05 and p < .005, respectively.

See also  Can You Mail CBD Oil

Figure 2. Changes in median levels of blood leukocyte subsets and serum cortisol levels during the days without and with THC/CBD. For simplicity, only median values are shown here, detailed data are represented in Table 3 . (A) Leukemic B cells. (B) Normal B cells. (C) CD3+ T cells. (D) CD4/CD8 ratio. (E) CD56+ NK cells. (F) Platelets. (G) Neutrophils. (H) Serum cortisol. Dashed black lines are from the day without treatment (n = 13) and solid gray lines are from the day with treatment (n = 23). All results are presented in relation to sampling at baseline (9 am) for each day. All cell-subset analyses were calculated from absolute blood counts, except CD4/CD8 (ratio). One circumflex (^) indicates significant changes at the day without treatment, with respect to baseline with p < .05. One asterisk (*) and two asterisks (**) indicate significant changes at the day with treatment, with respect to baseline with p < .05 and p < .005, respectively.

Published online:

Table 3. Changes with and without THC/CBD.

Influence of cannabinoid receptor expression

The leukemic B cells in all 23 patients expressed CB2 while 17/23 expressed CB1 ( Table 1 ). Neither CB1 nor CB2 mRNA levels changed after the administration of THC/CBD at any timepoint (p > .05 for every comparison). The six CB1-negative cases, all CLL, showed a deeper reduction after THC/CBD (15% decrease at 1 pm; p = .028) than in the CB1-positive cases (10% decrease; p = .013; Figure 3(A)).

Published online:

Figure 3. Reduction of CB1-expressing and non-expressing malignant B cells and CXCR4 surface expression. For simplicity, only median values are shown here, detailed data are represented in Table 3 . (A) Reduction of leukemic B cells after THC/CBD in CB1 positive (dashed gray line; n = 17) and CB1 negative (dotted gray line; n = 6) cases. Changes in CXCR4+/CXCR4- ratio in (B) leukemic B cells and (C) T cells.

Figure 3. Reduction of CB1-expressing and non-expressing malignant B cells and CXCR4 surface expression. For simplicity, only median values are shown here, detailed data are represented in Table 3 . (A) Reduction of leukemic B cells after THC/CBD in CB1 positive (dashed gray line; n = 17) and CB1 negative (dotted gray line; n = 6) cases. Changes in CXCR4+/CXCR4- ratio in (B) leukemic B cells and (C) T cells.

Effects on CXCR4 expression, apoptosis, and proliferation

Ratios of CXCR4high/CXCR4low were similar in CB1-negative and CB1-positive cases (median 9.4 and 9.5, respectively; p = .54) and were stable in leukemic cells and T cells when no drug had been given. However, after THC/CBD administration CXCR4high/CXCR4low ratios increased in leukemic B cells (Figure 3(B)) and T cells (Figure 3(C)) at 1 and 3 pm ( Table 3 ). Apoptosis and cell proliferation did not change at any timepoint (Supplementary Figure S3).

Existence of a diurnal rhythm in patients with CLL

Thirteen patients (12 with CLL) were sampled on a date prior to THC/CBD (median 6 d before [range, 1–26]), to ascertain any hitherto unknown diurnal rhythm of normal lymphocytes or leukemic cells. Without THC/CBD, there was a late significant reduction in leukemic cells at 1 pm only (11%; Table 3 ); other leukocyte subsets including T cells did not change (Figure 2; Table 3 ).

Long-term follow-up

Leukemic cell counts moderately increased between the non-THC/CBD day (approximately one week before therapy), the THC/CBD day, and one week after THC/CBD. The 9 am leukocyte counts went from 23.2 (day without THC/CBD) to 24.7 (immediately before THC/CBD) to 26.0 (a week after THC/CBD) x 10 9 /L (Supplementary Figure S4(A)). Thus, the increase in leukemic cells that was observed one week after THC/CBD was considered a natural, gradual increase caused by the disease.

Median follow-up was 2.8 years (range, 1.4–4.2). Seven patients required treatment after the trial, six with rituximab-bendamustine and one with ibrutinib. One patient died from a cerebral stroke and one from kidney cancer, both >2 years after the trial and without any evidence of leukemia progression. Overall survival and time to next treatment are shown in Supplementary Figure S4(B).

Discussion

Cannabinoids are increasingly prescribed for treatment of spasticity, pain, and epilepsy [ 29 ]. Some patients use cannabinoids during chemotherapy, to alleviate adverse events, such as nausea and fatigue [ 30 , 31 ]. A recent study showed that almost one-fifth of cancer patients use cannabinoids as self-treatment [ 32 ]. The effects these cannabinoids have on benign and malignant cells in vivo are not fully known, since most knowledge comes from descriptive studies and animal models.

In this trial, repeated sampling after a single dose of THC/CBD showed a quick decrease in circulating leukemic and normal B and T cells in patients with indolent B cell leukemia. To investigate whether this was due to diurnal rhythms, the same repeated samplings were conducted on a day prior to THC/CBD administration on subsequent patients. We then found that CLL cells in untreated patients display a diurnal fluctuation, with similarities to circadian rhythms. Circadian rhythms are 24-h variations in physiological processes and are generated by the expression of circadian clock genes in humans. In the CLL cells, the significant diurnal change in untreated patients might be due to an aberrant expression of clock genes. The transcription factor BMAL1 and the gene CRY1, both part of the circadian system, are described as being epigenetically inactivated in CLL [ 33 ]. We did not detect any diurnal changes in normal B or T cells within the time frame of 9–3 pm.

It was safe to administrate a single dose of THC/CBD to these elderly patients. Still, psychotropic adverse events were frequent, being the main dose-limiting toxicity. For most patients, the side effects were unpleasant, but they all could return home at the end of the day. After the first 24 h, there were neither beneficial nor adverse effects of this single THC/CBD dose, and the natural course of the disease remained unperturbed.

Sativex, containing a mixture of THC/CBD, was the only approved cannabinoid compound available to us, therefore we could not separate the effects of THC and CBD. This is a limitation of the study. Our trial did not reproduce in vitro findings of induced cell death caused by high concentrations of synthetic [ 3 , 5 , 26 ] and natural [ 4 , 34 ] cannabinoids. Indeed, the psychotropic side effects prohibited the attainment of tumoricidal plasma concentrations of cannabinoids. We cannot, however, exclude that THC/CBD acts differently than other cannabinoids previously used for in vitro studies.

Patients with CB1-negative leukemia showed a faster and deeper reduction of leukemic cell counts compared to CB1-positive cases. Normal B cells, which also have very low CB1 expression [ 7 ], behaved similarly, with a more profound decrease than leukemic B cells. We cannot in this study mechanistically explain the slower reduction of the leukemic cells in blood when both cannabinoid receptors are expressed, but it has been shown that CB1 and CB2 can form heterodimers in neurons and when such heterodimers were formed, stimulation of one receptor led to negative modulation of its partner [ 35 ]. If this also would occur in leukemic cells, CB1 stimulation would impair the stimulation of CB2. Since CB2 is involved in homing of leukocytes to secondary lymphoid tissues, this could partly explain why CB1-negative cases and normal B cells, which have very low CB1 expression, had a more profound decrease after exposure to the study drug [ 14–16 ].

We detected an increased expression of CXCR4 on the cell surface of leukemic cells and T cells from blood, at 6 h after THC/CBD. CXCR4, together with other chemokine receptors and integrins, plays an important role in the interaction between lymphoma cells and the microenvironment, increasing cell survival and drug resistance [ 36 , 37 ]. We also found that the administration of THC/CBD increased cortisol levels. Cortisol is known to affect circadian rhythms in T cells [ 38 ], and to increase CXCR4 expression in T lymphocytes [ 39 ]. It is likely that the increase of cortisol was secondary to stress from adverse events rather than directly induced by the THC/CBD [ 40 ]. Based on our findings we believe that the increase of CXCR4high expressing cells (both leukemic B cells and T cells) seen 6 h after THC/CBD is a secondary effect due to elevated cortisol levels and that this increased expression of CXCR4 is associated to a redistribution of lymphocytes from blood at 6 h. The increase of neutrophils after THC/CBD is probably also a secondary effect of cortisol and has also been observed in a study investigating the chronic use of synthetic cannabinoids [ 41 ].

However, our main finding, the fast decrease of circulating leukemic cells 1–2 h after a single dose of THC/CBD, cannot be explained by the later changes in CXCR4 expression or cortisol levels. Furthermore, THC/CBD did not affect cell proliferation or apoptosis on leukemic cells in blood. Therefore, we propose that cannabinoids induce a redistribution of malignant B cells away from blood. However, we do not know where the cells relocate to. It is possible that the cells adhere to the endothelium of blood vessels, or migrate from blood to spleen, lymph nodes, and/or bone marrow. Nevertheless, our data point toward the involvement of the cannabinoid receptors in regulation of the tissue localization of lymphocytes, as previously suggested in experimental studies in mice [ 14–16 ]. Whether chronic use of cannabinoids might result in a sustained redistribution of lymphocyte subsets is not known. In a small study of 20 multiple sclerosis patients, Sativex intake for up to six weeks did not significantly affect the levels of different blood cells populations [ 42 ].

Cannabinoids may also impact immune checkpoint control: a recent study of cancer patients with solid tumors given immune checkpoint inhibitors showed that concomitant cannabinoid use correlated with inferior time to progression and overall survival [ 43 ]. Our study demonstrates that THC/CBD affects a wide variety of immune cells in vivo, and this should be taken into consideration when cannabinoids are used to treat, for example, nausea from chemotherapy, because cannabinoid-induced immune modulation could have unforeseen effects.

We conclude that a single dose of THC/CBD causes considerable adverse events in elderly, cannabis-naïve patients but did not affect apoptosis or proliferation of the malignant cells. Instead, THC/CBD probably induced an early redistribution of malignant and benign blood cells away from blood. If the malignant cells home to lymphoid tissues and bone marrow, such a redistribution would be opposite of that induced by successful anti-tumoral therapies such as inhibitors of Bruton’s tyrosine kinase and phosphoinositide 3-kinase, where malignant cells egress from the bone marrow to the peripheral blood [ 44 , 45 ]. It is important to consider that cannabinoids might negatively interfere with anti-leukemia/lymphoma treatment. Based on our findings, this mixture of cannabinoids should not be considered as treatment for indolent lymphomas.

Cannabis Extract Treatment for Terminal Acute Lymphoblastic Leukemia with a Philadelphia Chromosome Mutation

This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Users may download, print and share this work on the Internet for noncommercial purposes only, provided the original work is properly cited, and a link to the original work on http://www.karger.com and the terms of this license are included in any shared versions.

Abstract

Acute lymphoblastic leukemia (ALL) is a cancer of the white blood cells and is typically well treated with combination chemotherapy, with a remission state after 5 years of 94% in children and 30–40% in adults. To establish how aggressive the disease is, further chromosome testing is required to determine whether the cancer is myeloblastic and involves neutrophils, eosinophils or basophils, or lymphoblastic involving B or T lymphocytes. This case study is on a 14-year-old patient diagnosed with a very aggressive form of ALL (positive for the Philadelphia chromosome mutation). A standard bone marrow transplant, aggressive chemotherapy and radiation therapy were revoked, with treatment being deemed a failure after 34 months. Without any other solutions provided by conventional approaches aside from palliation, the family administered cannabinoid extracts orally to the patient. Cannabinoid resin extract is used as an effective treatment for ALL with a positive Philadelphia chromosome mutation and indications of dose-dependent disease control. The clinical observation in this study revealed a rapid dose-dependent correlation.

Presentation of the Case

A 14-year-old female, P.K., presented with symptoms of weakness, shortness of breath and bruising when she was taken to the Hospital for Sick Children, Toronto, Canada, on the 10th March 2006. She was diagnosed with acute lymphoblastic leukemia (ALL), with >300,000 blast cells present. Acute chemotherapy followed by a standard chemotherapy regimen went on for 6 months after the diagnosis. Upon further analysis, she was found to be positive for the Philadelphia chromosome mutation. A mutation in the Philadelphia chromosome is a much more aggressive form of ALL. When standard treatment options were unsuccessful, a bone marrow transplant was pursued. She successfully received the transplant in August 2006 and was able to be released from isolation 45 days later. She was observed posttransplant by following the presence of blast cells, noted 6 months after treatment. Consequently, in February 2007, aggressive chemotherapy procedures (AALL0031) were administered along with a tyrosine kinase inhibitor, imatinib mesylate (Gleevac), 500 mg orally twice a day. In November 2007, 9 months after the transplant, the presence of premature blast cells was observed and it was determined that another bone marrow transplant would not be effective. In February 2008, in an effort to sustain the patient, another tyrosine kinase inhibitor, disatinib (Sprycel), was administered at 78 mg twice a day with no additional rounds of chemotherapy. The patient experienced increased migraine-like headaches in June 2008. After conducting a CT scan of the head in July 2008, cerebellitis was noted. It was assumed by the primary oncologist that the blast cells could have infiltrated the CNS and be present in the brain, although none were noted in the blood. By October 2008, ten treatments of radiation therapy had been administered to the brain.

See also  Peels CBD Oil

On the 4th February 2009, blood was noted in the patient’s stools and a blood cell count revealed the presence of blast cells. As a result, all treatment including the disatinib was suspended and the patient’s medical staff acknowledged failure in treating her cancer. It was charted by the patient’s hematologist/oncologist that the patient ‘suffers from terminal malignant disease. She has been treated to the limits of available therapy… no further active intervention will be undertaken’. She was placed in palliative home care and told to prepare for her disease to overwhelm her body and from which she would suffer a stroke within the next 2 months.

Cannabinoid Treatment

After this, disease progression was observed with rising counts of blast cells. The patient was receiving frequent blood transfusions and platelets during this period. Through research conducted by the patient’s family, it was observed, in a particular paper by Guzman [1] published in Nature Reviews Cancer, that cannabinoids have been shown to inhibit the growth of tumor cells in culture and in animal models by modulating key cell-signaling pathways. Cannabinoids are usually well tolerated and do not produce the generalized toxic effects of conventional chemotherapies. The family found promise in an organization known as Phoenix Tears, led by Rick Simpson who had treated several cancers with hemp oil, an extract from the cannabis plant. Rick worked with the family to help them prepare the extract.

From the 4th to the 20th of February, the patient’s blast cell count had risen from 51,490 to 194,000. The first dose of cannabinoid resin, also referred to as ‘hemp oil’, was administered orally (1 drop about the size of half a grain of rice) at 6:30 a.m. on the 21st February 2009 (day 0 in fig. ​ fig.1). 1 ). A 2-ounce Cannabis indica strain (known as ‘Chronic Strain’) was used to extract 7.5 ml of hemp oil using 1.2 liters of 99%-isopropyl-alcohol solution, which was boiled off in a rice cooker. Immediately after the dosing, the patient attempted to vomit; nausea had been observed previously and is common with this condition. To deal with the bitter taste and viscous nature of the hemp oil, it was suspended in honey, a known natural digestive aid, and then administered to the patient in daily doses. The objective was to quickly increase the frequency and amount of the dose and to hopefully build up the patient’s tolerance to cannabinoid resin (refer to fig. ​ fig.1). 1 ). The patient was observed to have periods of panic early on during administration of the hemp oil, along with increased appetite and fatigue.

Blast cell counts, days 0–15: Chronic Strain.

The blast cell count reached a peak of 374,000 on the 25th February 2009 (day 5), followed by a decrease, which correlated with the increasing dose. The daily dosing is the amount administered per dose; the doses were initially given once per day up to a total of 3 times per day by day 15, and were continued with the same average frequency throughout the treatment. A decreased use of morphine for pain, an increase in euphoria symptoms, a disoriented memory and an increase in alertness were observed; these are typical with cannabinoid use.

After day 15, the original Chronic Strain had been consumed and administration of a new strain (referred to as Hemp Oil #2) was started. This was obtained by the family from an outside source. It was noted that administering the same dose yielded a decreased response in terms of the side effects of euphoria and appetite, and the patient suffered more nausea with this hemp oil. The blast cells began to increase, demonstrated in figure ​ figure2 2 .

Blast cell counts, days 18–39: Hemp Oil #2.

There is a wide amount of variance in cannabinoid concentration amongst different strains and even in the same strain with changes in growing conditions. The amount of each dose was increased to match the response of the blast cells that had been declining previously (fig. ​ (fig.1). 1 ). After day 27, there was another peak blast cell count of 66,000 followed by a rapid decrease. There were elevated levels of urate present in the blood with corresponding joint pain; it was established that this was caused by tumor lysis syndrome of the blast cells. Allopurinol was administered.

On the 1st April 2009 (day 41), an infected central line with tunnel infection was noted on a blood test and the patient was admitted with a heavy antibiotic regimen of intravenous tazocin, gentamicin and vancomycin. On day 43, a new batch of hemp oil from an Afghan/Thai strain (referred to as Hemp Oil #3) prepared by the family was administered. A stronger psychosomatic response and increased fatigue were observed, so dosing was adjusted to 0.5 ml, shown in figure ​ figure3. 3 . Due to hospital restrictions, dosing was limited to twice a day.

Blast cell counts, days 44–49: Hemp Oil #3.

A new batch of hemp oil was obtained by the family from an outside source and the dosing regimen continued twice a day, shown in figure ​ figure4 4 .

Blast cell counts, days 50–67: Hemp Oil #4.

After returning home from the hospital on the 11th April (day 51), the patient suffered from intense nausea, an inability to eat and overall weakness. On the 13th April, the patient was readmitted to the SickKids Hospital and was treated for refeeding syndrome. This was the outcome of stopping total parenteral nutrition too quickly and causing shock to the patient’s body while she was being treated for the infection. The dosing regimen was intermittent until day 59, remaining at 1–2 doses per day of 0.5 ml. As the blast cells began to increase and the patient’s appetite increased, the dosing frequency was again increased to 3 times per day starting on day 62, and the amount administered was increased from day 65.

On day 68, a new batch of medicine was obtained by the family from an outside source (referred to as Hemp Oil #5), shown in figure ​ figure5 5 .

Blast cell counts, days 69–78: Hemp Oil #5.

Dosing was maintained 3 times a day at 1.0 ml. On day 78, the patient had stomach pain in the morning and was admitted to hospital. Upon X-ray, it was noted that gastrointestinal bleeding had occurred. The patient was under a DNR order and ultimately passed away due to the bowel perforation. A prior history of pancolitis documented by CT scan in March 2009 pointed to neutropenic colitis with perforation as the cause of death. Furthermore, prior to starting on the hemp oil treatment, the patient had been extremely ill, severely underweight and had endured numerous sessions of chemotherapy and radiation therapy in the course of 34 months.

As reported by Hematology/Oncology at SickKids: ‘At admission her total WBC was 1.4, hemoglobin was 82, platelet count 8,000. She was profoundly neutropenic… a prior history of pancolitis documented by CT scan in March 2009 was neutropenic colitis with perforation… her abdomen was distended and obviously had some signs of diffuse peritonitis. The abdomen X-ray was in favour a perforation…she passed away at 10:05 in the present (sic) of family…’.

Discussion

Figure ​ Figure6 6 is a summary of dose response to all the batches of hemp oil administered over a total of 78 days.

Response to hemp oil treatment over 78 days.

The results shown here cannot be attributed to the phenomenon of ‘spontaneous remission’ because a dose response curve was achieved. Three factors, namely frequency of dosing, amount given (therapeutic dosing) and the potency of the cannabis strains, were critical in determining response and disease control. In the figure, it can be seen that introducing strains that were less potent, dosing at intervals >8 h and suboptimal therapeutic dosing consistently showed increases in the leukemic blast cell count. It could not be determined which cannabinoid profiles constituted a ‘potent’ cannabis strain because the resin was not analyzed. Research is needed to determine the profile and ratios of cannabinoids within the strains that exhibit antileukemic properties.

These results cannot be explained by any other therapies, as the child was under palliative care and was solely on cannabinoid treatment when the response was documented by the SickKids Hospital. The toxicology reports ruled out chemotherapeutic agents, and only showed her to be positive for THC (tetrahydrocannabinol) when she had ‘a recent massive decrease of WBC from 350,000 to 0.3’ inducing tumor lysis syndrome, as reported by the primary hematologist/oncologist at the SickKids Hospital.

This therapy has to be viewed as polytherapy, as many cannabinoids within the resinous extract have demonstrated targeted, antiproliferative, proapoptotic and antiangiogenic properties. This also needs to be explored further, as there is potential that cannabinoids might show selectivity when attacking cancer cells, thereby reducing the widespread cytotoxic effects of conventional chemotherapeutic agents. It must be noted that where our most advanced chemotherapeutic agents had failed to control the blast counts and had devastating side effects that ultimately resulted in the death of the patient, the cannabinoid therapy had no toxic side effects and only psychosomatic properties, with an increase in the patient’s vitality.

The nontoxic side effects associated with cannabis may be minimized by slowly titrating the dosing regimen upwards, building up the patient’s tolerance. The possibility of bypassing the psychoactive properties also exists, by administering nonpsychoactive cannabinoids such as cannabidiol that have demonstrated antiproliferative properties. Furthermore, future therapies could examine the possibility of upregulating a patient’s endogenous cannabinoids to help combat leukemic cells. It goes without saying that much more research and, even more importantly, phase clinical trials need to be implemented to determine the benefits of such therapies. Laboratory analysis is critical to figure out the constituents/profiles/ratios of the vast cannabis strains that show the most favored properties for exerting possible anticancer effects. Despite the nonstandardization of the medicines, the dose was readily titrated according to the biological response of the patient and produced a potentially life-saving response, namely, the drop in the leukemic blast cell count.

There has been an abundance of research exhibiting the cytotoxic effects of cannabinoids on leukemic cell lines in the form of in vitro and in vivo studies [1, 2, 3, 4]. An oncology and hematology journal, Blood, has published numerous papers [2] over the years constructing the biochemical pathway to be elicited by the anticancer properties of cannabinoids. Our goal, upon examination of this significant case study which demonstrated complete disease control and a dose response curve, is to invest effort in and to focus on research and development to advance this therapy. An emphasis needs to be placed on determining the correct cannabinoid ratios for different types of cancer, the best method of administration, quality control and standardization of the cannabis strains and their growing conditions as well as therapeutic dosing ranges for various cancers contingent on staging and ages. Toxicity profiles favor therapies deriving from cannabis because toxicity within the body is greatly reduced and the devastating side effects of chemoradiation (i.e. secondary cancers or death) can be eliminated. It is unfortunate that this therapy does come with some unwanted psychosomatic properties; however, these might be eliminated by target therapies of nonpsychoactive cannabinoids such as cannabidiol which has garnered much attention as being a potent anti-inflammatory and possible antileukemic and anticancer agent. It is acknowledged that significant research needs to be conducted to reproduce these results and that in vitro studies cannot always be reproduced in clinical trials and the human physiological microenvironment. However, the numerous research studies and this particular clinical case are powerful enough to warrant implementing clinical trials to determine dose ranges, cannabinoid profiles and ratios, the methods of administration that produce the most efficacious therapeutic responses and the reproducibility of the results. It is tempting to speculate that, with integration of this care in a setting of full medical and laboratory support, a better outcome may indeed be achieved in the future.

References

1. Guzman M. Cannabinoids: potential anti-cancer agent. Nat Rev Cancer. 2003; 3 :745–755. [PubMed] [Google Scholar]

2. Powles T, Poele RT, Shamash J, Chaplin T, Propper D, Joel S, Oliver T, Liu WM. Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway. Blood. 2005; 105 :1214–1221. [PubMed] [Google Scholar]

3. McKallip RJ, Jia W, Schlomer J, Warren JW, Nagarkatti PS, Nagarkatti M. Cannabidiol-induced apoptosis in human leukemia cells: a novel role of cannabidiol in the regulation of p22 phox and Nox4 expression. Mol Pharmacol. 2006; 70 :897–908. [PubMed] [Google Scholar]

4. Murison G, Chubb C, Maeda S, Gemmell MA, Huberman E. Cannabinoids induce incomplete maturation of cultured human leukemia cells. Proc Natl Acad Sci. 1987; 84 :5414–5418. [PMC free article] [PubMed] [Google Scholar]

Leukemia

Did you know that cannabis can alleviate some symptoms of cancer and the painful side effects of certain cancer treatments? Since cannabinoid treatments are growing in availability, cancer patients are increasingly beginning to look to medical marijuana to help fight their cancer.

Medical marijuana is becoming more popular as a treatment for leukemia due to its cancer cell fighting properties and therapeutic effects. You may find that knowing more about the benefits of medical marijuana and leukemia may help you better cope with the condition and its treatment.

How Marijuana Can Be an Effective Treatment for Leukemia

New research has revealed that cannabinoids increase the effectiveness of chemotherapy treatments in leukemia patients. UK researchers found that THC and CBD, the two major cannabinoids, were both effective when combined with chemo. However, the effect dramatically improved when used simultaneously. Pot’s overall medical effects also increase when you pair marijuana with coconut oil or other substances.

See also  CBD Oil Crossfit

To relieve nausea associated with chemo and cancer-related pain, many patients often turn to cannabis and leukemia treatment. But weed has recently been growing in popularity as a treatment for leukemia and other types of cancer.

Evidence shows that medical cannabis is a viable treatment option for leukemia. Researchers found that the THC cannabinoids in medical marijuana can kill leukemia cells. Research also shows that, unlike chemo that targets cancer cells and healthy cells alike, medical pot only targets the cancer cells, not the healthy cells.

Researchers credit the widespread medical applications of marijuana to the endocannabinoid system (the natural cannabinoid system of your body.) What they found is that cannabinoid receptors are in many parts of your body, even your white blood cells. Because of this, researchers are continuing their promising investigation of marijuana for leukemia.

Leukemia & Medical Marijuana Research

A study from 2005 looked into the role of mitogen-activated protein kinases (MAPKs) in cannabinoid-induced leukemia cell death. Some types of MAPKs take part in apoptosis and autophagy, or cell death and turnover. Understanding how cannabis causes cancer cell death can help us learn how to make better treatments, so the researchers behind this study specifically examined the CB2 receptor.

Before observing the cell death process, the team reaffirmed that their leukemia cells had CB2 receptors. After confirming their presence, they administered THC and another CB2-related cannabinoid. A type of MAPK called p38 MAPK activated in response to CB2 receptor stimulation, showing a link. Blocking p38 MAPK lessened the CB2 receptor’s ability to kill leukemia cells.

Another study supported the possibility of using cannabis as a supplement to radiation therapy. When a team from Israel observed the effects of CBD and a synthetic counterpart on leukemia cells, they recorded the effects that occurred in cells with and without prior gamma radiation exposure.

While the compounds killed plenty of leukemia cells on their own, they worked even better when used after radiation therapy. Without radiation, CBD killed about 61% of cells, while the synthetic counterpart killed around 43% of leukemia cells. But, those numbers respectively rose to 93% and 95% for cells with previous radiation exposure.

What Symptoms of Leukemia Can Medical Marijuana Treat?

Medical marijuana helps ease the following cancer symptoms in patients:

  • Nausea
  • Vomiting
  • Pain
  • Lack of appetite

Best Strains of Marijuana to Use for Leukemia

Pain is a common and dreaded chemotherapy side effect. While marijuana might not be something you’re interested in, it can help relieve chronic pain. Many patients prefer it over opioid painkillers.

Painkilling strains of marijuana include:

  • Chemo (Indica)
  • Blackberry Kush (Indica)
  • Death Star (Indica)

Depression fighting strains include:

  • Harlequin (Sativa)
  • Trainwreck (Hybrid)
  • CBD Critical Cure (Indica)
  • White Widow (Hybrid)

Fatigue and Insomnia fighting strains include:

  • White Widow (Hybrid)
  • Granddaddy Purple (Indica)

Nausea and Vomiting strains include:

  • Lavender (Indica)
  • Chernobyl (Hybrid)

Stress fighting strains include:

  • Moby Dick (Sativa)
  • Blue Dream (Hybrid)

Lack of Appetite strains include:

  • Granddaddy Purple (Indica)

Best Methods of Marijuana Treatment to Treat Leukemia Symptoms

With medical cannabis growing in popularity, there are many new methods of consuming marijuana. These newer methods allow you to benefit from the plant’s therapeutic potential for leukemia and other medical conditions.

When you think about medical weed, your first thought is probably an image of someone lighting up a joint. Although this is a popular way to consume this miracle drug, it’s not the healthiest. By inhaling cannabis, most of the cannabinoids are entering your body through your lungs and passed to your bloodstream. Because of this direct exchange, you’re shortening its effect.

Some better methods of consuming your medical weed include:

  • Vaporizing
  • Edibles
  • Juicing
  • Transdermal patches
  • Sublingual uptake
  • Oils
  • Tinctures
  • Topicals

Even though medical marijuana is presently federally illegal in the U.S., it’s legal in many states for valid medical use. To qualify for medical cannabis, you must first receive a diagnosis of a qualifying condition and obtain a local doctor’s recommendation for a medical marijuana card.

To find out if your state has legalized the use of medical cannabis, you can check our list. Then just search for a medical marijuana doctor to receive your cannabis for leukemia.

What Is Leukemia?

Leukemia is blood cell cancer. It begins in your bone marrow, which creates your blood cells. With leukemia, immature blood cells turn into cancer. Blood cells have different functions:

  • Red blood cells transport oxygen to all areas of your body.
  • White blood cells assist your body in fighting infection.
  • Platelets help with blood clotting.

With leukemia, abnormal white blood cells known as leukemia cells form from your bone marrow. These abnormal cells don’t do the work that your normal white blood cells do. They grow faster than normal cells, and they continue to grow when they shouldn’t.

As time passes, leukemia cells begin crowding out your healthy blood cells. Serious problems can arise from this such as bleeding, infections and anemia. Leukemia cells may also begin spreading to your lymph nodes or other organs, resulting in pain or swelling.

Leukemia may come on quickly or gradually. Slow growing leukemia is chronic. With acute leukemia, abnormal cells increase in number quickly.

Patients who have slow-growing leukemia may not have symptoms. Patients who have quick-growing types of leukemias may experience symptoms, including:

  • Frequent infections
  • Weight loss
  • Fatigue
  • Physical weakness
  • Easy bruising
  • Bleeding easily
  • Slow-healing wounds
  • Anemia
  • Bone pain
  • Petechiae
  • Shortness of breath
  • Swollen or enlarged gums
  • Feeling full or bloated
  • Enlarged spleen
  • Fever and chills
  • Night sweats
  • Headaches
  • Unusual pallor
  • Swollen lymph nodes

These symptoms may start off mildly but can become more pronounced as leukemia advances.

Children often develop acute leukemia while adults may have either acute or chronic. Doctors can cure some types of leukemia. Other types of leukemia can’t be cured and can only be controlled.

Treatments might include radiation, chemotherapy or stem cell transplantation. These are the most common treatments although there are several others described below. You may require therapy even if your symptoms go away, to prevent a relapse.

Types of Leukemia

There are several types of leukemia, categorized by the type of white blood cells affected and the rate in which it worsens.

The four primary types of leukemia are:

  • Acute myelogenous leukemia (AML)
  • Acute lymphoblastic leukemia (ALL)
  • Chronic myelogenous leukemia (CML)
  • Chronic lymphocytic leukemia (CLL)

Acute Myelogenous Leukemia (AML)

AML causes your body to generate too many white blood cells, known in this case as myelocytes. Leukemia cells begin building up in your bone marrow and blood, leaving less room for your healthier blood cells. The symptoms of AML include easy bleeding, infections and anemia. AML affects men more than women. It also affects kids. As you age, the incidence of AML can increase.

Acute Lymphoblastic Leukemia (ALL)

ALL also causes your body to generate too many white blood cells known as lymphocytes. These leukemia cells can’t fight infection effectively. The cells build up in your bone marrow and blood and don’t leave much room for your healthy blood cells. Easy bleeding, infections and anemia can result. ALL typically develops and worsens in a very short span of time.

Chronic Myelogenous Leukemia (CML)

CML causes the same reaction as AML and ALL. It worsens slowly and is more common in men than it is in women. CML is most common in adults in their 50s, and rarely affects children.

Chronic Lymphocytic Leukemia (CLL)

The same reaction happens with CLL as the other leukemia types. It’s most common in adults who are in their 60s, and more common in men than women. Children don’t often develop CLL. Patients with CLL tend to get more infections since it compromises the immune system.

There are other types of leukemia that aren’t as common, such as hairy cell leukemia. Leukemia also has subtypes, like the subtype of AML known as acute promyelocytic leukemia.

History of Leukemia

In 1845, John Hughes Benett officially identified leukemia as a diagnosis in Edinburgh. In the 19th century, other European physicians recognized abnormally high white blood cell levels in their patients, calling it “weisses blut” that meant “white blood.” Today, “leukemia” comes from the Greek terms “leukos” and “heima” that also means “white blood.”

The formation of four types of leukemia occurred in 1913. They were:

  • Chronic myelogenous leukemia
  • Chronic lymphocytic leukemia
  • Erythroleukemia
  • Acute lymphocytic leukemia

In 1970, doctors confirmed that some patients could be cured of leukemia. By the 1980s, leukemia survival rates were approximately 70 percent.

Effects of Leukemia

The symptoms you experience with leukemia depend on what type of the disease you have. Common signs and symptoms of leukemia may include:

  • Weakness, persistent fatigue
  • Chills or fever
  • Weight loss without trying
  • Severe or frequent infections
  • Recurrent nosebleeds
  • Enlarged spleen or liver, swollen lymph nodes
  • Easy bruising or bleeding
  • Excessive sweating, particularly at night
  • Bone tenderness or pain
  • Petechiae (small red spots on the skin)

Besides the physical effects of leukemia, this disease can also affect your mental well-being. A cancer diagnosis can change your life. It may overwhelm you, and the side effects of treatment can make it difficult to handle everyday life stresses.

Your mood can change at any time once you receive your diagnosis. Some people struggle with anxiety or depression immediately following their diagnosis. Other people’s mood may change during treatment. Your body may have both mental and physical reactions to cancer treatment.

Although it’s harder to recognize mental changes, they can be just as hard to deal with as physical changes. However, it’s important to recognize and manage changes in mood. Some mood change symptoms may include:

  • Depression or feeling down
  • Irritability
  • Difficulty remembering and concentrating
  • Changing emotions like anger or crying
  • Problems with sexual performance or loss of sexual interest
  • Loss of motivation and energy
  • Excessive sleeping, insomnia or other changes in sleep
  • Fatigue
  • Loss of interest in socializing, activities and social events
  • Changes in appetite (loss of appetite or overeating)
  • Suicidal thoughts or feeling life isn’t worth living
  • Feelings of worthlessness or hopelessness
  • Anxiety
  • Excessive or frequent fear, worry, or uneasiness
  • Increasing interest in alcohol
  • Panic attacks

Leukemia Statistics

  • Around every three minutes, in the U.S., one person receives a blood cancer diagnosis
  • In the U.S. in 2017, around 172,910 individuals are expected to get a diagnosis of leukemia
  • New leukemia cases in 2017 in the U.S. are projected to comprise around 10.2 percent of the 1,688,780 new cancer diagnosis case estimate
  • Leukemia accounts for nearly one out of three cancers and is the most common cancer in teens and children
  • Acute lymphocytic leukemia makes up around three out of four leukemia cases among teens and children
  • Acute lymphocytic leukemia is the most common cancer in early childhood and peaks between two and four-year olds

Current Treatments Available for Leukemia and Their Side Effects

To recommend a treatment protocol for leukemia, doctors perform several tests to diagnose the condition. These include conducting a complete blood count and performing a tissue biopsy from your bone marrow and possibly other organs such as your spleen and liver.

Treatments for cancer, such as chemotherapy medications, may impact how you feel physically and emotionally. They may disrupt your sleep and cause nausea, depression, loss of appetite, fatigue and anxiety.

Your leukemia treatment plan depends on several factors. Your physician recommends the treatment best for your leukemia case based on your overall health, age, the type you have and if the cancer is spreading to other body parts.

Common treatments doctors typically prescribe for leukemia include:

Chemotherapy

Chemo is a major type of leukemia treatment. It consists of chemicals that kill leukemia cells. Your doctor may give you one dose or a mixture of drugs depending on your type of leukemia. It may come as an injection or a pill.

Side effects of chemotherapy include:

  • Pain
  • Fatigue
  • Nausea and vomiting
  • Throat and mouth sores
  • Constipation
  • Diarrhea
  • Nervous system effects
  • Blood disorders

Biological Therapy

Biological therapy helps your immune system identify leukemia cells and attack them.

Side effects of biological therapy include:

  • Weakness
  • Fever
  • Chills
  • Joint or muscle aches
  • Nausea or vomiting
  • Headache
  • Dizziness
  • Fatigue
  • Heightened or lowered blood pressure
  • Occasional breathing difficulties

Targeted Therapy

Targeted therapy attacks specific cancer cell vulnerabilities. For instance, Gleevec (imatinib) stops protein action in leukemia cells when you have chronic myelogenous leukemia helping to control leukemia.

Side effects of targeted therapy include:

  • High blood pressure
  • Skin problems such as dry skin, hair depigmentation, acneiform rash, nail changes
  • Gastrointestinal perforation
  • Problems with wound healing and blood clotting

Radiation Therapy

Radiation therapy consists of high-energy beams like X-rays that damage leukemia cells, stopping them from growing. Your doctor may apply radiation over your entire body or just a certain area of your body if there’s a concentrated group of leukemia cells. The doctor may give you radiation therapy before a stem cell transplant to prepare you for the procedure.

Side effects of radiation therapy include:

  • Fatigue
  • Skin problems such as itching, dryness, peeling
  • Dry mouth
  • Nausea
  • Shortness of breath
  • Diarrhea

Stem Cell Transplant

A stem cell transplant replaces unhealthy bone marrow with bone marrow that’s healthy. You’ll receive a high dose of radiation therapy or chemotherapy before your stem cell transplant procedure to destroy your unhealthy bone marrow. Your doctor will then give you an infusion that contains stem cells that form blood to help rebuild your bone marrow. Your doctor may use your stem cells or stem cells from a donor.

How useful was this post?

Click on a star to rate it!

Average rating 3 / 5. Vote count: 1

No votes so far! Be the first to rate this post.